Subarachnoid haemorrhage Flashcards
Define SAH.
Bleeding into space between pia mater and arachnoid membrane.
What is the aetiology of SAH?
Traumatic or spontaneous
Rupture of blood vessel in subarachnoid space –> release of blood into CSF –> rapid rise in ICP
What are the causes of SAH?
What is the most common cause?
Traumatic - head injury e.g. bridging vein tear
Spontaneous - arterial origin e.g. saccular ‘berry’ aneurysm (85% of all SAH cases) rupture, AVM
What are the risk factors for SAH?
- Female, elderly
- Smokers
- Associated conditions e.g. saccular aneurysms, Ehlers-Danlos syndrome, Marfan syndrome, PCKD
- SCD
- Coagulopathy
What are the complications of SAH?
- Rebleeding - most occur within 12hrs, affects 10% of cases and has 70% mortality. May occur 2 weeks after SAH, increased in those with HTN, anxiety, seizures post-SAH
- Vasospasm (delayed cerebral ischaemia) - usually 7-14 days after onset
- Hydrocephalus
- Sympathetic hyperactivity due to increased ICP –> raised adrenaline levels, pulmonary vasoconstriction –> neurogenic pulmonary oedema
- Hyponatraemia (SIADH)
- Meningitis
- Seizures
What are the clinical features of SAH?
- Thunderclap headache
- Severe headache (‘worst ever’)
- Nausea, vomiting
- Focal neurological deficit e.g. CNIII palsy (ptosis, down and out eye, mydriasis, loss of pupillary reflex), CNVI palsy
- Aseptic meningitis due to irritation –> neck pain, stiffness, photophobia
- Optic disc swelling, retinal haemorrhages, tachycardia
- ECG changes- wide QRS, long QT, short PR, U waves, dysrhythmias
How is SAH graded on CT?
Fisher scale grading
* Group 1 - no haemorrhage
* Group 2 - blood depositions <1mm without blood clots
* Group 3 - blood depositions >1mm with localised clots
* Group 4 - diffuse/lack of SAH with extension to ventricles, brain parenchyma
Hydrocephalus - causes a “mickey mouse” ventricular system appearance
What do investigations show in SAH?
- CT (first line) - hyperdense/bright bleed on CT typically seen in basal cisterns, sulci and ventricles in severe cases
- LP - raised erythrocytes, yellow colouration on centrifugation due to xanthochromia (only positive about 3-4 weeks after SAH)
- Bloods - may show coagulopathy abnormalities
What is the management of SAH?
Needs to be done within 24hrs otherwise rise of rebleeding.
Medical:
* Antihypertensives - beta-blockers, hydralazine, calcium channel blockers, ACE inhibitors - keep BP < 140 to avoid rebleed
* Anti-vascoconstriction treatment - CCB (nimodipine), recombinant TPA
* ICP treatment - osmotic, loop diuretics
* IV midazolam
* Seizure tx - penytoin, phenobarbital
* Pulmonary oedema treatment - diuretics, dobutamine
Once CT or LP confirms SAH give medical treatment and prepare to have CT angiography +/- coiling if there are aneurysms.
Surgical:
* Endovascular coiling
* Craniotomy with clipping/coiling of aneurysm
* CSF drainage
* Transluminal balloon angioplasty
* Shunt
* Ventriculostomy
What % of cases of SAH is CT negative in?
7%
What distinguishes true SAH from ‘traumatic tap’ on LP?
Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).
NB: LP is performed at least 12 hours following the onset of symptoms and up to 2 weeks, to allow the development of xanthochromia (the result of red blood cell breakdown).
What should be done once SAH is confirmed on CT?
Referral to neurosurgery as soon as SAH confirmed
Need to identify cause of spontaneous SAH:
* CT angiogram
* +/- digital subtraction angiogram (catheter angiogram)
What is shown on this CT?
CT image shows:
* diffuse subarachnoid haemorrhage in all basal cisterns, bilateral sylvian fissures and the inter-hemispheric fissure.
This case demonstrates the typical distribution that takes the blood into the subarachnoid space in a subarachnoid hemorrhage.
How is vasospasm prevented in SAH?
Nimodipine (CCB) which targets brain vasculature - not fully understood how it works
