Subarachnoid Haemorrhage
Understanding the headache none of use want to miss
About 2% of ED headaches (goes to 12% when “worst ever headache” is considered)
Traumatic and Non traumatic
(will skip over traumatic as we are talking about the presenting complaint of headache, not trauma)
Fatality around 50% BUT many die prior to reaching hospital, of survivors 1/3 significantly disabled
Has a mean age of 50 (younger than other strokes)
Can be split into Vascular Rarities eg AMV, dissection, tumour, aneurismal and non aneurismal
Aneurismal
¾ of all non traumatic SAH from rupture of saccular aneurysm
2-3% of the population has these aneurysms
Linked to polycystic kidneys and connective tissue disorders
Risk factors: Modifiable: smoking, alcohol, HTN
Non Aneurismal
Half of these are due to perimesencephalic haemorrhage
- Have normal angios
- Good outcome with no specific treatment needed
Most SAHs are arterial bleeds with direct communication between BP and subarachnoid space causing the sudden onset of symptoms (particularly headache and LOC)
Suggestions that perimesencephalic haemorrhages maybe venous (slower onset but also better outcomes)
Blood in the subarachnoid space can lead to
- Meningism
- Hydrocephalus
- Cerebral oedema
- Raised ICP
Post intial insult morbitity and mortality related to rebleeding or vasospasm
Complications
- Neurogenic cardiac dysfunction]
- Electrolyte problems (particularly hyponatraemia, hyperglycaemia and hypomagnesaemia)
Presentation
Likelihood corrolates with reduced GCS or neurology
BUT about 50% have normal neurology at presentation
Features of the headache: worst ever, rapid onset, seizure, >40 neck pain, neck stiffness/ limited flexion or transient LOC
Headache failing to reach maximal intensity within a few mins is unlikely to be SAH, usually SAH headache is within seconds.
The headache will last atleast an hour and usually 1-2 weeks
Severity of the headache is less important than the onset time (more subjective)
Site and character irrelevant (maybe helpful in chronic headache suffers, ?is it different to their usual headache)
Signs:
Maybe specific ie hard neurology
Sometimes more vague eg vomiting, visual disturbance
Complications can be clues eg neurogenic cardiac disturbance/pulmonary oedema, ECG changes suggesting MI
Investigate
Easy ones are the reduced GCS or focal neurology
Neurologically pristine patients (or subjective neurology) provide a different challenge
Ottawa SAH rule (useful but the study to make it valid in the UK was delayed by COVID)
Non- Con CT head
Intial weapon of choice
About 92-3% sensitive (pushes towards 100% if performed within 6hrs)
At 3 days about 85% sensitive and 50% at 1 week
Pattern of blood can help suggest perimesencephalic haemorrhage or aneurismal
The sensitivity gap means that non-diagnostic or normal CTs need an LP
LP
Allows for measuring of opening pressures as well as xanthachromia
12hrs from index episode of headache to allow for the production of Haemoglobin break down products (Oxyhaemoglobin in 2-3hrs, bilirubin closer to 12hrs and methaemoglobin)
The bilirubin content allows for distigishing between traumatic tap and SAH – but will degrade in light or when the cells haemolyse (ie pneumatic pods or delay in getting to the lab)
To summarise investigations
- Non- con CT as initial
- If done in 6hrs SAH can be ruled out
- If needing LP, should be done 12hr post headache
- If both negative within 2 weeks then SAH can be ruled out
>2 weeks need specialist involvement ?MRA
CTA tends to be the next investigation after diagnosis to look for an aneurysm, this doesn’t really change on the type of bleed as perimesencephalic bleeds can be from a basilar artery aneurysm
Catheter angiography is the gold standard and is used in appropriate patients
Classifications
Hunt and Hess:
World Federation of Neurosurgeons SAH grading system
Management
Initial management of all headaches should be analgesia and antiemetics
Needs definitive management if concerns about aneurismal SAH
- Rebleed rate of 2-4% in first 24hrs and 15-20% in 2 weeks
No evidence for use of antifibrinolytics eg TXA, aminocaproic acid
Best way to reduce rebleeding risk is BP control to 160mmHg as a max ( have maintain cerebral perfusion – Cerebral Perfusion = BP-ICP) (mannitol, labetalol)
Vasospasm
If presents clinically (doesn’t always) then typically with a “delayed cerebral ischaemia” – unlike thromboembolic stroke its gradual onset
The bigger the SAH the more likely spasm is to happen – also if there was any LOC its more likely
Nimodipine is effective in prevention and treatment of vasospasm