hrhodes's version from 2015-10-13 19:22

SAH General demographics and features

Question Answer
Who gets SAH?F>M, mean age 50-55yrs; 1-4% of headache presentations to ED
What are the Causes of SAH?1. Ruptured berry (saccular) aneurysm (70%) 2. Isolated perimesencephalic SAH (15%) 3. AVM: 0.01% 4. Other: mycotic aneurysm, TRAUMA, angioma, severe HTN, tumour, vasculitis
Where is the most common site for a berry aneurysm?85% = Anterior COW
Where are berry aneurysms found in descending order of likelihood?85% anterior COW, 30% ACA and accA, 25% ICA/PCA, 25% bifurcation ICA, 15% multiple, 5% VBA
Name some risk factors for SAH F:M 2:1; prev SAH (most important); FH in 1st/2nd deg 4x incr risk; smoking 3-10x incr risk; HTN mild incr risk; Con tissue disorders (coarctation, Marfan’s, Ehler-Danlos, neurofibromatotis, PCKD); ETOH binges; anticoagulation
How many people have a warning bleed and when?50%, 10 days before often during activity
What percentage of people have onset of symptoms during activity?20%

SAH Signs and symptoms

Question Answer
What features in PMH make SAH more likely?migraine; vomiting++; transient LOC (highly spec; 2/3 have decr LOC) 20% of people have one of these
When is maximal headache likely to occur?Within 2 hrs after thunderclap. If maximal headache >6hrs, less likely to be SAH
Aside from headache what other features can patients present with?meningism in 75% (takes 3-24hrs to develop); coma 50%; seizures 20%
Can SAH present with only syncope?Not typically. If syncope is part of symptoms usually accompanied by headache pre or post
What do isolated CN lesions suggest?progressive enlargement of enraptured aneurysm
Where do cranial nerve signs correspond to?CN III = PCA/ICA ; CN VI = cavernous sinus; also results from incr ICP; CN I = supraclinoid
What sign is pathognomonic of non-traumatic SAH and how often dod you find it?Subhyaloid haemorrhage. <25% This is called Terson syndrome

SAH grading system

Question Answer
What grading system is used and how many grades for SAH?Hunt and Hess. 5 grades. 1=good
Describe the grades of the Hess and Hunt systemI: minimal symptoms - 70% survival II: mod-severe headache; nuchal rigidity; maybe CN palsy - 60% survival III: drowsy, confused, mild FND - 50% survival IV: stupor, hemiparesis - 40% survival V: coma, decerebrate, moribund - 10% survival
What percentage of SAH is misdiagnosed on initial ED presentation?5-12%

SAH imaging

Question Answer
What investigations do you want to do in SAH?CT head, LP, ECG, ? angiography/MRI
how sensitive and specific is CT head?80-90% sens, 95% spec
When is CT most sensitive?<12hrs 97.5%. 12-24hrs = 95%, then drops by 10% per day
What will make a CT less sensitive?Hb <10, small aneurysm, few clinical signs
Is Non con CT helpful in finding site of aneurysm?Yes - particularly in anterior circulation
What test do you do if you find a SAH on CT?Helical CT angiogram: perform immediately after CT head if find SAH; 90% sens for >3mm aneurysm
When would you use Cerebral angiography? before OT or if –ive CT/LP and high suspicion (Prev SAH, history of polycystic disease); defines anatomy, shows vasospasm, shows AVM / mycotic aneurysm
What are the negatives of cerebral angiography?underestimates size of aneurysms; may miss up to 20% aneurysms; causes rupture in 2%
How sensitive is MRI in SAH?sens 85%; less sens than CT for blood
If you find an enraptured aneurysm on CTA, what is the risk of rupture when as symptomatic?8.3%

SAH other investigations

Question Answer
When do you do an LP?normal CT + no CI (GCS 15, no papilloedema, normal neuro exam, no neck stiffness)
What are the contraindications to doing a LP in SAH?GCS <15, papilloedema, abnormal clinical exam, neck stiffness
What combination of tests can reliably exclude SAH?Negative NCCT <12hrs, No xanthochromia >12 hrs and only 0-5 RBC
How quickly can xanthochromia develop?6-12 hrs from SAH, but as quickly as 2 hrs in CSF tube form bloody tap
How is xanthochromia produced?Bilirubin breakdown in vivo and oxyhameoglobin breakdown in vitro and in vivo
Does a reducing RBC count in successive tubes reliably confirm a traumatic tap and exclude SAH?NO, some SAH can produce this. You need absence of xanthochromia and <5 RBC
If you have a negative NCCT, LP with RBC >10 and no xanthochromia, can SAH be excluded?no, need CTA
What counts as a positive LP for SAH?>100,000 RBC traumatic tap in 20%; probably traumatic if clearing of blood in tubes 1-3 but this is not proven, xanthochromia, clot formation, proportion of RBC to WBC same as in blood
What ECG do you expect to find?ST changes in inf leads, wide QRS, prolonged QT, peaked/inverted T waves
What abnormalities will you find in Bloods?mild incr trop in 20%; hypoNa

SAH Complications

Question Answer
What is the incidence of rebleeding? 10-30% in 2-5 days 50% in 6/52 50% mortality if rebleed. Rebleed is BAD so coil or clip
What is the incidence of vasospasm and delayed neuro deficit? Rule of 30s - 30% 4-14 days 30% mortality, 30% permanent deficit;
When is vasospasm most likely to occur?2days - 3weeks
How can you prevent vasospasm related complications?nimodipine
How quickly should nimodipine be started?Within 96hrs
What is the best predictor of rebleed and vasospasm?amount of blood seen on initial CT trt with hypertension and hypervolaemia
What controllable features are associated with rebreeding?Hyperglycaemia, uncontrolled temperature
What aim of BP control?Premorbid, or around 140 systolic
Aside form rebreeding and vasospasm what other complications of SAH are there?CNS: Hydrocephalus 15% , seizures 35%, cerebral oedema, subdural haematoma, ICH, global cerebral ischameia. CVS: Prolonged QT, myocardial dysfunction, VTE, high trop, Resp: APO, resp failure, Metabolic: SIADH, low Na
Given that seizures can complicate up to 30% of SAH, should all ED pts get anticonvulsants prophylactically?No, Controversial. Not indicated but aggressive rx once had any suggestion of seizure

SAH Management

Question Answer
Outline ABCDE managementA: raise head 30deg; B: aim pCO2 30-35-40 C: aim for pre-haemorrhage BP / SBP 120-180 Treat if MAP >130 or evidence of end-organ dysfunction (GTN, labetalol, nitroprusside 0.3mg/kg/min etc...) Nimodipine: decr vasospasm - prevents 2Y ischaemia; significantly decr risk of poor outcome (NNT 20, 18% RRR, 5% ARR); benefit only proven PO; Give 60mg PO Q4h for 1/52, starting within 96hr D: analgesia; mannito
Outline supportive caresFASTHUGFIDDLER head up 30, antiemetics; quiet dark room; anticonvulsants (not prophylactically); correct electrolytes, normoglycaemia, normotension - AVOID HYPO ANYTHING, VTE prophylaxis, analgesia, normothermia
Dispositionurgent neurosurg; OT decr risk of re-bleed, allows aggressive hypertensive trt, prevents delayed ischaemic deficit, removes blood clots that may cause vasospasm and delayed deficit
When would coiling be indicated?<7mm and small neck; works best in ant circ in patients with good neuro fx; place within 72hrs; lower morbidity at 1yr, decr death/disability (23% vs 30%) compared with clipping
When would you choose OTif >7mm or wide neck

SAH Prognosis

Question Answer
Mortality from initial bleed?40-60%. 10% die before hospital; 30% die untreated
How many people get a good recovery and how many have significant neuro defect? 35% good recovery; 33% significant neuro deficit
Most important prognostic factor?Presenting GCS

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