> [!References]- > - on BP mgmt controversy; first two links are 2023 updates on SAH mgmt .from AHA/stroke and neurointensive care, respectively: [2023 Guideline for the Management of Patients With...](cubox://card?id=7124828344629070399) > - [Blood Pressure Targets for the Prevention of Reble...](cubox://highlight?id=7124833961750040230) > - [Blood Pressure Management After Intracerebral and ...](cubox://card?id=7124820175462860849) > > Fellowship resources: > - [Rosen SAH](x-devonthink-item://1781B09F-B327-4348-AA6F-F427FF97CA97?page=5) > - [Dunn SAH](x-devonthink-item://FC2A2A08-65F0-4CE6-A466-C44756664E22), [ Dunn investigation of suspected SAH](x-devonthink-item://7E6AD08C-BDB2-4128-86B6-90E833EE7E96), [Dunn management of SAH](x-devonthink-item://1F87C478-B735-4707-95B0-4E9D2C021903) > - [Core radiology - Subarachnoid Hemorrhage](x-devonthink-item://C1EF00FD-576C-4C41-AE08-CA966611F572?page=690) > - [Radiology Case studies - Subarachnoid Hemorrhage](x-devonthink-item://2A71AF1A-4715-4D5F-9841-03401D8E6C4E?page=461) > > NZ study on CTB timing: [[Multisclice CT for SAH]] > - single centre > - MSCT identified 253 (97.3%) of all aneurysmal SAH and 332 (95.7%) of all SAH. > - Sensitivity of MSCT was 99.6% (95% CI 97.6 to 100) for aneurysmal SAH and 99.0% (95% CI 97.1 to 99.8) for all SAH at 48 hours after headache onset. > - At 24 hours after headache onset, the sensitivity for aneurysmal SAH was 100% (95% CI 98.3 to 100). > - ==single-centre retrospective study suggests that it may be possible to extend the timeframe from headache onset in which modern MSCT can be used to rule out aneurysmal SAH== > > UK study on CTB timing: [[SHED]] > - prospective, observational, multicentre cohort study > > Nimodipine meta analysis: [Calcium antagonists for aneurysmal subarachnoid haemorrhage - cochrane 2007](https://www.cochranelibrary.com/web/cochrane/content?templateType=full&urlTitle=/cdsr/doi/10.1002/14651858.CD000277.pub3&doi=10.1002/14651858.CD000277.pub3&type=cdsr&contentLanguage=) > - “Calcium antagonists reduce the risk of poor outcome and secondary ischaemia after aneurysmal SAH. The results for 'poor outcome' depend largely on a single large trial of oral nimodipine; the evidence for other calcium antagonists is inconclusive. The evidence for nimodipine is not beyond all doubt, but given the potential benefits and modest risks of this treatment, oral nimodipine is currently indicated in patients with aneurysmal SAH. Intravenous administration of calcium antagonists cannot be recommended for routine practice on the basis of the present evidence. Magnesium sulphate is a promising agent but more evidence is needed before definite conclusions can be drawn.” > [!Key Points] > - nimodipine 60mg Q4h oral or ngt > - See also: [[Head trauma radiology#Traumatic Subarachnoid haemorrhage]], [[Lumbar puncture#interpretation|LP interpretation]] see: [Interpreting red blood cells in lumbar puncture: distinguishing true subarachnoid hemorrhage from traumatic tap.](bookends://sonnysoftware.com/ref/DL/250465) # causes - 70% ruptured berry aneurysm - 85% anterior circle of willis - 30% junction of anterior cerebral artery and ACOM - 25% junction of ICA and PCA ~ 3.5-7% of general population of asymptomatic aneurysms - F>M Isolated perimesencephalic SAH - 15% of cases - good prognosis - neurologic complications rare - recurrence rare ## risk factors - prior SAH - female > M - smoking - HTN - FMx - connective tissue disease: - autosomal dominant polycystic disease - marfans - NF1 - a-1-antitrypsin def - fibromuscular dysplasia - hereditary haemorrhagic telangiectasia - tuberous sclerosis - others - finish or japanese ethnicity - ethanol binges # history - headache - reaches peak intensity within 10 min - 1 hour - may improve spontaneously or with treatment; however, complete resolution within hours is rare - ==20% of pts with SAH also have a history of migraine== - occipital or neck pain suggests aneurysm of PICA or AICA - eye or temple pain suggests MCA aneurysm - other sx - vomiting common - transient LOC → due to cerebral perfusion pressure fall at onset as ICP approaches MAP. highly specific for SAH. a/w worse prognosis ## DDx for "thunderclap headache" - idiopathic - [[carotid and vertebral artery dissection|carotid or vertebral artery dissection]] - [[intracerebral haemorrhage|ICH]] - [[Cerebral venous thrombosis|cerebral venous sinus thrombosis]] - although usually more gradual in onset - benign post coital sudden onset headache - benign post exertional sudden onset HA - pituitary apoplexy - RCVS # complications **immediate complications** - myocardial dysfunction - [[STEMI mimics]] / [[#ecg changes|cerebral t waves]] - APO **delayed complications** - re-bleeding - vasospasm and delayed neuro deficit - 30% - usually btn days 4-14 - occurs in response to breakdown of blood products in subarachnoid space - ==may be prevented by nimodipine== - hydrocephalus - may require ventricular drainage - [[hyponatremia]] (cerebral salt wasting) - [[Seizures]] # Decision tools ## Hunt and Hess clinical grading for SAH | Grade | condition | outcomes <br>(independent / death) | | ----- | ----------------------------------------------------------------------------------- | ---------------------------------- | | 0 | unruptured aneurysm | | | 1 | asymptomatic or minimal HA and slight nuchal rigidity | 90-95% /<br>1-2% | | 2 | mod or severe HA, nuchal rigidity, no neuro deficity other than cranial nerve palsy | | | 3 | drowsiness, confusion, or mild focal deficit | | | 4 | stupor, moderate to severe hemiparesis | 10% /<br>80% | | 5 | deep coma, decerebrate posturing, moribund appearance | | ## Ottawa SAH clinical decision rule - age ≥ 40 - neck pain or stiffness - loss of consciousness - onset during exertion - thunderclap (instantly peaking) HA - limited neck flexion on exam if 0 of these, SAH ruled out # ecg changes See also: [[T inversion DDx]] - [Cerebral t waves LITFL](https://litfl.com/raised-intracranial-pressure-ecg-library/) - [[Long QT]] - Bradycardia SAH ECG - Widespread, giant T-wave inversions (“cerebral T waves”) secondary to subarachnoid haemorrhage. The QT interval is also grossly prolonged: ![[75E40827-3E23-4520-BE51-86EEEB982EF1.jpeg]] Severe [[traumatic brain injury|TBI]] with ↑ ICP: ![[B390B53F-CEA5-4C8C-AA6E-59B9EC24099D.jpeg]] # CTB distributions of blood location of blood suggests the cause - aneurysmal/AVM/dissection -- diffuse: blood in basal cisterns, sylvian fissure, interhemispheric fissure - isolated convexity SAH near cortex : - young RCVS - older cerebral amyloid angipathy or traumatic - permesencephalic pre-pontine - venous bleeding origin, better prognosis # sensitivity of CT <6 hours? ~ 95-98% in first 24 hours can demonstrate presence of SAH blood in >95% of cases. <6 hours closer to 98%. do LP if high clinical index of concern in spite of negative CTB. per Dunn, multi-detector CTB (most common in Aus/Nz) negative within 48-72 hours mostly rules out SAH; claim LP following negative plain CT in ED has a true positive yield of 0.4% overall, and 1:2000 if new generation CT within 6 hours.   *factors that may decrease sensitivity of non-con CTB?* - HCT <30 - small vol bleed - posterior fossa bleed - increased time from sx onset - radiology reporting from non-neurospecialist radiologist # LP criteria - generally need >100 x 10\^6 RBCs (usually more like 1000) - xanthochromia better; needs to be >12 hours # Treatment - ==nimodipine 60mg Q4H oral or NGT== - analgesia - maintain cerebral perfusion pressure while avoiding excess rise in MAP - BP 110-160 systolic - [[labetalol]] (esmolol would also work) - [[Nicardipine]] - [[hydralazine]] - reduce raised ICP - head up 30 deg - [[traumatic brain injury#Hypertonic saline|hypertonic saline]] 3mL/kg over 10 min (or 100mL 3%) or manitol 0.5-1mg/kg IV if ↑ ICP - keppra loading dose 60mg/kg - may need EVD if interventricular blood or high grade SAH (risk of obstructive hydrocephalus > do NOT use GTN or sodium nitropruside; these vasodilate and can cause increased intracranial pressure # Deep dive The topic of whether or not to LP to exclude SAH after a negative CTB is a topic of debate[^1]. Although emergency physicians have mostly adopted Perry's [6 hour 'rule'](https://pubmed.ncbi.nlm.nih.gov/31805846), there is lingering equipoise about the reliability of non-contrast CT beyond 6 hours, and traditionally, lumbar puncture would be used to exclude SAH. Due in large part to the time, difficulty, and perceived low diagnostic yield, CTA has become an attractive alternative to lumbar puncture to further exclude SAH. Although CT angio is ~97.9% sensitive for aneurysms and 90% specific, the rate of SAH due to aneurysm is estimated at 85%; therefore, CTA on its own would only be 83.2% sensitive for SAH overall. When combined with a CTB with a sensitivity of ~90%, the false negative rate of CTB + CTA is approximately 1.7% using the back-of-the-envelope: $(1 - \text{CTB SAH sensitivity}) * (1 - \text{CTA SAH sensitivity})$. With a pre-test probability of SAH of 10%, from Bayes' we can calculate a post-test probability of any SAH of 0.194%. This can be a bit abstract, but to put it in perspective, if the pre-test probability is as high as 50%, the post-test probability of any SAH would only be 1.72% after negative CTB+CTA. **McCormack 2010** analysed the CT + CTA strategy, on the basis that aneurysmal SAH is clinically significant and ~85% of SAH are due to aneurysm or AVM. Rather than analysing study data, they constructed a mathematical model to assess the post-test probability of both SAH and aneurysm, hypothesising that CT+CTA can replace CT+LP to exclude SAH. Estimating a pre-test probability of 15%, CTB sensitivity of 91% and specificity of 100%, they calculated a post-test probability of 99.98% (95% CI = 99.75% to 100%) that aneurysm and SAH are not present after negative CTB + CTA/ A key assumption of this approach is that non-aneurysmal SAH, eg perimesencephalic bleeding, does not carry the same risk of a poor outcome. The authors conclude that while a small number of SAHs that are not caused by AVM or aneurysms may be missed, in patients who are neurologically intact with headaches controlled, discharge should not cause harm to the patient. There are limitations to this approach. [Carpenter et al](https://pubmed.ncbi.nlm.nih.gov/27306497/) note some of the downsides of using CTA, including that aneurysms occur in 1-2% of the population, and it is problematic to link a non-ruptured aneurysm detected via CTA to an individual's headache. Others have noted that the sensitivity of CTA is only 92.3% for aneurysms >4mm, remarking that morbidity and mortality are not directly related to the size of the aneurysm. In 2019, [ACEP](https://www.annemergmed.com/article/S0196-0644%2819%2930577-3/fulltext) notes that CTA will miss significant alternative diagnoses that would be found on LP, approximating a 10.6% incidence of alternative diagnoses, including viral meningitis, IIH, bacterial meningitis. There is also the risk of increasing ionising radiation risk and cataract risks. Overall, the decision to CTA, rather than LP, has been gradually adopted into Emergency Medical practice worldwide, with ACEP advocating for 'shared decision making.' Other key stakeholders are less convinced of this approach. In 2025, A [neurosurgery group](https://pubmed.ncbi.nlm.nih.gov/40034490) estimated that 24-58 cases of aneurysmal SAH would be missed each year in the UK if LP was removed from the diagnostic pathway for SAH if CT head is negative at 6 hours, and total 336 missed aneurysmal SAH each year. However, this study did not compare the value of LP to the CTB+CTA approach. [April et al (2021)](https://pubmed.ncbi.nlm.nih.gov/33838968/) calculated a Pauker and Kassirer testing threshold for SAH at 1% (Carpenter 2016 calculated 2%), and based on available research, found a post negative CT head probability of disease at 1.1%. Noting that calculations are highly dependent on the values used to estimate probability of disease and testing thresholds, they conclude that ED physicians might reasonably decide to either perform or forego the procedure, and argue that LP is an excellent candidate for shared decision-making. Overall, the discussion of SAH 'rule out' often conflates two distinct questions that affect our comfort with discharging headaches: test 'miss-rate' (sensitivity) is a much different issue than the probability that <em>any</em> patient with a headache peaking in <1 hour has a SAH after a negative CT brain. These are fundamentally different issues. Many papers and podcasts tend to cite the 'number needed to LP' to find a clinically-significant SAH at about 250, but this should be taken with caution, as the studies often involved patients presenting with negative CTB within 6 hours; the NNTLP is likely lower for negative non-contrast CTB beyond 6 hours. Furthermore, considering the potentially-lethal nature of SAH, 250 tests to potentially prevent one death would be generally reasonable -- consider that every patient with chest pain gets an ECG to review for STEMI -- if not for the practical constraints of performing an LP. Shared decision making is a commendable target for ED physicians. However, using the approach in select settings such as whether or not to proceed to LP itself suggests a different standard of medical guidance than a 'recommendation' that would be issued for most other investigations performed in the ED. We should acknowledge whether true clinical equipoise exists about the role of CTA vs LP, or whether our tepid support for LP is a function of inconvenience, procedural difficulty, time constraints, and resource limitations. # Related Questions ## collapse - [x] 2Q: [Collapse, cause unclear](x-devonthink-item://8AAAF35C-CCF4-4157-9551-5B05727AA0CD?page=13) -- [Answer](x-devonthink-item://FDFBA3A1-6207-4204-AB6D-7483D80C5B5C?page=13) ## confusion - [x] 3Q: [Confused patient with VP shunt](x-devonthink-item://4BE7EDE1-1843-4BA0-B8D2-0DCEF50784D4?page=1) -- [Answer](x-devonthink-item://15F8F701-8EC8-4F9A-8DEC-5220C8561C8A?page=1) - [x] 4Q: [Cirrhosis and Confusion](x-devonthink-item://C4CCEB12-61D5-4308-AA41-5078F3D96CC0?page=10) -- [Answer](x-devonthink-item://75D8E35B-EE77-4D1B-A665-438451C976AE?page=16) - [ ] 5Q: [Confused Adult](x-devonthink-item://7061D1B4-0AB9-4963-B3B0-23BDD975B2CD?page=24) -- [Answer](x-devonthink-item://3F30C77E-E23E-4200-89FE-48A41618E0C2?page=16) ## headache - [ ] 11Q: [Possible meningitis](x-devonthink-item://554C45F7-8661-4467-BD61-8A79B6ECABF4?page=34) -- [Answer](x-devonthink-item://554C45F7-8661-4467-BD61-8A79B6ECABF4?page=36) - [ ] 12Q: [Headache](x-devonthink-item://F0498813-9350-484C-AD5B-6FF7C3AE9015?page=46) -- [Answer](x-devonthink-item://A491A3F6-FD6D-492F-BCBE-7F7BAE101EDF?page=50) - [ ] 13Q: [VP Shunt Complication](x-devonthink-item://7FCD3940-4BB4-45FE-86A6-E5707E82D5B5?page=28) -- [Answer](x-devonthink-item://3263A68A-96A6-43EC-985B-43260C3509BF?page=9) ## sah - [ ] 15Q: [Subarachnoid haemorrhage](x-devonthink-item://FE3157C2-07B3-43F2-9ECE-AFACE1355E13?page=2) -- [Answer](x-devonthink-item://DDC959EB-0C1E-448A-8380-C397BF734322?page=0) - [ ] 16Q: [Headache and Collapse with Abnormal CT](x-devonthink-item://3D57C3FE-3B52-42E0-9FBD-E4034F60C5B7?page=11) -- [Answer](x-devonthink-item://75D8E35B-EE77-4D1B-A665-438451C976AE?page=25) ## subarachnoid haemorrhage - [x] 17Q: [Severe headache and confusion](x-devonthink-item://554C45F7-8661-4467-BD61-8A79B6ECABF4?page=43) -- [Answer](x-devonthink-item://554C45F7-8661-4467-BD61-8A79B6ECABF4?page=45) - [x] 18Q: [Subarachnoid haemorrhage](x-devonthink-item://4134DDB3-6E12-474A-9F6F-64135C0C6048?page=25) -- [Answer](x-devonthink-item://AC92B5F1-8EE6-461A-B03E-F70AE7DC1275?page=25) - [x] 19Q: [Subarachnoid haemorrhage](x-devonthink-item://310EEEDE-D794-4365-8865-5B3DD1C20510?page=4) -- [Answer](x-devonthink-item://6D5125AD-DE4D-435B-8D13-6EA35DB8E785?page=4) - [x] DUPLICATE Q: [Subarachnoid haemorrhage](x-devonthink-item://FE3157C2-07B3-43F2-9ECE-AFACE1355E13?page=2) -- [Answer](x-devonthink-item://DDC959EB-0C1E-448A-8380-C397BF734322?page=0) - [x] DUPLICATE Q: [Headache and Collapse with Abnormal CT](x-devonthink-item://3D57C3FE-3B52-42E0-9FBD-E4034F60C5B7?page=11) -- [Answer](x-devonthink-item://75D8E35B-EE77-4D1B-A665-438451C976AE?page=25) - [ ] 20Q: [Collapse and Reduced GCS](x-devonthink-item://09CFA1A7-00F1-4151-979E-8F3984924D54?page=19) -- [Answer](x-devonthink-item://CF5E9C2B-42F9-4F9C-AC29-877E20134927?page=12) ## ottawa SAH - [ ] [question](x-devonthink-item://09493372-578D-4C97-972A-EEC617B38B53?page=4) -- [Answer](x-devonthink-item://A0D348CE-FCD4-4ECD-BE21-6CA73F6DE8CD?page=1) [^1]: [Sayer et al 2015](https://pubmed.ncbi.nlm.nih.gov/26480290) observed 2,248 patients presenting with headache suggestive of SAH who had LP following a normal CTB. The trial is limited by not characterising what percentage of these patients had CT scans within 6 hours vs >6 hours. Overall, they found vascular abnormalities in 0.47% of all LPs undertaken, requiring 204 LPs to identify one vascular abnormality. Other trials have demonstrated a lower NNLP. Regardless of the specific number, neurosurgical research (see [here](https://pubmed.ncbi.nlm.nih.gov/40676358) and [here](https://pubmed.ncbi.nlm.nih.gov/40034490)) has argued that LPs are still critical in the diagnosis SAH.