View source for Subarachnoid hemorrhage

{{short description|Bleeding into the brain's subarachnoid space}}
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{{See also|Pseudosubarachnoid hemorrhage}}
{{Use dmy dates|date=August 2018}}
{{Infobox medical condition (new)
| name            = Subarachnoid hemorrhage
| image           = SubarachnoidP.png
| caption         = CT scan of the brain showing subarachnoid hemorrhage as a white area in the center (marked by the arrow) and stretching into the [[sulcus (neuroanatomy)|sulci]] to either side
| field           = [[Neurosurgery]], [[Neurology]]
| pronounce       = {{IPAc-en|ˌ|s|ʌ|b|ə|ˈ|r|æ|k|n|ɔɪ|d|_|ˈ|h|ɛ|m|ər|ɪ|dʒ}}
| synonyms        = Subarachnoid haemorrhage
| symptoms        = [[Thunderclap headache|Severe headache of rapid onset]], [[vomiting]], [[decreased level of consciousness]]<ref name=EM2016/>
| complications   = Delayed [[cerebral ischemia]], [[cerebral vasospasm]], [[seizure]]s<ref name=EM2016/>
| onset           =
| duration        =
| types           = Traumatic, spontaneous (aneurysmal, nonaneurysmal, perimesencephalic)<ref name=EM2016/>
| causes          = [[Head injury]], [[cerebral aneurysm]]<ref name=EM2016/>
| risks           = [[High blood pressure]], [[smoking]], [[alcoholism]], [[cocaine]]<ref name=EM2016/>
| diagnosis       = [[CT scan]], [[lumbar puncture]]<ref name=Car2016/>
| differential    = [[Meningitis]], [[migraine]], [[cerebral venous sinus thrombosis]]<ref name=Ox2007/>
| prevention      =
| treatment       = [[Neurosurgery]] or [[interventional radiology|radiologically guided interventions]]<ref name=EM2016/>
| medication      = [[Labetalol]], [[nimodipine]]<ref name=EM2016/>
| prognosis       = 45% risk of death at 30 days (aneurysmal)<ref name=EM2016/>
| frequency       = 1 per 10,000 per year<ref name=EM2016/>
| deaths          =
}}
<!-- Definition and symptoms -->
'''Subarachnoid hemorrhage''' ('''SAH''') is [[bleeding]] into the [[subarachnoid space]]—the area between the [[arachnoid (brain)|arachnoid membrane]] and the [[pia mater]] surrounding the [[human brain|brain]].<ref name=EM2016/> Symptoms may include a [[thunderclap headache|severe headache of rapid onset]], vomiting, [[decreased level of consciousness]], [[fever]], weakness, numbness, and sometimes [[seizure]]s.<ref name=EM2016/> Neck stiffness or neck pain are also relatively common.<ref name=Car2016>{{cite journal | vauthors = Carpenter CR, Hussain AM, Ward MJ, Zipfel GJ, Fowler S, Pines JM, Sivilotti ML | title = Spontaneous Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis Describing the Diagnostic Accuracy of History, Physical Examination, Imaging, and Lumbar Puncture With an Exploration of Test Thresholds | journal = Academic Emergency Medicine | volume = 23 | issue = 9 | pages = 963–1003 | date = September 2016 | pmid = 27306497 | pmc = 5018921 | doi = 10.1111/acem.12984 }}</ref> In about a quarter of people a small bleed with resolving symptoms occurs within a month of a larger bleed.<ref name=EM2016/>

<!-- Cause and diagnosis -->
SAH may occur as a result of a [[head injury]] or spontaneously, usually from a ruptured [[cerebral aneurysm]].<ref name=EM2016/> Risk factors for spontaneous cases include [[high blood pressure]], smoking, family history, alcoholism, and [[cocaine]] use.<ref name=EM2016/> Generally, the diagnosis can be determined by a [[computed tomography|CT scan]] of the head if done within six hours of symptom onset.<ref name=Car2016/> Occasionally, a [[lumbar puncture]] is also required.<ref name=Car2016/> After confirmation further tests are usually performed to determine the underlying cause.<ref name=Car2016/>

<!-- Treatment and prognosis -->
Treatment is by prompt [[neurosurgery]] or [[endovascular coiling]].<ref name=EM2016>{{cite journal | vauthors = Abraham MK, Chang WW | title = Subarachnoid Hemorrhage | journal = Emergency Medicine Clinics of North America | volume = 34 | issue = 4 | pages = 901–916 | date = November 2016 | pmid = 27741994 | doi = 10.1016/j.emc.2016.06.011 }}</ref> Medications such as [[labetalol]] may be required to lower the blood pressure until repair can occur.<ref name=EM2016/> Efforts to treat fevers are also recommended.<ref name=EM2016/> [[Nimodipine]], a [[calcium channel blocker]], is frequently used to prevent [[cerebral vasospasm|vasospasm]].<ref name=EM2016/> The routine use of medications to prevent further seizures is of unclear benefit.<ref name=EM2016/> Nearly half of people with a SAH due to an underlying aneurysm die within 30 days and about a third who survive have ongoing problems.<ref name=EM2016/> Between ten and fifteen percent die before reaching a hospital.<ref name=VanGijn2007>{{cite journal | vauthors = van Gijn J, Kerr RS, Rinkel GJ | title = Subarachnoid haemorrhage | journal = Lancet | volume = 369 | issue = 9558 | pages = 306–18 | date = January 2007 | pmid = 17258671 | doi = 10.1016/S0140-6736(07)60153-6 | s2cid = 29126514 }}</ref>

<!-- Epidemiology and history -->
Spontaneous SAH occurs in about one per 10,000 people per year.<ref name=EM2016/> Females are more commonly affected than males.<ref name=EM2016/> While it becomes more common with age, about 50% of people present under 55 years old.<ref name=VanGijn2007/> It is a form of [[stroke]] and comprises about 5 percent of all strokes.<ref name=VanGijn2007/> Surgery for aneurysms was introduced in the 1930s.<ref name=Todd>{{cite journal | vauthors = Todd NV, Howie JE, Miller JD | title = Norman Dott's contribution to aneurysm surgery | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 53 | issue = 6 | pages = 455–8 | date = June 1990 | pmid = 2199609 | pmc = 1014202 | doi = 10.1136/jnnp.53.6.455 }}</ref> Since the 1990s many aneurysms are treated by a less invasive procedure called [[endovascular coiling]], which is carried out through a large blood vessel.<ref name=St2001>{{cite journal | vauthors = Strother CM | title = Historical perspective. Electrothrombosis of saccular aneurysms via endovascular approach: part 1 and part 2 | journal = AJNR. American Journal of Neuroradiology | volume = 22 | issue = 5 | pages = 1010–2 | date = May 2001 | pmid = 11337350 | url = http://www.ajnr.org/cgi/content/full/22/5/1011 | url-status = live | archive-url = https://web.archive.org/web/20051114124323/http://www.ajnr.org/cgi/content/full/22/5/1011 | archive-date = 14 November 2005 }}</ref>

A true subarachnoid hemorrhage may be confused with a [[pseudosubarachnoid hemorrhage]], an apparent increased [[attenuation]] on [[CT scan]]s within the [[interpeduncular cistern|basal cisterns]] that mimics a true subarachnoid hemorrhage.<ref>{{cite web |last1=Dixon |first1=Andrew |title=Pseudosubarachnoid hemorrhage {{!}} Radiology Reference Article {{!}} Radiopaedia.org |url=https://radiopaedia.org/articles/pseudosubarachnoid-haemorrhage?lang=us |website=Radiopaedia}}</ref> This occurs in cases of severe [[cerebral edema]], such as by [[cerebral hypoxia]]. It may also occur due to [[intrathecal administration|intrathecally administered]] [[contrast material]],<ref>{{cite journal |last1=Given |first1=Curtis A. |last2=Burdette |first2=Jonathan H. |last3=Elster |first3=Allen D. |last4=Williams |first4=Daniel W. |title=Pseudo-Subarachnoid Hemorrhage: A Potential Imaging Pitfall Associated with Diffuse Cerebral Edema |url=http://www.ajnr.org/content/24/2/254 |journal=AJNR. American Journal of Neuroradiology |pages=254–256 |language=en |date=1 February 2003|volume=24 |issue=2 |pmid=12591643 |pmc=7974121 }}</ref> leakage of high-dose [[intravenous administration|intravenous]] contrast material into the [[subarachnoid space]]s, or in patients with [[cerebral venous sinus thrombosis]], severe [[meningitis]], [[Leptomeningeal cancer|leptomeningeal carcinomatosis]],<ref>{{cite journal |last1=Marder |first1=Carrie P. |last2=Narla |first2=Vinod |last3=Fink |first3=James R. |last4=Tozer Fink |first4=Kathleen R. |title=Subarachnoid Hemorrhage: Beyond Aneurysms |url=https://www.ajronline.org/doi/full/10.2214/AJR.12.9749 |journal=American Journal of Roentgenology |pages=25–37 |doi=10.2214/AJR.12.9749 |date=26 December 2013|volume=202 |issue=1 |pmid=24370126 |url-access=subscription }}</ref> [[Intracranial pressure#Low ICP|intracranial hypotension]], [[Cerebellar stroke syndrome|cerebellar infarctions]], or [[Anatomical terms of location#Medial and lateral|bilateral]] [[subdural hematoma]]s.<ref>{{cite journal |last1=Coulier |first1=Bruno |title=Pseudo-subarachnoid Hemorrhage |journal=Journal of the Belgian Society of Radiology |pages=32 |doi=10.5334/jbsr.1509 |date=1 March 2018|volume=102 |issue=1 |pmid=30039044 |pmc=6032606 |doi-access=free }}</ref>

==Signs and symptoms==
The classic symptom of subarachnoid hemorrhage is [[thunderclap headache]] (a headache described as "like being kicked in the head",<ref name=Ox2007>{{cite book | vauthors = Longmore M, Wilkinson I, Turmezei T, Cheung CK |title=Oxford Handbook of Clinical Medicine, 7th edition |publisher=Oxford University Press |year=2007 |page=841 |isbn=978-0-19-856837-7}}</ref> or the "worst ever", developing over seconds to minutes). This headache often pulsates towards the [[occiput]] (the back of the head).<ref name="oxford2">{{cite book | vauthors = Ramrakha P, Moore K |title=Oxford Handbook of Acute Medicine, 2nd edition |publisher=Oxford University Press |year=2007 |pages=466–470 |isbn=978-0-19-852072-6}}</ref> About one-third of people have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid hemorrhage.<ref name=VanGijn2007/> Vomiting may be present, and 1 in 14 have [[seizure]]s.<ref name=VanGijn2007/> [[Confusion]], decreased level of consciousness or [[coma]] may be present, as may neck stiffness and other signs of [[meningism]].<ref name=VanGijn2007/>

Neck stiffness usually presents six hours after initial onset of SAH.<ref name=OTV3>{{cite book |title=Oxford Textbook of Medicine | edition = Fourth | volume = 3 | vauthors = Warrell DA, Cox TM |year=2003 |publisher=Oxford |isbn=978-0-19-857013-4 |pages=1032–34|display-authors=etal}}</ref> Isolated [[pupillary response|dilation]] of a pupil and loss of the [[pupillary light reflex]] may reflect [[brain herniation]] as a result of rising [[intracranial pressure]] (pressure inside the skull).<ref name=VanGijn2007/> [[Intraocular hemorrhage]] (bleeding into the eyeball) may occur in response to the raised pressure: subhyaloid hemorrhage (bleeding under the [[vitreous membrane|hyaloid membrane]], which envelops the [[vitreous body]] of the eye) and vitreous hemorrhage may be visible on [[fundoscopy]]. This is known as [[Terson syndrome]] (occurring in 3–13 percent of cases) and is more common in more severe SAH.<ref name=mccarron>{{cite journal | vauthors = McCarron MO, Alberts MJ, McCarron P | title = A systematic review of Terson's syndrome: frequency and prognosis after subarachnoid haemorrhage | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 75 | issue = 3 | pages = 491–3 | date = March 2004 | pmid = 14966173 | pmc = 1738971 | doi = 10.1136/jnnp.2003.016816 }}</ref>

[[Oculomotor nerve]] abnormalities (affected eye looking downward and outward and [[ptosis (eyelid)|inability to lift the eyelid on the same side]]) or [[:wikt:palsy|palsy]] (loss of movement) may indicate bleeding from the [[posterior communicating artery]].<ref name=VanGijn2007/><ref name=oxford2/> Seizures are more common if the hemorrhage is from an aneurysm; it is otherwise difficult to predict the site and origin of the hemorrhage from the symptoms.<ref name=VanGijn2007/> SAH in a person known to have seizures is often diagnostic of a [[cerebral arteriovenous malformation]].<ref name=oxford2/>

The combination of intracerebral hemorrhage and raised intracranial pressure (if present) leads to a "sympathetic surge", i.e. over-activation of the sympathetic system. This is thought to occur through two mechanisms, a direct effect on the [[medulla oblongata|medulla]] that leads to activation of the descending [[sympathetic nervous system]] and a local release of inflammatory mediators that circulate to the peripheral circulation where they activate the sympathetic system. As a consequence of the sympathetic surge there is a sudden increase in [[blood pressure]]; mediated by increased [[Myocardial contractility|contractility]] of the [[ventricular system|ventricle]] and increased [[vasoconstriction]] leading to increased [[systemic vascular resistance]]. The consequences of this sympathetic surge can be sudden, severe, and are frequently life-threatening. The high [[blood plasma|plasma]] concentrations of adrenaline also may cause [[cardiac arrhythmia]]s (irregularities in the heart rate and rhythm), [[electrocardiogram|electrocardiographic changes]] (in 27 percent of cases)<ref name="OHA">{{cite book | vauthors = Allman KG, Wilson IH |title=Oxford Handbook of Anaesthesia | edition = 2nd |publisher=Oxford University Press |year=2006 |pages=408–409 |isbn=978-0-19-856609-0}}</ref> and [[cardiac arrest]] (in 3 percent of cases) may occur rapidly after the onset of hemorrhage.<ref name=VanGijn2007/><ref>{{cite journal | vauthors = Banki NM, Kopelnik A, Dae MW, et al | title = Acute neurocardiogenic injury after subarachnoid hemorrhage | journal = Circulation | volume = 112 | issue = 21 | pages = 3314–9 | date = November 2005 | pmid = 16286583 | doi = 10.1161/CIRCULATIONAHA.105.558239 | doi-access = free }}</ref> A further consequence of this process is [[neurogenic]] [[pulmonary edema]],<ref>{{cite journal| vauthors = O'Leary R, McKinlay J |title=Neurogenic pulmonary oedema|journal=[[Continuing Education in Anaesthesia, Critical Care & Pain]]|volume=11|issue=3|pages=87–92|doi=10.1093/bjaceaccp/mkr006|year=2011|s2cid=18066655|doi-access=free}}</ref> where a process of increased pressure within the pulmonary circulation causes leaking of fluid from the pulmonary [[capillaries]] into the air spaces, the [[Pulmonary alveolus|alveoli]], of the lung.<ref>{{cite journal |vauthors=Lee VH, Oh JK, Mulvagh SL, Wijdicks EF |title=Mechanisms in neurogenic stress cardiomyopathy after aneurysmal subarachnoid hemorrhage |journal=Neurocrit Care |volume=5 |issue=3 |pages=243–249 |date=2006 |pmid=17290097 |doi=10.1385/NCC:5:3:243 |s2cid=20268064 }}</ref><ref>{{cite journal |vauthors=Wartenberg KE, Mayer SA |title=Medical complications after subarachnoid hemorrhage: new strategies for prevention and management |journal=Curr Opin Crit Care |volume=12 |issue=2 |pages=78–84 |date=April 2006 |pmid=16543780 |doi=10.1097/01.ccx.0000216571.80944.65 |s2cid=29858980 }}</ref>

Subarachnoid hemorrhage may also occur in people who have had a head injury. Symptoms may include headache, decreased level of consciousness and [[hemiparesis]] (weakness of one side of the body). SAH is a frequent occurrence in traumatic brain injury and carries a poor prognosis if it is associated with deterioration in the level of consciousness.<ref>{{cite journal | vauthors = Servadei F, Murray GD, Teasdale GM, et al | title = Traumatic subarachnoid hemorrhage: demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries | journal = Neurosurgery | volume = 50 | issue = 2 | pages = 261–7; discussion 267–9 | date = February 2002 | pmid = 11844260 | doi = 10.1097/00006123-200202000-00006 | s2cid = 38900336 }}</ref>

While thunderclap headache is the characteristic symptom of subarachnoid hemorrhage, less than 10% of those with concerning symptoms have SAH on investigations.<ref name=Car2016/> A number of other causes may need to be considered.<ref name=Schwedt>{{cite journal | vauthors = Schwedt TJ, Matharu MS, Dodick DW | title = Thunderclap headache | journal = The Lancet. Neurology | volume = 5 | issue = 7 | pages = 621–31 | date = July 2006 | pmid = 16781992 | doi = 10.1016/S1474-4422(06)70497-5 | s2cid = 5511658 }}</ref>

==Causes==
[[File:Circulus arteriosus SAB Lokalisationen SVG.svg|thumb|Circle of Willis with the most common locations of ruptured aneurysms marked]]
Most cases of SAH are due to [[trauma (medicine)|trauma]] such as a blow to the head.<ref name=EM2016/><ref>{{cite book| vauthors = Parrillo J |title=Critical care medicine: principles of diagnosis and management in the adult|year=2013|publisher=Elsevier/Saunders|location=Philadelphia, PA|isbn=9780323089296|page=1154|url=https://books.google.com/books?id=NXuzAQAAQBAJ&pg=PA1154|edition=4th|url-status=live|archive-url=https://web.archive.org/web/20170910173751/https://books.google.com/books?id=NXuzAQAAQBAJ&pg=PA1154|archive-date=10 September 2017}}</ref> Traumatic SAH usually occurs near the site of a [[skull fracture]] or [[intracerebral contusion]].<ref name="Rinkel93"/> It often happens in the setting of other forms of traumatic brain injury. In these cases prognosis is poorer; however, it is unclear if this is a direct result of the SAH or whether the presence of subarachnoid blood is simply an indicator of a more severe head injury.<ref name="Armin06">{{cite journal | vauthors = Armin SS, Colohan AR, Zhang JH | title = Traumatic subarachnoid hemorrhage: our current understanding and its evolution over the past half century | journal = Neurological Research | volume = 28 | issue = 4 | pages = 445–52 | date = June 2006 | pmid = 16759448 | doi = 10.1179/016164106X115053 | s2cid = 23726077 }}</ref>

In 85 percent of spontaneous cases the cause is a [[cerebral aneurysm]]—a weakness in the wall of one of the [[artery|arteries]] in the brain that becomes enlarged. They tend to be located in the [[circle of Willis]] and its branches. While most cases are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture.<ref name=VanGijn2007/> [[Aspirin]] also appears to increase the risk.<ref>{{cite journal | vauthors = Phan K, Moore JM, Griessenauer CJ, Ogilvy CS, Thomas AJ | title = Aspirin and Risk of Subarachnoid Hemorrhage: Systematic Review and Meta-Analysis | journal = Stroke | volume = 48 | issue = 5 | pages = 1210–1217 | date = May 2017 | pmid = 28341753 | doi = 10.1161/strokeaha.116.015674 | s2cid = 227321 | doi-access = free }}</ref>

In 15–20 percent of cases of spontaneous SAH, no aneurysm is detected on the first [[angiogram]].<ref name="Rinkel93">{{cite journal | vauthors = Rinkel GJ, van Gijn J, Wijdicks EF | title = Subarachnoid hemorrhage without detectable aneurysm. A review of the causes | journal = Stroke | volume = 24 | issue = 9 | pages = 1403–9 | date = September 1993 | pmid = 8362440 | doi = 10.1161/01.STR.24.9.1403 | doi-access = free }}</ref> About half of these are attributed to non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the subarachnoid spaces around the [[midbrain]] (i.e. mesencephalon). In these, the origin of the blood is uncertain.<ref name=VanGijn2007/> The remainder are due to other disorders affecting the blood vessels (such as [[cerebral arteriovenous malformation]]s), disorders of the blood vessels in the [[spinal cord]], and bleeding into various [[tumor]]s.<ref name=VanGijn2007/>

[[Cocaine]] abuse and [[sickle cell anemia]] (usually in children) and, rarely, [[anticoagulant]] therapy, [[coagulopathy|problems with blood clotting]] and [[pituitary apoplexy]] can also result in SAH.<ref name=OTV3/><ref name="Rinkel93"/> [[Vertebral artery dissection|Dissection of the vertebral artery]], usually caused by trauma, can lead to subarachnoid hemorrhage if the dissection involves the part of the vessel inside the skull.<ref name=Santos>{{cite journal | vauthors = Santos-Franco JA, Zenteno M, Lee A | title = Dissecting aneurysms of the vertebrobasilar system. A comprehensive review on natural history and treatment options | journal = Neurosurgical Review | volume = 31 | issue = 2 | pages = 131–40; discussion 140 | date = April 2008 | pmid = 18309525 | doi = 10.1007/s10143-008-0124-x | s2cid = 8755665 }}</ref>

==Pathophysiology==
Cerebral vasospasm is one of the complications caused by subarachnoid hemorrhage. It usually happens from the third day after the aneurysm event, and reaches its peak on 5th to 7th day.<ref name="ChineseNeurosurg">{{cite journal|last1=Fei Liu|first1=Yong|last2=Qiu|first2=Han Cheng|last3=Jiang|first3=Wei-Jian |title=Drug treatment of cerebral vasospasm after subarachnoid hemorrhage following aneurysms|journal=Chinese Neurosurgical Journal|date=18 February 2016|volume=2|issue=4|doi=10.1186/s41016-016-0023-x|doi-access=free}}</ref> There are several mechanisms proposed for this complication. Blood products released from subarachnoid hemorrhage stimulates the [[tyrosine kinase]] pathway causing the release of calcium ions from intracellular storage, resulting in smooth muscle contraction of cerebral arteries. [[Oxyhaemoglobin]] in [[cerebrospinal fluid]] (CSF) causes vasoconstriction by increasing [[free radicals]], [[endothelin-1]], [[prostaglandin]] and reducing the level of [[nitric oxide]] and [[prostacyclin]]. Besides, the disturbances of [[autonomic nervous system]] innervating cerebral arteries is also thought to cause vasospasm.<ref>{{cite journal | vauthors = Kolias AG, Sen J, Belli A |author-link3=Anna-Maria Belli| title = Pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage: putative mechanisms and novel approaches | journal = Journal of Neuroscience Research | volume = 87 | issue = 1 | pages = 1–11 | date = January 2009 | pmid = 18709660 | doi = 10.1002/jnr.21823 | s2cid = 23626380 }}</ref>

==Diagnosis==
[[File:Wikipedian getting a lumbar puncture (2006).jpg|thumb|upright=1.3|left|A [[lumbar puncture]] in progress. A large area on the back has been washed with an [[Povidone-iodine|iodine]]-based disinfectant, leaving brown coloration.]]
As only 10 percent of people admitted to the emergency department with a thunderclap headache are having an SAH, other possible causes are usually considered simultaneously, such as [[meningitis]], [[migraine]], and [[cerebral venous sinus thrombosis]].<ref name=Ox2007/> [[Intracerebral hemorrhage]], in which bleeding occurs within the brain itself, is twice as common as SAH and is often misdiagnosed as the latter.<ref name="Teunissen96"/> It is not unusual for SAH to be initially misdiagnosed as a migraine or [[tension headache]], which can lead to a delay in obtaining a CT scan. In a 2004 study, this occurred in 12 percent of all cases and was more likely in people who had smaller hemorrhages and no impairment in their mental status. The delay in diagnosis led to a worse outcome.<ref name=Kowalski>{{cite journal | vauthors = Kowalski RG, Claassen J, Kreiter KT, Bates JE, Ostapkovich ND, Connolly ES, Mayer SA |author6-link=E. Sander Connolly |author7-link=Stephan A. Mayer| title = Initial misdiagnosis and outcome after subarachnoid hemorrhage | journal = JAMA | volume = 291 | issue = 7 | pages = 866–9 | date = February 2004 | pmid = 14970066 | doi = 10.1001/jama.291.7.866 | doi-access = free }}</ref> In some people, the headache resolves by itself, and no other symptoms are present. This type of headache is referred to as "sentinel headache", because it is presumed to result from a small leak (a "warning leak") from an aneurysm. A sentinel headache still warrants investigations with CT scan and lumbar puncture, as further bleeding may occur in the subsequent three weeks.<ref name=Suarez>{{cite journal | vauthors = Suarez JI, Tarr RW, Selman WR | title = Aneurysmal subarachnoid hemorrhage | journal = The New England Journal of Medicine | volume = 354 | issue = 4 | pages = 387–96 | date = January 2006 | pmid = 16436770 | doi = 10.1056/NEJMra052732 | s2cid = 45645505 }}</ref>

The initial steps for evaluating a person with a suspected subarachnoid hemorrhage are obtaining a [[medical history]] and performing a [[physical examination]]. The diagnosis cannot be made on clinical grounds alone and in general [[medical imaging]] and possibly a lumbar puncture is required to confirm or exclude bleeding.<ref name="Car2016"/>

===Imaging===
The modality of choice is [[computed tomography]] (CT scan), without [[Contrast CT|contrast]], of the brain. This has a high [[sensitivity (tests)|sensitivity]] and will correctly identify 98.7% of cases within six hours of the onset of symptoms.<ref>{{cite journal | vauthors = Dubosh NM, Bellolio MF, Rabinstein AA, Edlow JA | title = Sensitivity of Early Brain Computed Tomography to Exclude Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis | journal = Stroke | volume = 47 | issue = 3 | pages = 750–5 | date = March 2016 | pmid = 26797666 | doi = 10.1161/STROKEAHA.115.011386 | s2cid = 7268382 | doi-access = free }}</ref> A CT scan can rule out the diagnosis in someone with a normal neurological exam if done within six hours.<ref name=ACEP2019>{{cite journal | vauthors = Godwin SA, Cherkas DS, Panagos PD, Shih RD, Byyny R, Wolf SJ | title = Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache | journal = Annals of Emergency Medicine | volume = 74 | issue = 4 | pages = e41–e74 | date = October 2019 | pmid = 31543134 | doi = 10.1016/j.annemergmed.2019.07.009 | doi-access = free }}</ref> Its efficacy declines thereafter,<ref name=EM2016/> and [[magnetic resonance imaging]] (MRI) is more sensitive than CT after several days.<ref name=VanGijn2007/>

====Angiography====
After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as determined by the CT scan appearance), the choice is between [[cerebral angiography]] (injecting radiocontrast through a [[catheter]] to the brain arteries) and [[computed tomography angiography|CT angiography]] (visualizing [[blood vessel]]s with [[radiocontrast]] on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm (see below).<ref name=VanGijn2007/><ref name=Suarez/>

In emergency department patients complaining of acute-onset headache without significant risk factors for SAH, evidence suggests that CT scanning of the head followed by CT angiography can reliably exclude SAH without the need for a lumbar puncture.<ref name="AEM-CTA">{{cite journal |vauthors=McCormack RF, Hutson A |title=Can computed tomography angiography of the brain replace lumbar puncture in the evaluation of acute-onset headache after a negative noncontrast cranial computed tomography scan? |journal=Acad Emerg Med |volume=17 |issue=4 |pages=444–51 |date=April 2010 |pmid=20370785 |doi=10.1111/j.1553-2712.2010.00694.x }}</ref> The risk of missing an aneurysmal bleed as the cause of SAH with this approach is less than 1%.<ref name="AEM-CTA"/>

===Lumbar puncture===
[[File:Xanthochromia.jpg|thumb|110px|[[Xanthochromia]] versus normal CSF]]
[[Lumbar puncture]], in which [[cerebrospinal fluid]] (CSF) is removed from the [[subarachnoid space]] of the [[spinal canal]] using a [[hypodermic needle]], shows evidence of bleeding in three percent of people in whom a non-contrast CT was found normal.<ref name=VanGijn2007/> A lumbar puncture or CT scan with contrast is therefore regarded as mandatory in people with suspected SAH when imaging is delayed to after six hours from the onset of symptoms and is negative.<ref name=VanGijn2007/><ref name=ACEP2019/> At least three tubes of CSF are collected.<ref name=OTV3/> If an elevated number of [[red blood cell]]s is present equally in all bottles, this indicates a subarachnoid hemorrhage. If the number of cells decreases per bottle, it is more likely that it is due to damage to a small blood vessel during the procedure (known as a "traumatic tap").<ref name=Suarez/> While there is no official cutoff for red blood cells in the CSF no documented cases have occurred at less than "a few hundred cells" per high-powered field.<ref>{{cite journal| vauthors = Thomas L |title=Evidence-Based Approach to Diagnosis and Management of Aneurysmal Subarachnoid Hemorrhage in the Emergency Department|journal=Emergency Medicine Practice|date=July 2009|volume=11|issue=7|url=http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=193|display-authors=etal|url-status=live|archive-url=https://web.archive.org/web/20120314230344/http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=193|archive-date=14 March 2012}}</ref>

The CSF sample is also examined for [[xanthochromia]]—the yellow appearance of [[centrifugation|centrifugated]] fluid. This can be determined by [[spectrophotometry]] (measuring the absorption of particular wavelengths of light) or visual examination. It is unclear which method is superior.<ref>{{cite journal | vauthors = Chu K, Hann A, Greenslade J, Williams J, Brown A | title = Spectrophotometry or visual inspection to most reliably detect xanthochromia in subarachnoid hemorrhage: systematic review | journal = Annals of Emergency Medicine | volume = 64 | issue = 3 | pages = 256–264.e5 | date = September 2014 | pmid = 24635988 | doi = 10.1016/j.annemergmed.2014.01.023 | doi-access = free }}</ref> Xanthochromia remains a reliable ways to detect SAH several days after the onset of headache.<ref name=Cruickshank/> An interval of at least 12&nbsp;hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the hemoglobin from the red blood cells to be metabolized into [[bilirubin]].<ref name=VanGijn2007/><ref name=Cruickshank>{{cite journal | vauthors = Cruickshank A, Auld P, Beetham R, et al| title = Revised national guidelines for analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage | journal = Annals of Clinical Biochemistry | volume = 45 | issue = Pt 3 | pages = 238–44 | date = May 2008 | pmid = 18482910 | doi = 10.1258/acb.2008.007257 | s2cid = 24393459 | doi-access = free }}</ref>

===ECG===
[[File:CNSinjury.JPG|thumb|upright=1.3|ECG changes resembling those of an STEMI in a woman who had an acute CNS injury from a subarachnoid hemorrhage]]

[[Electrocardiography|Electrocardiographic]] changes are relatively common in subarachnoid hemorrhage, occurring in 40–70 percent of cases. They may include [[QT prolongation]], [[Q waves]], [[cardiac dysrhythmia]]s, and [[ST elevation]] that mimics a [[heart attack]].<ref>{{cite journal | vauthors = Nguyen H, Zaroff JG | title = Neurogenic stunned myocardium | journal = Current Neurology and Neuroscience Reports | volume = 9 | issue = 6 | pages = 486–91 | date = November 2009 | pmid = 19818236 | doi = 10.1007/s11910-009-0071-0 | s2cid = 9169045 }}</ref> 

Also one of the characteristic [[ECG]] changes that could be found in patients with subarachnoid hemorrhage, is the [[J wave]]s or Osborn waves, which are positive deflections that occur at the junction between [[QRS complexes]] and [[ST segment]]s, where the S point, also known as the J point, has a myocardial infarction-like elevation.<ref>{{cite journal |last1=De Sweit J. |title=Changes simulating hypothermia in the electrocardiogram in subarachnoid hemorrhage. |journal=Journal of Electrocardiology |year=1972 |volume=5 |issue=2 |pages=93–95 |pmid=5033416}}</ref> J waves or Osborn waves, which represent an early [[repolarization]] and delayed [[depolarization]] of the heart ventricles, are thought to be caused by the high [[catecholamines]] surge released in patients with subarachnoid hemorrhage or brain damage, the issue that might lead to [[ventricular fibrillation]] and [[cardiac arrest]] in unmanaged patients.<ref>{{cite journal |last1=Gussak I, Bjerregaard P, Egan TM, Chaitman BR. |title=ECG phenomenon called the J wave. History, pathophysiology, and clinical significance. |journal=Journal of Electrocardiology |year=1995 |volume=28 |issue=1 |pages=49–58 |doi=10.1016/s0022-0736(05)80007-x |pmid=7897337}}</ref><ref>{{cite journal |last1=SCHER AM, YOUNG AC. |title=The pathway of ventricular depolarization in the dog |journal=Circulation Research |year=1956 |volume=4 |issue=4 |pages=461–469 |doi=10.1161/01.res.4.4.461 |pmid=13330192|s2cid=8830952 |doi-access=free }}</ref>

===Classification===
There are several grading scales available for SAH. The [[Glasgow Coma Scale]] (GCS) is ubiquitously used for assessing consciousness. Its three specialized scores are used to evaluate SAH; in each, a higher number is associated with a worse outcome.<ref>{{cite journal | vauthors = Rosen DS, Macdonald RL | title = Subarachnoid hemorrhage grading scales: a systematic review | journal = Neurocritical Care | volume = 2 | issue = 2 | pages = 110–8 | year = 2005 | pmid = 16159052 | doi = 10.1385/NCC:2:2:110 | s2cid = 13925503 }}</ref> These scales have been derived by retrospectively matching characteristics of people with their outcomes.

The first widely used scale for neurological condition following SAH was published by [[Harry Botterell|Botterell]] and Cannell in 1956 and referred to as the Botterell Grading Scale. This was modified by Hunt and Hess<ref name="Wang2016">{{cite journal |journal=[[Journal of Neurosurgery]] |publisher=[[American Association of Neurological Surgeons]] |title=Editorial: Subarachnoid hemorrhage grading scales |last1=Wang |first1=Anthony C. |last2=Heros |first2=Roberto C. |doi=10.3171/2015.3.JNS15336 |year=2016 |volume=124 |number=2 |pages=296–298 |pmid=26381258 |doi-access=free }}</ref><ref name="CJNS">{{cite journal |journal=[[The Canadian Journal of Neurological Sciences]] |title=E. Harry Botterell: A Series of Papers Commemorating his Life and Contributions |volume=26 |number=3 |pages=230–246 |date=August 1999|doi=10.1017/S0317167100000305 |url=https://www.cambridge.org/core/services/aop-cambridge-core/content/view/1F003B2E5DABA00D83816F245AA6D4BD/S0317167100000305a.pdf/e_harry_botterell_a_series_of_papers_commemorating_his_life_and_contributions.pdf|last1=Schatz |first1=Stanley W. |last2=Morley |first2=T.P. |last3=Fleming |first3=J.F. Ross |last4=Geisler |first4=William O. |last5=Tator |first5=Charles H. |last6=Tasker |first6=Ronald R. |last7=Gentili |first7=F. |last8=Vandewater |first8=Stuart L. |last9=Lougheed |first9=William M. |doi-access=free }}</ref><ref name="Rosen2005">{{cite journal |journal=Neurocritical Care |publisher=[[Neurocritical Care Society]] |title=Subarachnoid hemorrhage grading scales: a systematic review |last1=Rosen |first1=David S. |last2=Macdonald |first2=R. Loch |year=2005 |volume=2 |number=2 |pages=110–118 |url=http://cmp-manual.wbs.cz/skaly/subarachnoid_hemorrhage_grading_scales.pdf |doi=10.1385/NCC:2:2:110 |pmid=16159052 |s2cid=13925503 }}</ref> in 1968:<ref name="H&H">{{cite journal | vauthors = Hunt WE, Hess RM | title = Surgical risk as related to time of intervention in the repair of intracranial aneurysms | journal = Journal of Neurosurgery | volume = 28 | issue = 1 | pages = 14–20 | date = January 1968 | pmid = 5635959 | doi = 10.3171/jns.1968.28.1.0014 | s2cid = 2871628 }}</ref>

{| class="wikitable" style = "width:75%; font-size:85%; margin-left:15px; text-align:center"
|-
!width="50"| Grade
! Signs and symptoms
! Survival
|-
! 1
| style="text-align:left;"|[[Asymptomatic]] or minimal headache and slight neck stiffness ||70%
|-
!2
| style="text-align:left;"| Moderate to severe headache; neck stiffness; no [[neurology|neurologic]] deficit except [[cranial nerve]] [[:wikt:palsy|palsy]] || 60%
|-
!3
|align="left"| [[Drowsy]]; minimal neurologic deficit || 50%
|-
!4
| style="text-align:left;"| Stuporous; moderate to severe hemiparesis; possibly early [[decerebrate rigidity]] and vegetative disturbances || 20%
|-
!5
| style="text-align:left;"| Deep coma; [[abnormal posturing|decerebrate rigidity]]; [[death|moribund]] || 10%
|}

The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan.<ref name="Fisher">{{cite journal | vauthors = Fisher CM, Kistler JP, Davis JM | title = Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning | journal = Neurosurgery | volume = 6 | issue = 1 | pages = 1–9 | date = January 1980 | pmid = 7354892 | doi = 10.1097/00006123-198001000-00001 }}</ref>

{| class="wikitable" style = "width:75%; font-size:85%; margin-left:15px; text-align:center"
|-
!width="50"| Grade
! Appearance of hemorrhage
|-
! 1
| style="text-align:left;"|None evident
|-
!2
| style="text-align:left;"| Less than 1&nbsp;mm thick
|-
!3
|align="left"| More than 1&nbsp;mm thick
|-
!4
| style="text-align:left;"| Diffuse or none with intraventricular hemorrhage or [[parenchymal]] extension
|}

This scale has been modified by Claassen and coworkers, reflecting the additive risk from SAH size and accompanying [[intraventricular hemorrhage]] (0 – none; 1 – minimal SAH w/o IVH; 2 – minimal SAH with IVH; 3 – thick SAH w/o IVH; 4 – thick SAH with IVH);.<ref name="Claassen">{{cite journal | vauthors = Claassen J, Bernardini GL, Kreiter K, et al| title = Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited | journal = Stroke | volume = 32 | issue = 9 | pages = 2012–20 | date = September 2001 | pmid = 11546890 | doi = 10.1161/hs0901.095677 | doi-access = free }}</ref>

The World Federation of Neurosurgeons (WFNS) classification uses Glasgow coma score and [[focal neurological deficit]] to gauge severity of symptoms.<ref name="WorldFed">{{cite journal | vauthors = Teasdale GM, Drake CG, Hunt W, Kassell N, Sano K, Pertuiset B, De Villiers JC | title = A universal subarachnoid hemorrhage scale: report of a committee of the World Federation of Neurosurgical Societies | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 51 | issue = 11 | pages = 1457 | date = November 1988 | pmid = 3236024 | pmc = 1032822 | doi = 10.1136/jnnp.51.11.1457 }}</ref>
{| class="wikitable" style = "width:75%; font-size:85%; margin-left:15px; text-align:center"
|-
!width="50"| Grade
! GCS
! Focal neurological deficit
|-
! 1
| 15 || Absent
|-
! 2
| 13–14 || Absent
|-
! 3
| 13–14 || Present
|-
! 4
| 7–12 || Present or absent
|-
! 5
| <7 || Present or absent
|}

A comprehensive [[classification scheme]] has been suggested by Ogilvy and Carter to predict outcome and gauge therapy.<ref name="pmid9588539">{{cite journal | vauthors = Ogilvy CS, Carter BS | title = A proposed comprehensive grading system to predict outcome for surgical management of intracranial aneurysms | journal = Neurosurgery | volume = 42 | issue = 5 | pages = 959–68; discussion 968–70 | date = May 1998 | pmid = 9588539 | doi = 10.1097/00006123-199805000-00001 | doi-access = free }}</ref> The system consists of five grades and it assigns one point for the presence or absence of each of five factors: age greater than 50; Hunt and Hess grade 4 or 5; Fisher scale 3 or 4; aneurysm size greater than 10&nbsp;mm; and posterior circulation aneurysm 25&nbsp;mm or more.<ref name="pmid9588539"/>

==Screening and prevention==
[[Screening (medicine)|Screening]] for aneurysms is not performed on a population level; because they are relatively rare, it would not be [[cost-effectiveness analysis|cost-effective]]. However, if someone has two or more first-degree relatives who have had an aneurysmal subarachnoid hemorrhage, screening may be worthwhile.<ref name=VanGijn2007/><ref name=WhiteWardlaw>{{cite journal | vauthors = White PM, Wardlaw JM | title = Unruptured intracranial aneurysms | journal = Journal of Neuroradiology |volume = 30 | issue = 5 | pages = 336–50 | date = December 2003 | pmid = 14752379 | url = http://www.em-consulte.com/article/126528 | url-status = live | archive-url = https://web.archive.org/web/20101220061605/http://www.em-consulte.com/article/126528 | archive-date = 20 December 2010 }}</ref>

[[Polycystic kidney disease#Autosomal dominant form|Autosomal dominant polycystic kidney disease]] (ADPKD), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8 percent of cases, but most such aneurysms are small and therefore unlikely to rupture. As a result, screening is only recommended in families with ADPKD where one family member has had a ruptured aneurysm.<ref>{{cite journal | vauthors = Gibbs GF, Huston J, Qian Q, Kubly V, Harris PC, Brown RD, Torres VE | title = Follow-up of intracranial aneurysms in autosomal-dominant polycystic kidney disease | journal = Kidney International | volume = 65 | issue = 5 | pages = 1621–7 | date = May 2004 | pmid = 15086900 | doi = 10.1111/j.1523-1755.2004.00572.x | doi-access = free }}</ref>

An aneurysm may be detected incidentally on brain imaging; this presents a conundrum, as all treatments for cerebral aneurysms are associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic data both in people having previously had a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those having previously had a SAH were more likely to bleed from other aneurysms. In contrast, those having never bled and had small aneurysms (smaller than 10&nbsp;mm) were very unlikely to have a SAH and were likely to sustain harm from attempts to repair these aneurysms.<ref name=ISUIA/> On the basis of the ISUIA and other studies, it is now recommended that people are considered for [[preventive healthcare|preventive treatment]] only if they have a reasonable [[life expectancy]] and have aneurysms that are highly likely to rupture.<ref name=WhiteWardlaw/> Moreover, there is only limited evidence that endovascular treatment of unruptured aneurysms is actually beneficial.<ref>{{cite journal | vauthors = Naggara ON, White PM, Guilbert F, Roy D, Weill A, Raymond J | title = Endovascular treatment of intracranial unruptured aneurysms: systematic review and meta-analysis of the literature on safety and efficacy | journal = Radiology | volume = 256 | issue = 3 | pages = 887–97 | date = September 2010 | pmid = 20634431 | doi = 10.1148/radiol.10091982 }}</ref>

==Treatment==
Management involves general measures to stabilize the person while also using specific investigations and treatments. These include the prevention of rebleeding by obliterating the bleeding source, prevention of a phenomenon known as [[vasospasm]], and prevention and treatment of complications.<ref name=VanGijn2007/>

Stabilizing the person is the first priority. Those with a depressed level of consciousness may need to be [[intubation|intubated]] and [[mechanical ventilation|mechanically ventilated]]. Blood pressure, [[pulse]], [[respiratory rate]], and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an [[intensive care unit]] may be preferable, especially since 15 percent may have further bleeding soon after admission. Nutrition is an early priority, mouth or [[nasogastric intubation|nasogastric tube]] feeding being preferable over [[parenteral nutrition|parenteral]] routes. In general, pain control is restricted to less-sedating agents such as [[codeine]], as [[sedation]] may impact on the mental status and thus interfere with the ability to monitor the level of consciousness. [[Deep vein thrombosis]] is prevented with [[compression stockings]], intermittent [[pneumatic]] compression of the [[calf (anatomy)|calves]], or both.<ref name=VanGijn2007/> A [[urinary catheterization|bladder catheter]] is usually inserted to monitor fluid balance. [[Benzodiazepine]]s may be administered to help relieve distress.<ref name=OTV3/> [[Antiemetic]] drugs should be given to awake persons.<ref name="oxford2"/>

People with poor clinical grade on admission, acute neurologic deterioration, or progressive enlargement of ventricles on CT scan are, in general, indications for the placement of an [[external ventricular drain]] by a neurosurgeon. The external ventricular drain may be inserted at the bedside or in the operating room. In either case, strict [[aseptic technique]] must be maintained during insertion. In people with aneurysmal subarachnoid hemorrhage the EVD is used to remove [[cerebrospinal fluid]], blood, and blood byproducts that increase [[intracranial pressure]] and may increase the risk for [[cerebral vasospasm]].<ref>{{cite web|title=Care of the Patient with Anuerysmal Subarachnoid Hemorrhage|url=http://www.aann.org/apps/ws_downloads/download.php?file=62|work=AANN Clinical Practice Guidelines|publisher=American Association of Neuroscience Nurses|access-date=14 June 2013|url-status=dead|archive-url=https://web.archive.org/web/20131229074041/http://www.aann.org/apps/ws_downloads/download.php?file=62|archive-date=29 December 2013}}</ref>

===Preventing rebleeding===
[[File:Coiled PCA residual aneurysm arteriogram.JPG|thumb|upright=1.3|[[Arteriogram]] showing a partially coiled aneurysm (''indicated by yellow arrows'') of the [[posterior cerebral artery]] with a residual aneurysmal sac. The person was a 34-year-old woman initially treated for a subarachnoid hemorrhage.]]
Efforts to keep a person's [[systolic blood pressure]] somewhere between 140 and 160 mmHg is generally recommended.<ref name=EM2016/> Medications to achieve this may include [[labetalol]] or [[nicardipine]].<ref name=EM2016/>

People whose CT scan shows a large [[hematoma]], depressed level of consciousness, or [[focal neurologic signs]] may benefit from urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are stabilized more extensively and undergo a [[cerebral angiography|transfemoral angiogram]] or CT angiogram later. It is hard to predict who will have a rebleed, yet it may happen at any time and carries a dismal prognosis. After the first 24&nbsp;hours have passed, rebleeding risk remains around 40 percent over the subsequent four&nbsp;weeks, suggesting that interventions should be aimed at reducing this risk as soon as possible.<ref name=VanGijn2007/> Some predictors of early rebleeding are high systolic blood pressure, the presence of a hematoma in the brain or ventricles, poor Hunt-Hess grade (III-IV), aneurysms in the posterior circulation, and an aneurysm >10&nbsp;mm in size.<ref>{{cite journal | vauthors = Tang C, Zhang TS, Zhou LF | title = Risk factors for rebleeding of aneurysmal subarachnoid hemorrhage: a meta-analysis | journal = PLOS ONE | volume = 9 | issue = 6 | pages = e99536 | date = 9 June 2014 | pmid = 24911172 | pmc = 4049799 | doi = 10.1371/journal.pone.0099536 | bibcode = 2014PLoSO...999536T | doi-access = free }}</ref>

If a [[cerebral aneurysm]] is identified on angiography, two measures are available to reduce the risk of further bleeding from the same aneurysm: [[clipping (medicine)|clipping]]<ref name=Dandy1938>{{cite journal | vauthors = Dandy WE | title = Intracranial Aneurysm of the Internal Carotid Artery Cured by Operation | journal = Annals of Surgery | volume = 107 | issue = 5 | pages = 654–9 | date = May 1938 | pmid = 17857170 | pmc = 1386933 | doi = 10.1097/00000658-193805000-00003 }}</ref> and [[Guglielmi Detachable Coil|coiling]].<ref name=Guiglielmi1991>{{cite journal | vauthors = Guglielmi G, Viñuela F, Dion J, Duckwiler G | title = Electrothrombosis of saccular aneurysms via endovascular approach. Part 2: Preliminary clinical experience | journal = Journal of Neurosurgery | volume = 75 | issue = 1 | pages = 8–14 | date = July 1991 | pmid = 2045924 | doi = 10.3171/jns.1991.75.1.0008 }}</ref> Clipping requires a [[craniotomy]] (opening of the skull) to locate the aneurysm, followed by the placement of clips around the neck of the aneurysm. Coiling is performed through the large blood vessels (endovascularly): a catheter is inserted into the [[femoral artery]] in the groin and advanced through the [[aorta]] to the arteries (both [[carotid artery|carotid arteries]] and both [[vertebral artery|vertebral arteries]]) that supply the brain. When the aneurysm has been located, [[platinum]] coils are deployed that cause a [[thrombosis|blood clot to form]] in the aneurysm, obliterating it. The decision as to which treatment is undertaken is typically made by a multidisciplinary team consisting of a [[neurosurgery|neurosurgeon]], [[neuroradiology|neuroradiologist]], and often other health professionals.<ref name=VanGijn2007/>

In general, the decision between clipping and coiling is made on the basis of the location of the aneurysm, its size and the condition of the person. Aneurysms of the [[middle cerebral artery]] and its related vessels are hard to reach with angiography and tend to be amenable to clipping. Those of the [[basilar artery]] and posterior cerebral artery are hard to reach surgically and are more accessible for endovascular management.<ref name=ISAT2005>{{cite journal | vauthors = Molyneux AJ, Kerr RS, Yu LM, Clarke M, Sneade M, Yarnold JA, Sandercock P | title = International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion | journal = Lancet | volume = 366 | issue = 9488 | pages = 809–17 | year = 2005 | pmid = 16139655 | doi = 10.1016/S0140-6736(05)67214-5 | s2cid = 18777412 }}</ref> These approaches are based on general experience, and the only [[randomized controlled trial]] directly comparing the different modalities was performed in relatively well people with small (less than 10&nbsp;mm) aneurysms of the [[anterior cerebral artery]] and [[anterior communicating artery]] (together the "anterior circulation"), who constitute about 20 percent of all people with aneurysmal SAH.<ref name=ISAT2005/><ref>{{cite journal | vauthors = Lindgren A, Vergouwen MD, van der Schaaf I, Algra A, Wermer M, Clarke MJ, Rinkel GJ | title = Endovascular coiling versus neurosurgical clipping for people with aneurysmal subarachnoid haemorrhage | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | issue = 8 | pages = CD003085 | date = August 2018 | pmid = 30110521 | pmc = 6513627 | doi = 10.1002/14651858.CD003085.pub3 }}</ref> This trial, the ''International Subarachnoid Aneurysm Trial'' (ISAT), showed that in this group the likelihood of death or being dependent on others for [[activities of daily living]] was reduced (7.4 percent [[absolute risk reduction]], 23.5 percent [[relative risk]] reduction) if endovascular coiling was used as opposed to surgery.<ref name=ISAT2005/> The main drawback of coiling is the possibility that the aneurysm will recur; this risk is extremely small in the surgical approach. In ISAT, 8.3 percent needed further treatment in the longer term. Hence, people who have undergone coiling are typically followed up for many years afterwards with angiography or other measures to ensure recurrence of aneurysms is identified early.<ref>{{cite journal | vauthors = Campi A, Ramzi N, Molyneux AJ, et al | title = Retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT) | journal = Stroke | volume = 38 | issue = 5 | pages = 1538–44 | date = May 2007 | pmid = 17395870 | doi = 10.1161/STROKEAHA.106.466987 | doi-access = free }}</ref> Other trials have also found a higher rate of recurrence necessitating further treatments.<ref>{{cite journal | vauthors = Piotin M, Spelle L, Mounayer C, Salles-Rezende MT, Giansante-Abud D, Vanzin-Santos R, Moret J | title = Intracranial aneurysms: treatment with bare platinum coils--aneurysm packing, complex coils, and angiographic recurrence | journal = Radiology | volume = 243 | issue = 2 | pages = 500–8 | date = May 2007 | pmid = 17293572 | doi = 10.1148/radiol.2431060006 }}</ref><ref>{{cite journal | vauthors = Raymond J, Guilbert F, Weill A, et al | title = Long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils | journal = Stroke | volume = 34 | issue = 6 | pages = 1398–403 | date = June 2003 | pmid = 12775880 | doi = 10.1161/01.STR.0000073841.88563.E9 | doi-access = free }}</ref>

===Vasospasm===
[[Vasospasm]], in which the blood vessels constrict and thus restrict [[blood flow]], is a serious complication of SAH. It can cause [[ischemia|ischemic]] [[acquired brain injury|brain injury]] (referred to as "delayed ischemia") and permanent [[brain damage]] due to lack of oxygen in parts of the brain.<ref name=CochraneNimo/> It can be fatal if severe. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by [[transcranial doppler]] or cerebral angiography. About one third of people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those have permanent damage as a result.<ref name=CochraneNimo>{{cite journal | vauthors = Dorhout Mees SM, Rinkel GJ, Feigin VL, Algra A, van den Bergh WM, Vermeulen M, van Gijn J | title = Calcium antagonists for aneurysmal subarachnoid haemorrhage | journal = The Cochrane Database of Systematic Reviews | issue = 3 | pages = CD000277 | date = July 2007 | volume = 2007 | pmid = 17636626 | pmc = 7044719 | doi = 10.1002/14651858.CD000277.pub3 | s2cid = 1767194 | veditors = Rinkel GJ }}</ref> It is possible to screen for the development of vasospasm with transcranial Doppler every 24–48&nbsp;hours. A blood flow velocity of more than 120&nbsp;[[metre per second|centimeters per second]] is suggestive of vasospasm.<ref name=Suarez/>

The pathogenesis of cerebral vasospasm following subarachnoid hemorrhage is attributed to the higher levels of [[endothelin 1]], a potent vasoconstrictor, and the lower levels of [[endothelial NOS]] (eNOS), a potent vasodilator. Both of which are produced from a series of events that begin from the inflammatory reaction caused by the products released from erythrocytes' degradation. Following subarachnoid hemorrhage, different clotting factors and blood products are released into the surrounding [[perivascular spaces]] known as ([[Virchow-Robin spaces]]). The released clotting factors like; [[fibrinopeptides]], [[thromboxane A2]] and others lead to microthrombosis around near vessels that leads to extrinsic vasoconstriction of these vessels. Besides that extrinsic vasoconstriction, the erythrocytes' degradation products like; [[bilirubin]] and [[oxyhemoglobin]] lead to neuroinflammation that in turn increases the production of [[reactive oxygen species]] (ROS) which increases and decreases the production of endothelin 1 and endothelial NOS, respectively, the issue that yields in intrinsic vasoconstriction of the neighboring blood vessels and results in cerebral ischemia if left untreated.<ref>{{cite journal |last1=Kolias AG, Sen J, Belli A. |title=Pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage: putative mechanisms and novel approaches. |journal=Journal of Neuroscience Research |year=2009 |volume=87 |issue=1 |pages=1–11 |doi=10.1002/jnr.21823 |pmid=18709660|s2cid=23626380 }}</ref><ref>{{cite journal |last1=Suhardja A. |title=Mechanisms of disease: roles of nitric oxide and endothelin-1 in delayed cerebral vasospasm produced by aneurysmal subarachnoid hemorrhage. |journal=Nature Clinical Practice Cardiovascular Medicine |year=2004 |volume=1 |issue=2 |pages=110–116 |doi=10.1038/ncpcardio0046 |pmid=16265315|s2cid=23446475 }}</ref><ref>{{cite journal |last1=Pluta RM. |title=Delayed cerebral vasospasm and nitric oxide: review, new hypothesis, and proposed treatment. |journal=Pharmacology & Therapeutics |year=2005 |volume=105 |issue=1 |pages=23–56 |doi=10.1016/j.pharmthera.2004.10.002 |pmid=15626454}}</ref><ref>{{cite book |last1=Zhou Y, Martin RD, Zhang JH. |title=Early Brain Injury or Cerebral Vasospasm |chapter=Advances in Experimental Subarachnoid Hemorrhage |journal=Acta Neurochirurgica. Supplement |year=2011 |volume=110 |issue=Pt 1 |pages=15–21 |doi=10.1007/978-3-7091-0353-1_3 |pmid=21116908|isbn=978-3-7091-0352-4 }}</ref><ref>{{cite journal |last1=Xie A, Aihara Y, Bouryi VA, Nikitina E, Jahromi BS, Zhang ZD, Takahashi M, Macdonald RL. |title=Novel mechanism of endothelin-1-induced vasospasm after subarachnoid hemorrhage. |journal=Journal of Cerebral Blood Flow & Metabolism |year=2007 |volume=27 |issue=10 |pages=1692–1701 |doi=10.1038/sj.jcbfm.9600471 |pmid=17392694|s2cid=6830602 |doi-access=free }}</ref>

The use of [[calcium channel blocker]]s, thought to be able to prevent the spasm of blood vessels by preventing [[calcium]] from entering smooth muscle cells, has been proposed for prevention.<ref name="Armin06"/> The calcium channel blocker [[nimodipine]] when taken by mouth improves outcome if given between the fourth and twenty-first day after the bleeding, even if it does not reduce the amount of vasospasm detected on angiography.<ref name=Allen>{{cite journal | vauthors = Allen GS, Ahn HS, Preziosi TJ, et al | title = Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage | journal = The New England Journal of Medicine | volume = 308 | issue = 11 | pages = 619–24 | date = March 1983 | pmid = 6338383 | doi = 10.1056/NEJM198303173081103 }}</ref> It is the only [[Food and Drug Administration]] (FDA)-approved drug for treating cerebral vasospasm.<ref name="ChineseNeurosurg"/> In ''traumatic'' subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended.<ref>{{cite journal | vauthors = Vergouwen MD, Vermeulen M, Roos YB | title = Effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: a systematic review | journal = The Lancet. Neurology | volume = 5 | issue = 12 | pages = 1029–32 | date = December 2006 | pmid = 17110283 | doi = 10.1016/S1474-4422(06)70582-8 | s2cid = 43488740 }}</ref> Other calcium channel blockers and [[magnesium sulfate]] have been studied, but are not presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously.<ref name=CochraneNimo/>

Nimodipine is readily authorized in the form of tablets and solution for infusion for the prevention and treatment of complications due to vasospasm following subarachnoid hemorrhage. Another sustained formulation of nimodipine administered via an [[external ventricular drain]] (EVD), called EG-1962, is also available. In contrast to the tablets and solution formulations of Nimodipine which require an administration every 4hrs for a total of 21 days, the sustained formulation, EG-1962, needs to be administered once directly into the ventricles. The CSF concentrations from EG-1962, however, were at least 2 orders of magnitude higher than those with oral nimodipine. These results supported a phase 3 study that demonstrated a favorable safety profile for EG-1962 but yielded inconclusive efficacy results due to notable differences in clinical outcome based on baseline disease severity.<ref>{{cite journal |last1=Macdonald RL, Hänggi D, Strange P, Steiger HJ, Mocco J, Miller M, Mayer SA, Hoh BL, Faleck HJ, Etminan N, Diringer MN, Carlson AP, Aldrich F; NEWTON Investigators. |title=Nimodipine pharmacokinetics after intraventricular injection of sustained-release nimodipine for subarachnoid hemorrhage. |journal=Journal of Neurosurgery |year=2021 |volume=134 |issue=1 |pages=95–101 |doi=10.3171/2019.9.JNS191366 |pmid=31812149|s2cid=208870207 }}</ref><ref>{{cite journal |last1=Carlson AP, Hänggi D, Wong GK, Etminan N, Mayer SA, Aldrich F, Diringer MN, Schmutzhard E, Faleck HJ, Ng D, Saville BR, Bleck T, Grubb R Jr, Miller M, Suarez JI, Proskin HM, Macdonald RL; NEWTON Investigators |title=Single-Dose Intraventricular Nimodipine Microparticles Versus Oral Nimodipine for Aneurysmal Subarachnoid Hemorrhage. |journal=Stroke |year=2020 |volume=51 |issue=4 |pages=1142–1149 |doi=10.1161/STROKEAHA.119.027396 |pmid=32138631|s2cid=212569228 |doi-access=free }}</ref><ref>{{cite journal |last1=Zussman B, Weiner GM, Ducruet A. |title=Intraventricular Nimodipine for Aneurysmal Subarachnoid Hemorrhage: Results of the NEWTON Phase 1/2a Study. |journal=Neurosurgery |year=2017 |volume=81 |pages=N3–N4 |doi=10.1093/neuros/nyx260 |pmid=28873993|doi-access=free }}</ref>  

Some older studies have suggested that [[statin]] therapy might reduce vasospasm, but a subsequent meta-analysis including further trials did not demonstrate benefit on either vasospasm or outcomes.<ref>{{cite journal | vauthors = Vergouwen MD, de Haan RJ, Vermeulen M, Roos YB | title = Effect of statin treatment on vasospasm, delayed cerebral ischemia, and functional outcome in patients with aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis update | journal = Stroke | volume = 41 | issue = 1 | pages = e47-52 | date = January 2010 | pmid = 19875741 | doi = 10.1161/STROKEAHA.109.556332 | doi-access = free }}</ref> While corticosteroids with mineralocorticoid activity may help prevent vasospasm their use does not appear to change outcomes.<ref>{{cite journal | vauthors = Mistry AM, Mistry EA, Ganesh Kumar N, Froehler MT, Fusco MR, Chitale RV | title = Corticosteroids in the Management of Hyponatremia, Hypovolemia, and Vasospasm in Subarachnoid Hemorrhage: A Meta-Analysis | journal = Cerebrovascular Diseases | volume = 42 | issue = 3–4 | pages = 263–71 | date = 2016 | pmid = 27173669 | doi = 10.1159/000446251 | doi-access = free }}</ref>

{{Anchor|Triple H}}
A protocol referred to as "triple H" is often used as a measure to treat vasospasm when it causes symptoms; this is the use of [[intravenous fluid]]s to achieve a state of [[hypertension]] (high blood pressure), [[hypervolemia]] (excess fluid in the circulation), and hemodilution (mild dilution of the blood).<ref name=Kassell>{{cite journal | vauthors = Kassell NF, Peerless SJ, Durward QJ, Beck DW, Drake CG, Adams HP | title = Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension | journal = Neurosurgery | volume = 11 | issue = 3 | pages = 337–43 | date = September 1982 | pmid = 7133349 | doi = 10.1097/00006123-198209000-00001 }}</ref> Evidence for this approach is inconclusive; no randomized controlled trials have been undertaken to demonstrate its effect.<ref>{{cite journal | vauthors = Sen J, Belli A, Albon H, Morgan L, Petzold A, Kitchen N | author-link2=Anna-Maria Belli|title = Triple-H therapy in the management of aneurysmal subarachnoid haemorrhage | journal = The Lancet. Neurology | volume = 2 | issue = 10 | pages = 614–21 | date = October 2003 | pmid = 14505583 | doi = 10.1016/S1474-4422(03)00531-3 | s2cid = 38149776 }}</ref>

If the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of vasospasms and administer [[vasodilator]] medication (drugs that relax the blood vessel wall) directly into the artery. [[Angioplasty]] (opening the constricted area with a balloon) may also be performed.<ref name=Suarez/>

===Other complications===
[[Hydrocephalus]] (obstruction of the flow of cerebrospinal fluid) may complicate SAH in both the short and long term. It is detected on CT scanning, on which there is enlargement of the [[lateral ventricles]]. If the level of consciousness is decreased, drainage of the excess fluid is performed by therapeutic lumbar puncture, [[extraventricular drain]] (a temporary device inserted into one of the ventricles), or occasionally a permanent [[cerebral shunt|shunt]].<ref name=VanGijn2007/><ref name=Suarez/> Relief of hydrocephalus can lead to an enormous improvement in a person's condition.<ref name=oxford2/> Fluctuations in blood pressure and [[electrolyte imbalance]], as well as [[pneumonia]] and [[left ventricular failure|cardiac decompensation]] occur in about half the hospitalized persons with SAH and may worsen prognosis.<ref name=VanGijn2007/> [[Seizure]]s occur during the hospital stay in about a third of cases.<ref name=Suarez/>

People have often been treated with [[prophylaxis|preventative]] [[antiepileptic drugs|antiepileptic medications]].<ref name=Suarez/><ref name="pmid17695377">{{cite journal | vauthors = Rosengart AJ, Huo JD, Tolentino J, Novakovic RL, Frank JI, Goldenberg FD, Macdonald RL | title = Outcome in patients with subarachnoid hemorrhage treated with antiepileptic drugs | journal = Journal of Neurosurgery | volume = 107 | issue = 2 | pages = 253–60 | date = August 2007 | pmid = 17695377 | doi = 10.3171/JNS-07/08/0253 | s2cid = 37400347 }}</ref> This is controversial and not [[evidence-based medicine|based on good evidence]].<ref name="pmid16424735">{{cite journal | vauthors = Naval NS, Stevens RD, Mirski MA, Bhardwaj A | title = Controversies in the management of aneurysmal subarachnoid hemorrhage | journal = Critical Care Medicine | volume = 34 | issue = 2 | pages = 511–24 | date = February 2006 | pmid = 16424735 | doi = 10.1097/01.CCM.0000198331.45998.85 | s2cid = 24028808 }}</ref><ref name="pmid17763834">{{cite journal | vauthors = Liu KC, Bhardwaj A | title = Use of prophylactic anticonvulsants in neurologic critical care: a critical appraisal | journal = Neurocritical Care | volume = 7 | issue = 2 | pages = 175–84 | year = 2007 | pmid = 17763834 | doi = 10.1007/s12028-007-0061-5 | s2cid = 18547651 }}</ref> In some studies, use of these medications was associated with a worse prognosis; although it is unclear whether this might be because the drugs themselves actually cause harm, or because they are used more often in persons with a poorer prognosis.<ref name="prognostic"/><ref name="pmid15662039">{{cite journal | vauthors = Naidech AM, Kreiter KT, Janjua N, et al | title = Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage | journal = Stroke | volume = 36 | issue = 3 | pages = 583–7 | date = March 2005 | pmid = 15662039 | doi = 10.1161/01.STR.0000141936.36596.1e | doi-access = free }}</ref> There is a possibility of a gastric hemorrhage due to stress ulcers.<ref>{{cite book |title=Neurology and Neurosurgery Illustrated | vauthors = Lindsay KW, Bone I, Callander R |year=1993 |publisher=Churchill Livingstone |location=United States |isbn=978-0-443-04345-1}}</ref>

==Prognosis==

===Short-term outcomes===
SAH is often associated with a poor outcome.<ref name=Feigin05>{{cite journal | vauthors = Feigin VL, Rinkel GJ, Lawes CM, Algra A, Bennett DA, van Gijn J, Anderson CS | title = Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies | journal = Stroke | volume = 36 | issue = 12 | pages = 2773–80 | date = December 2005 | pmid = 16282541 | doi = 10.1161/01.STR.0000190838.02954.e8 | doi-access = free }}</ref> The death rate ([[mortality rate|mortality]]) for SAH is between 40 and 50 percent,<ref name="Teunissen96"/> but trends for survival are improving.<ref name=VanGijn2007/> Of those that survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever.<ref name=ISAT2005/> Delay in diagnosis of minor SAH (mistaking the sudden headache for migraine) contributes to poor outcome.<ref name=Kowalski/> Factors found on admission that are associated with poorer outcome include poorer neurological grade; [[systolic hypertension]]; a previous diagnosis of [[myocardial infarction|heart attack]] or SAH; [[liver disease]]; more blood and larger aneurysm on the initial CT scan; location of an aneurysm in the [[posterior (anatomy)|posterior]] [[circle of Willis|circulation]]; and higher age.<ref name="prognostic"/> Factors that carry a worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from [[vasospasm]], development of [[intracerebral hematoma]], or intraventricular hemorrhage (bleeding into the [[ventricular system|ventricles]] of the brain) and presence of [[fever]] on the eighth&nbsp;day of admission.<ref name="prognostic">{{cite journal | vauthors = Rosengart AJ, Schultheiss KE, Tolentino J, Macdonald RL | title = Prognostic factors for outcome in patients with aneurysmal subarachnoid hemorrhage | journal = Stroke | volume = 38 | issue = 8 | pages = 2315–21 | date = August 2007 | pmid = 17569871 | doi = 10.1161/STROKEAHA.107.484360 | doi-access = free }}</ref>

So-called "angiogram-negative subarachnoid hemorrhage", SAH that does not show an aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysm, but it is still associated with a risk of ischemia, rebleeding, and [[hydrocephalus]].<ref name="Rinkel93"/> Perimesencephalic SAH (bleeding around the [[mesencephalon]] in the brain), however, has a very low rate of rebleeding or delayed [[ischemia]], and the prognosis of this subtype is excellent.<ref>{{cite journal | vauthors = Greebe P, Rinkel GJ | title = Life expectancy after perimesencephalic subarachnoid hemorrhage | journal = Stroke | volume = 38 | issue = 4 | pages = 1222–4 | date = April 2007 | pmid = 17332451 | doi = 10.1161/01.STR.0000260093.49693.7a | doi-access = free }}</ref>

The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding.<ref name="Armin06"/> It is difficult to isolate the effects of SAH from those of other aspects of traumatic brain injury; it is unknown whether the presence of subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred.<ref name="Armin06"/> People with moderate and severe traumatic brain injury who have SAH when admitted to a hospital have as much as twice the risk of dying as those who do not.<ref name="Armin06"/> They also have a higher risk of severe disability and [[persistent vegetative state]], and traumatic SAH has been correlated with other markers of poor outcome such as [[post traumatic epilepsy]], hydrocephalus, and longer stays in the intensive care unit.<ref name="Armin06"/>  More than 90 percent of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12 have a good outcome.<ref name="Armin06"/>

There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of the gene encoding [[apolipoprotein E]] that also plays a role in [[Alzheimer's disease]]) seems to increase risk for delayed ischemia and a worse outcome.<ref name="pmid17709709">{{cite journal | vauthors = Lanterna LA, Ruigrok Y, Alexander S, Tang J, Biroli F, Dunn LT, Poon WS | title = Meta-analysis of APOE genotype and subarachnoid hemorrhage: clinical outcome and delayed ischemia | journal = Neurology | volume = 69 | issue = 8 | pages = 766–75 | date = August 2007 | pmid = 17709709 | doi = 10.1212/01.wnl.0000267640.03300.6b | s2cid = 8596810 }}</ref> The occurrence of [[hyperglycemia]] (high blood sugars) after an episode of SAH confers a higher risk of poor outcome.<ref>{{cite journal | vauthors = Kruyt ND, Biessels GJ, de Haan RJ, Vermeulen M, Rinkel GJ, Coert B, Roos YB | title = Hyperglycemia and clinical outcome in aneurysmal subarachnoid hemorrhage: a meta-analysis | journal = Stroke | volume = 40 | issue = 6 | pages = e424-30 | date = June 2009 | pmid = 19390078 | doi = 10.1161/STROKEAHA.108.529974 | s2cid = 7684816 | doi-access = free }}</ref>

===Long-term outcomes===
[[File:Gross pathology of subarachnoid hemorrhage.jpg|thumb|[[Autopsy]] of a case with subarachnoid hemorrhage. The arachnoid mater is left in place on the exterior surface, containing extensive hemorrhage that also fills the sulci, as detailed in magnified image.]]
Neurocognitive symptoms, such as [[fatigue (medical)|fatigue]], mood disturbances, and other related symptoms, are common [[sequela]]e. Even in those who have made good neurological recovery, anxiety, depression, [[posttraumatic stress disorder]], and cognitive impairment are common; 46 percent of people who have had a subarachnoid hemorrhage have cognitive impairment that affects their quality of life.<ref name=Suarez/> Over 60 percent report frequent headaches.<ref>{{cite journal | vauthors = Powell J, Kitchen N, Heslin J, Greenwood R | title = Psychosocial outcomes at three and nine months after good neurological recovery from aneurysmal subarachnoid haemorrhage: predictors and prognosis | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 72 | issue = 6 | pages = 772–81 | date = June 2002 | pmid = 12023423 | pmc = 1737916 | doi = 10.1136/jnnp.72.6.772 }}</ref> Aneurysmal subarachnoid hemorrhage may lead to damage of the [[hypothalamus]] and the [[pituitary gland]], two areas of the brain that play a central role in hormonal regulation and production. More than a quarter of people with a previous SAH may develop [[hypopituitarism]] (deficiencies in one or more of the [[Hypothalamic–pituitary hormone|hypothalamic–pituitary hormones]] such as [[growth hormone]], [[luteinizing hormone]], or [[follicle-stimulating hormone]]).<ref>{{cite journal | vauthors = Schneider HJ, Kreitschmann-Andermahr I, Ghigo E, Stalla GK, Agha A | title = Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review | journal = JAMA | volume = 298 | issue = 12 | pages = 1429–38 | date = September 2007 | pmid = 17895459 | doi = 10.1001/jama.298.12.1429 | doi-access = free }}</ref> SAH is also associated with [[SIADH]] and [[cerebral salt wasting]], and is the most common cause of the latter.

==Epidemiology==

[[File:SAH incidence graph.svg|thumb|upright=1.3|Average number of people with SAH per 100,000 person-years, broken down by age<ref name=DeRooij2007/>]]

According to a review of 51 studies from 21 countries, the average [[incidence (epidemiology)|incidence]] of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.<ref name=DeRooij2007>{{cite journal | vauthors = de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ | title = Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 78 | issue = 12 | pages = 1365–72 | date = December 2007 | pmid = 17470467 | pmc = 2095631 | doi = 10.1136/jnnp.2007.117655 }}</ref>

Although the group of people at risk for SAH is younger than the population usually affected by stroke,<ref name=Feigin05/> the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage.<ref name=DeRooij2007/> The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55.<ref name=DeRooij2007/> Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the [[menopause]], such as a decrease in [[estrogen]] levels.<ref name=DeRooij2007/>

Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage.<ref name=Ox2007/> But lifestyle factors are more important in determining overall risk.<ref name=Feigin05/> These risk factors are [[tobacco smoking|smoking]], hypertension (high blood pressure), and excessive [[alcohol consumption]].<ref name="Teunissen96">{{cite journal | vauthors = Teunissen LL, Rinkel GJ, Algra A, van Gijn J | title = Risk factors for subarachnoid hemorrhage: a systematic review | journal = Stroke | volume = 27 | issue = 3 | pages = 544–9 | date = March 1996 | pmid = 8610327 | doi = 10.1161/01.STR.27.3.544 }}</ref> Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked.<ref name=Feigin05/> Some protection of uncertain significance is conferred by [[caucasian race|caucasian ethnicity]], [[hormone therapy|hormone replacement therapy]], and [[diabetes mellitus]].<ref name=Feigin05/> There is likely an inverse relationship between total serum [[cholesterol]] and the risk of non-traumatic SAH, though confirmation of this association is hindered by a lack of studies.<ref name="Wang13">{{cite journal | vauthors = Wang X, Dong Y, Qi X, Huang C, Hou L | title = Cholesterol levels and risk of hemorrhagic stroke: a systematic review and meta-analysis | journal = Stroke | volume = 44 | issue = 7 | pages = 1833–9 | date = July 2013 | pmid = 23704101 | doi = 10.1161/STROKEAHA.113.001326 | doi-access = free }}</ref> Approximately 4 percent of aneurysmal bleeds occur after [[sexual intercourse]] and 10 percent of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.<ref name=oxford2/>

Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these are small and unlikely to rupture.<ref name=ISUIA>{{cite journal | vauthors = Wiebers DO | collaboration = International Study of Unruptured Intracranial Aneurysms Investigators | title = Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention | journal = The New England Journal of Medicine | volume = 339 | issue = 24 | pages = 1725–33 | date = December 1998 | pmid = 9867550 | doi = 10.1056/NEJM199812103392401 | doi-access = free }}</ref>

==History==
While the clinical picture of subarachnoid hemorrhage may have been recognized by [[Hippocrates]], the existence of cerebral aneurysms and the fact that they could rupture was not established until the 18th&nbsp;century.<ref name=Longstreth>{{cite journal | vauthors = Longstreth WT, Koepsell TD, Yerby MS, van Belle G | title = Risk factors for subarachnoid hemorrhage | journal = Stroke | volume = 16 | issue = 3 | pages = 377–85 | year = 1985 | pmid = 3890278 | doi = 10.1161/01.STR.16.3.377 | doi-access = free }}</ref> The associated symptoms were described in more detail in 1886 by [[Edinburgh]] physician Dr [[Byrom Bramwell]].<ref>{{cite journal |author=Bramwell B |title=Spontaneous meningeal haemorrhage |journal=Edinburgh Medical Journal |year=1886 |volume=32 |page=101}}</ref> In 1924, London [[neurologist]] Sir [[Charles Symonds|Charles P. Symonds]] (1890–1978) gave a complete account of all major symptoms of subarachnoid hemorrhage, and he coined the term "spontaneous subarachnoid hemorrhage".<ref name=Todd/><ref name=Longstreth/><ref>{{cite journal |author=Symonds CP |title=Spontaneous subarachnoid hemorrhage |journal=Quarterly Journal of Medicine |year=1924 |volume=18 |issue=69 |pages=93–122 |doi=10.1093/qjmed/os-118.69.93 }}</ref> Symonds also described the use of [[lumbar puncture]] and [[xanthochromia]] in diagnosis.<ref>{{cite journal | vauthors = Symonds CP | title = Spontaneous Sub-arachnoid Haemorrhage | journal = Proceedings of the Royal Society of Medicine | volume = 17 | issue = Neurol Sect | pages = 39–52 | year = 1924 | pmid = 19983808 | pmc = 2201441 | doi = 10.1177/003591572401700918 }}</ref>

The first surgical intervention was performed by Norman Dott, who was a pupil of [[Harvey Cushing]] then working in Edinburgh. He introduced the wrapping of aneurysms in the 1930s, and was an early pioneer in the use of angiograms.<ref name=Todd/> American [[neurosurgeon]] Dr [[Walter Dandy]], working in [[Baltimore]], was the first to introduce clips in 1938.<ref name=Dandy1938/> [[Microsurgery]] was applied to aneurysm treatment in 1972 in order to further improve outcomes.<ref>{{cite journal | vauthors = Krayenbühl HA, Yaşargil MG, Flamm ES, Tew JM | title = Microsurgical treatment of intracranial saccular aneurysms | journal = Journal of Neurosurgery | volume = 37 | issue = 6 | pages = 678–86 | date = December 1972 | pmid = 4654697 | doi = 10.3171/jns.1972.37.6.0678 }}</ref> The 1980s saw the introduction of triple H therapy<ref name=Kassell/> as a treatment for delayed ischemia due to [[vasospasm]], and trials with nimodipine<ref name=Allen/><ref>{{cite journal | vauthors = Pickard JD, Murray GD, Illingworth R, et al | title = Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial | journal = BMJ | volume = 298 | issue = 6674 | pages = 636–42 | date = March 1989 | pmid = 2496789 | pmc = 1835889 | doi = 10.1136/bmj.298.6674.636 }}</ref> in an attempt to prevent this complication. In 1983, the Russian neurosurgeon Zubkov and colleagues reported the first use of transluminal balloon angioplasty for vasospasm after aneurysmal SAH.<ref>{{cite journal | vauthors = Zubkov I, Nikiforov BM, Shustin VA | title = [1st attempt at dilating spastic cerebral arteries in the acute stage of rupture of arterial aneurysms] | journal = Zhurnal Voprosy Neirokhirurgii Imeni N. N. Burdenko | volume = 5 | issue = 5 | pages = 17–23 | date = September–October 1983 | pmid = 6228084 }}</ref><ref>{{cite journal | vauthors = Zubkov YN, Nikiforov BM, Shustin VA | title = Balloon catheter technique for dilatation of constricted cerebral arteries after aneurysmal SAH | journal = Acta Neurochirurgica | volume = 70 | issue = 1–2 | pages = 65–79 | date = September–October 1984 | pmid = 6234754 | doi = 10.1007/BF01406044 | s2cid = 1628687 }}</ref> The Italian neurosurgeon Dr Guido Guglielmi introduced his endovascular coil treatment in 1991.<ref name=St2001/><ref name=Guiglielmi1991/>

== References ==
{{Reflist}}

== External links ==
{{Commons}}
{{Medical resources
| DiseasesDB      = 12602
| ICD10           = {{ICD10|I|60||i|60}}, {{ICD10|P|10|3|p|10}}, {{ICD10|S|06|6|s|00}}
| ICD9            = {{ICD9|430}}, {{ICD9|852.0}}-{{ICD9|852.1}}
| OMIM            = 105800
| MedlinePlus     = 000701
| eMedicineSubj   = med
| eMedicineTopic  = 2883
| eMedicine_mult  = {{eMedicine2|neuro|357}} {{eMedicine2|emerg|559}}
| MeshID          = D013345
}}
{{Spoken Wikipedia|Subarachnoid Haemorrhage.ogg|date=2008-08-09}}

{{Cerebrovascular diseases}}
{{Neurotrauma}}

{{Featured article}}

{{DEFAULTSORT:Subarachnoid Hemorrhage}}
[[Category:Central nervous system disorders]]
[[Category:Cerebrovascular diseases]]
[[Category:Disorders causing seizures]]
[[Category:Intensive care medicine]]
[[Category:Neurosurgery]]
[[Category:Neurotrauma]]
[[Category:Wikipedia medicine articles ready to translate]]
[[Category:Wikipedia emergency medicine articles ready to translate]]