Subarachnoid hemorrhage: Difference between revisions
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{{Infobox_Disease | |
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Name = Subarachnoid hemorrhage | |
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Image = Subarachnoid haemorrhage.jpg | |
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Caption = CT scan of the brain showing subarachnoid hemorrhage as a white area in the center | |
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DiseasesDB = 12602 | |
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ICD10 = {{ICD10|I|60||i|60}}, {{ICD10|S|06|6|s|00}} | |
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ICD9 = {{ICD9|430}}, {{ICD9|852.0}}-{{ICD9|852.1}} | |
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ICDO = | |
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OMIM = 105800 | |
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MedlinePlus = 000701 | |
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eMedicineSubj = med | |
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eMedicineTopic = 2883 | |
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eMedicine_mult = {{eMedicine2|neuro|357}} {{eMedicine2|emerg|559}} | |
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MeshID = D013345 | |
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}} |
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A '''subarachnoid hemorage''' ('''SAH''', {{pron-en|ˌsʌbəˈræknɔɪd ˈhɛm(ə)rɪdʒ}}), or '''subarachnoid haemorrhage''' in [[American and British English spelling differences|British English]], is [[bleeding]] into the [[subarachnoid space]]—the area between the [[arachnoid (brain)|arachnoid membrane]] and the [[pia mater]] surrounding the [[brain]]. This may occur spontaneously, usually from a ruptured [[cerebral aneurysm]], or may result from [[head injury]]. [[Symptom]]s include an intense [[headache]] with a rapid onset ("[[thunderclap headache]]"), [[vomiting]], and an altered [[level of consciousness]].<ref name=vanGijn/> The [[diagnosis]] is generally confirmed with a [[computed tomography|CT scan]] of the head, or occasionally by [[lumbar puncture]]. SAH is managed with close observation and prompt [[neurosurgery|neurosurgical]] and [[interventional radiology|radiological]] therapies, medications and other management methods to help prevent recurrence of the bleeding and complications. Surgery for aneurysms was introduced in the 1930s, but since the 1990s many aneurysms are treated by a less invasive procedure called "[[Guglielmi Detachable Coil|coiling]]", which is carried out by instrumentation through large blood vessels.<ref name=vanGijn/> |
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SAH is a [[medical emergency]] and can lead to death or severe [[disability]]—even when recognized and treated at an early stage. Up to half of all cases of SAH are fatal and 10–15% die before reaching a hospital,<ref name=vanGijn/> and those who survive often have neurological or cognitive impairment.<ref name=Suarez/> Subarachnoid hemorrhage is considered a form of [[stroke]] and causes 1–7% of all strokes.<ref name=Feigin05/> |
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==Signs and symptoms== |
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The classic symptom of subarachnoid hemorrhage is [[thunderclap headache]] (a headache described as "like being kicked in the head",<ref name="oxford">{{cite book | last=Longmore | first=Murray | coauthors=Ian Wilkinson, Tom Turmezei, Chee Kay Cheung | title=Oxford Handbook of Clinical Medicine, 7th edition | publisher=Oxford University Press | year=2007 | pages=841 | isbn=0-19-856837-1 }}</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 | last=Ramrakha | first=Punit | coauthors=Kevin Moore | title=Oxford Handbook of Acute Medicine, 2nd edition | publisher=Oxford University Press | year=2007 | pages=466–470 | isbn=0-19-852072-6 }}</ref> About one-third of sufferers have no symptoms apart from the characteristic headache, and about one in ten people who seek [[Health care|medical care]] with this symptom are later diagnosed with a subarachnoid hemorrhage.<ref name=vanGijn>{{cite journal |author=van Gijn J, Kerr RS, Rinkel GJ |title=Subarachnoid haemorrhage |journal=Lancet |volume=369 |issue=9558 |pages=306–18 |year=2007 |pmid=17258671 |doi=10.1016/S0140-6736(07)60153-6}}</ref> [[Vomiting]] may be present, and 1 in 14 have [[seizure]]s.<ref name=vanGijn/> [[Confusion]], decreased level of consciousness or [[coma]] may be present, as may neck stiffness and other signs of [[meningism]].<ref name=vanGijn/> Neck stiffness usually presents six hours after initial onset of SAH.<ref name=OTV3>{{cite book |title=Oxford Textbook of Medicine, Fourth Edition, Volume 3 |last=Warrell |first=David A |coauthors=Timothy M. Cox, ''et al'' |year=2003 |publisher=Oxford |isbn=0-19-857013-9 |pages=1032–1034}}</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=vanGijn/> [[Intraocular hemorrhage]] (bleeding into the eyeball) may occur in response to the raised pressure: subhyaloid hemorrhage (bleeding under the 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% of cases) and is more common in more severe SAH.<ref name=mccarron>{{cite journal |author=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 |year=2004 |pmid=14966173 |pmc=1738971 |url=http://jnnp.bmj.com/cgi/content/full/75/3/491 |doi=10.1136/jnnp.2003.016816}}</ref> |
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[[Oculomotor nerve]] abnormalities (affected eye looking downward and outward and [[Ptosis (eyelid)|inability to lift the eyelid on the same side]]) or [[palsy]] (loss of feeling) may indicate bleeding from the [[posterior communicating artery]].<ref name=vanGijn/><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=vanGijn/> SAH in a person known to have fits is often diagnostic of an [[arteriovenous malformation]].<ref name=oxford2/> |
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yal are all suckers for using this website when you know that you can add stuff in. suckers arrhythmia]]s (irregularities in the heart rate and rhythm), [[electrocardiogram|electrocardiographic changes]] (in 27% of cases)<ref name="OHA">{{cite book | last=Allman | first=Keith G. | coauthors=Iain H. Wilson | title=Oxford Handbook of Anaesthesia, 2nd edition | publisher=Oxford University Press | year=2006 | pages=408–409 | isbn=0198566090 }}</ref> and [[cardiac arrest]] (in 3% of cases) may occur rapidly after the onset of hemorrhage.<ref name=vanGijn/><ref>{{cite journal |author=Banki NM, Kopelnik A, Dae MW, ''et al'' |title=Acute neurocardiogenic injury after subarachnoid hemorrhage |journal=Circulation |volume=112 |issue=21 |pages=3314–9 |year=2005 |pmid=16286583 |doi=10.1161/CIRCULATIONAHA.105.558239 | url=http://circ.ahajournals.org/cgi/content/full/112/21/3314}}</ref> |
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Subarachnoid hemorrhage may also occur in people who have suffered 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 |author=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 |year=2002 |month=February |pmid=11844260 |doi=10.1097/00006123-200202000-00006}}</ref> |
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==Diagnosis== |
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[[Image:Coiled PCA residual aneurysm arteriogram.JPG|thumb|[[Arteriogram]] showing a partially coiled aneurysm (''indicated by yellow arrows'') of the [[posterior cerebral artery]] with a residual aneurysmal sac. The patient was a 34-year-old woman initially treated for a subarachnoid hemorrhage.]] |
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[[Image:Thisisspinaltap.jpg|thumb|A [[lumbar puncture]] in progress.]] |
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The initial steps for evaluating a person with a suspected subarachnoid hemorrhage are obtaining a [[medical history]] and performing a [[physical examination]]; these are aimed at determining whether the symptoms are due to SAH or to another cause. The diagnosis cannot, however, be made on clinical grounds alone; therefore [[medical imaging]] is generally required to confirm or exclude bleeding. The modality of choice is [[computed tomography]] (CT scan) of the brain. This has a high [[Sensitivity (tests)|sensitivity]] and will correctly identify over 95% of cases—especially on the first day after the onset of bleeding. [[Magnetic resonance imaging]] (MRI) may be more sensitive than CT after several days.<ref name=vanGijn/> |
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[[Lumbar puncture]], in which [[cerebrospinal fluid]] (CSF) is removed with a needle from the [[lumbar]] sac, will show evidence of hemorrhage in 3% of people in whom CT was found normal; lumbar puncture is therefore regarded as mandatory in people with suspected SAH if imaging is negative.<ref name=vanGijn/> 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/> The CSF sample is also examined for [[xanthochromia]]—the yellow appearance of [[Centrifugation|centrifugated]] fluid. More sensitive is [[spectrophotometry]] (measuring the absorption of particular wavelengths of light) for detection of [[bilirubin]], a breakdown product of [[hemoglobin]] from red blood cells.<ref name=vanGijn/><ref name=Cruickshank>{{cite journal |author=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 |year=2008 |month=May |pmid=18482910 |doi=10.1258/acb.2008.007257 |url=http://acb.rsmjournals.com/cgi/content/full/45/3/238}}</ref> Xanthochromia and spectrophotometry remain reliable ways to detect SAH several days after the onset of headache.<ref name=Cruickshank/> An interval of at least 12 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=vanGijn/><ref name=Cruickshank/> |
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As only 10% of people admitted to the emergency department with a thunderclap headache are suffering from an SAH, other possible causes are usually considered simultaneously, such as [[meningitis]], [[migraine]], and [[cerebral venous sinus thrombosis]].<ref name="oxford"/> [[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% 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 |author=Kowalski RG, Claassen J, Kreiter KT, ''et al'' |title=Initial misdiagnosis and outcome after subarachnoid hemorrhage |journal=Journal of the American Medical Association |volume=291 |issue=7 |pages=866–9 |year=2004 |month=February |pmid=14970066 |doi=10.1001/jama.291.7.866 |url=http://jama.ama-assn.org/cgi/content/full/291/7/866}}</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 |author=Suarez JI, Tarr RW, Selman WR |title=Aneurysmal subarachnoid hemorrhage |journal=New England Journal of Medicine |volume=354 |issue=4 |pages=387–96 |year=2006 |month=January |pmid=16436770 |doi=10.1056/NEJMra052732}}</ref> |
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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=vanGijn/><ref name=Suarez/> |
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==Causes== |
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In 85% of cases of spontaneous SAH, the cause is rupture of 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 of SAH are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture.<ref name=vanGijn/> |
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In 15–20% of cases of spontaneous SAH, no aneurysm is detected on the first [[angiogram]].<ref name="Rinkel93">{{cite journal |author=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 |year=1993 |pmid=8362440 | url=http://stroke.ahajournals.org/cgi/reprint/24/9/1403 | format=PDF |date=09/01/1993}}</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=vanGijn/> The remainder are due to other disorders affecting the blood vessels (such as [[Cerebral arteriovenous malformation|arteriovenous malformations]]), disorders of the blood vessels in the [[spinal cord]], and bleeding into various [[tumor]]s.<ref name=vanGijn/> [[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"/> |
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Subarachnoid blood can be detected on CT scanning in as many as 60% of people with [[traumatic brain injury]].<ref name="Armin06">{{cite journal |author=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 |year=2006 |month=June |pmid=16759448 |doi=10.1179/016164106X115053}}</ref> Traumatic SAH (tSAH) usually occurs near the site of a [[skull fracture]] or [[intracerebral contusion]].<ref name="Rinkel93"/> It usually happens in the setting of other forms of traumatic brain injury and has been linked with a poorer prognosis. It is unclear, however, if this is a direct result of the SAH or whether the presence of subarachnoid blood is simply an indicator of severity of the head injury and the prognosis is determined by other associated mechanisms.<ref name="Armin06"/> |
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==Classification== |
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There are several grading scales available for SAH. The [[Glasgow Coma Scale]] is ubiquitously used for assessing consciousness. Three specialized scores are used to evaluate SAH; in each, a higher number is associated with a worse outcome.<ref>{{cite journal |author=Rosen D, Macdonald R |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}}</ref> These scales have been derived by retrospectively matching characteristics of patients with their outcomes. |
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The first scale of severity was described by Hunt and Hess in 1968:<ref name="H&H">{{cite journal |author=Hunt W, Hess R |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 |year=1968 |pmid=5635959}}</ref> |
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{| class="prettytable" style = "width:75%; font-size:85%; margin-left:15px; text-align:center" |
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!width="50"| Grade |
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! Signs and symptoms |
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! Survival |
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|- |
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! 1 |
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| align="left" |[[Asymptomatic]] or minimal headache and slight neck stiffness ||70% |
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|- |
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!2 |
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| align="left"| Moderate to severe headache; neck stiffness; no [[neurology|neurologic]] deficit except [[cranial nerve]] [[palsy]] || 60% |
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|- |
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!3 |
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|align="left"| [[Drowsy]]; minimal neurologic deficit || 50% |
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|- |
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!4 |
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| align="left"| Stuporous; moderate to severe hemiparesis; possibly early [[decerebrate rigidity]] and vegetative disturbances || 20% |
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|- |
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!5 |
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| align="left" | Deep coma; [[abnormal posturing|decerebrate rigidity]]; [[moribund]] || 10% |
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|- |
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|} |
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The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan.<ref name="Fisher">{{cite journal |author=Fisher C, Kistler J, Davis J |title=Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning |journal=Neurosurgery |volume=6 |issue=1 |pages=1–9 |year=1980 |pmid=7354892 |doi=10.1097/00006123-198001000-00001}}</ref> This scale has been modified by Claassen and coworkers, reflecting the additive risk from SAH size and accompanying [[intraventricular hemorrhage]].<ref name="Claassen">{{cite journal |author=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 |year=2001 |month=September |pmid=11546890 |url=http://stroke.ahajournals.org/cgi/content/full/32/9/2012 |doi=10.1161/hs0901.095677}}</ref> |
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{| class="prettytable" style = "width:75%; font-size:85%; margin-left:15px; text-align:center" |
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!width="50"| Grade |
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! Appearance of hemorrhage |
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|- |
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! 1 |
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| align="left" |None evident |
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|- |
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!2 |
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| align="left"| Less than 1 mm thick |
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|- |
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!3 |
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|align="left"| More than 1 mm thick |
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|- |
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!4 |
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| align="left"| Any thickness with intraventricular hemorrhage or [[parenchymal]] extension |
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|- |
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|} |
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The World Federation of Neurosurgeons classification uses Glasgow coma score (GCS) and [[focal neurological deficit]] to gauge severity of symptoms.<ref name="WorldFed">{{cite journal |author=Teasdale G, Drake C, Hunt W, Kassell N, Sano K, Pertuiset B, De Villiers J |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 |year=1988 |pmid=3236024 | pmc=1032822}}</ref> |
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{| class="prettytable" style = "width:75%; font-size:85%; margin-left:15px; text-align:center" |
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!width="50"| Grade |
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! GCS |
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! Focal neurological deficit |
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|- |
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! 1 |
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| 15 || Absent |
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|- |
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! 2 |
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| 13–14 || Absent |
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|- |
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! 3 |
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| 13–14 || Present |
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|- |
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! 4 |
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| 7–12 || Present or absent |
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|- |
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! 5 |
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| <7 || Present or absent |
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|- |
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|} |
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A comprehensive [[classification scheme]] has been suggested by Ogilvy and Carter to predict outcome and gauge therapy.<ref name="pmid9588539">{{cite journal |author=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 |year=1998 |month=May |pmid=9588539 |doi=10.1097/00006123-199805000-00001}}</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 mm; and posterior circulation aneurysm 25 mm or more.<ref name="pmid9588539"/> |
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==Treatment== |
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Management involves general measures to stabilize the patient 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=vanGijn/> |
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===General measures=== |
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Stabilizing the patient 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% may have further bleeding soon after admission. Nutrition is an early priority, with [[mouth|oral]] or [[Nasogastric intubation|nasogastric tube]] feeding being preferable over [[parenteral]] routes. [[Analgesia]] (pain control) is generally 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 muscle|calves]] or both.<ref name=vanGijn/> 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"/> |
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===Prevention of rebleeding=== |
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[[Image:Arteries beneath brain Gray closer.jpg|right|thumb|The arteries of the brain, viewed from underneath. Image originally from [[Gray's Anatomy]], 1918.]] |
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People whose CT scan shows a large [[hematoma]], depressed level of consciousness or [[focal neurology|focal neurological symptoms]] may benefit from urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are stabilized more extensively and undergo an [[Cerebral angiography|transfemoral angiogram]] or CT angiogram later. It is hard to predict who will suffer a rebleed, yet it may happen at any time and carries a dismal prognosis. After the first 24 hours have passed, rebleeding risk remains around 40% over the subsequent four weeks, suggesting that interventions should be aimed at reducing this risk as soon as possible.<ref name=vanGijn/> |
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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 |author=Dandy WE |title=Intracranial aneurysm of the internal carotid artery: Cured by operation |journal=Annals of Surgery |volume=107 |issue=5 |pages=654–9 |year=1938 |pmid=17857170 |doi=10.1097/00000658-193805000-00003 | pmc=1386933}}</ref> and [[Guglielmi Detachable Coil|coiling]].<ref name=Guiglielmi1991>{{cite journal |author=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 |year=1991 |pmid=2045924}}</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=vanGijn/> |
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Generally, the decision between clipping and coiling is made on the basis of the location of the aneurysm, its size and the condition of the patient. 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 |author=Molyneux AJ, Kerr RS, Yu LM, ''et al'' |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}}</ref> These approaches are based on general experience, and the only [[randomized controlled trial]] directly comparing the different modalities was performed in relatively well patients with small (less than 10 mm) aneurysms of the [[anterior cerebral artery]] and [[anterior communicating artery]] (together the "anterior circulation"), who constitute about 20% of all patients with aneurysmal SAH.<ref name=ISAT2005/><ref>{{cite journal |author=van der Schaaf I, Algra A, Wermer M, ''et al'' |title=Endovascular coiling versus neurosurgical clipping for patients with aneurysmal subarachnoid haemorrhage |journal=Cochrane Database of Systematic Reviews (Online) |issue=4 |pages=CD003085 |year=2005 |pmid=16235314 |doi=10.1002/14651858.CD003085.pub2 |url=http://mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD003085/frame.html}}</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% [[absolute risk reduction]], 23.5% [[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% 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 |author=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 |year=2007 |pmid=17395870 |doi=10.1161/STROKEAHA.106.466987 |url=http://stroke.ahajournals.org/cgi/content/full/38/5/1538}}</ref> Other trials have also found a higher rate of recurrence necessitating further treatments.<ref>{{cite journal |author=Piotin M, Spelle L, Mounayer C, ''et al'' |title=Intracranial aneurysms: Treatment with bare platinum coils—aneurysm packing, complex coils, and angiographic recurrence |journal=Radiology |volume=243 |issue=2 |pages=500–8 |year=2007 |pmid=17293572 |doi=10.1148/radiol.2431060006 |url=http://radiology.rsnajnls.org/cgi/content/full/243/2/500}}</ref><ref>{{cite journal |author=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 |year=2003 |pmid=12775880 |doi=10.1161/01.STR.0000073841.88563.E9 | url=http://stroke.ahajournals.org/cgi/content/full/34/6/1398}}</ref> |
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===Vasospasm=== |
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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. 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 all people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those suffer permanent damage as a result.<ref name=CochraneNimo>{{cite journal |author=Dorhout Mees S, Rinkel G, Feigin V, ''et al'' |title=Calcium antagonists for aneurysmal subarachnoid haemorrhage |journal=Cochrane Database of Systematic Reviews (Online) |issue=3 |pages=CD000277 |year=2007 |pmid=17636626 |doi=10.1002/14651858.CD000277.pub3}}</ref> It is possible to screen for the development of vasospasm with transcranial doppler every 24–48 hours. A blood flow velocity of more than 120 [[Metre per second|centimeters per second]] is suggestive of vasospasm.<ref name=Suarez/> |
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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 the prevention of vasospasm.<ref name="Armin06"/> The oral calcium channel blocker [[nimodipine]] improves outcome if administered between the fourth and twenty-first day after the hemorrhage, even if it does not significantly reduce the amount of vasospasm detected on angiography.<ref name=Allen>{{cite journal |author=Allen GS, Ahn HS, Preziosi TJ, ''et al'' |title=Cerebral arterial spasm: A controlled trial of nimodipine in patients with subarachnoid hemorrhage |journal=New England Journal of Medicine |volume=308 |issue=11 |pages=619–24 |year=1983 |pmid=6338383}}</ref> In ''traumatic'' subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended.<ref>{{cite journal |author=Vergouwen MD, Vermeulen M, Roos YB |title=Effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: A systematic review |journal=Lancet Neurology |volume=5 |issue=12 |pages=1029–32 |year=2006 |month=December |pmid=17110283 |doi=10.1016/S1474-4422(06)70582-8}}</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/> |
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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 therapy#IV fluids|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 |author=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 |year=1982 |month=September |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 benefits.<ref>{{cite journal |author=Sen J, Belli A, Albon H, Morgan L, Petzold A, Kitchen N |title=Triple-H therapy in the management of aneurysmal subarachnoid haemorrhage |journal=Lancet Neurology |volume=2 |issue=10 |pages=614–21 |year=2003 |month=October |pmid=14505583 |doi=10.1016/S1474-4422(03)00531-3}}</ref> |
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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/> |
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===Other complications=== |
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[[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 the one of the ventricles) or occasionally a permanent [[cerebral shunt|shunt]].<ref name=vanGijn/><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 disturbance]]s, 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=vanGijn/> [[Seizure]]s occur during the hospital stay in about a third of cases.<ref name=Suarez/> Many believe that patients might benefit from [[prophylaxis|prevention]] with [[antiepileptic drug]]s.<ref name=Suarez/> Although this is widely practiced,<ref name="pmid17695377">{{cite journal |author=Rosengart AJ, Huo JD, Tolentino J, ''et al'' |title=Outcome in patients with subarachnoid hemorrhage treated with antiepileptic drugs |journal=Journal of Neurosurgery |volume=107 |issue=2 |pages=253–60 |year=2007 |month=August |pmid=17695377 |doi=10.3171/JNS-07/08/0253}}</ref> it is controversial and not [[evidence based medicine|based on good evidence]].<ref name="pmid16424735">{{cite journal |author=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 |year=2006 |month=February |pmid=16424735 | doi=10.1097/01.CCM.0000198331.45998.85}}</ref><ref name="pmid17763834">{{cite journal |author=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}}</ref> In some studies, use of these drugs was associated with a worse prognosis; this might be because they actually cause harm, or because they are used more often in persons with a poorer prognosis.<ref name="prognostic"/><ref name="pmid15662039">{{cite journal |author=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 |year=2005 |month=March |pmid=15662039 |doi=10.1161/01.STR.0000141936.36596.1e |url=http://stroke.ahajournals.org/cgi/content/full/36/3/583}}</ref> |
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==Prognosis== |
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===Early morbidity and mortality=== |
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SAH is often associated with a poor outcome.<ref name=Feigin05>{{cite journal |author=Feigin VL, Rinkel GJ, Lawes CM, ''et al'' |title=Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies |journal=Stroke |volume=36 |issue=12 |pages=2773–80 |year=2005 |pmid=16282541 |doi=10.1161/01.STR.0000190838.02954.e8 |url=http://stroke.ahajournals.org/cgi/content/full/36/12/2773}}</ref> The death rate ([[mortality rate|mortality]]) for SAH is between 40 and 50%,<ref name="Teunissen96"/> but trends for survival are improving.<ref name=vanGijn/> Of those who 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|liver disease]]; more blood and larger aneurysm on the initial CT scan; location of an aneurysm in the [[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 day of admission.<ref name="prognostic">{{cite journal |author=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 |year=2007 |month=August |pmid=17569871 |doi=10.1161/STROKEAHA.107.484360 | url=http://stroke.ahajournals.org/cgi/content/full/38/8/2315}}</ref> |
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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; however, 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 |author=Greebe P, Rinkel GJ |title=Life expectancy after perimesencephalic subarachnoid hemorrhage |journal=Stroke |volume=38 |issue=4 |pages=1222–4 |year=2007 |month=April |pmid=17332451 |doi=10.1161/01.STR.0000260093.49693.7a |url=http://stroke.ahajournals.org/cgi/content/full/38/4/1222}}</ref> |
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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"/> However, more than 90% of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12 have a good outcome.<ref name="Armin06"/> |
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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 |author=Lanterna LA, Ruigrok Y, Alexander S, ''et al'' |title=Meta-analysis of APOE genotype and subarachnoid hemorrhage: clinical outcome and delayed ischemia |journal=Neurology |volume=69 |issue=8 |pages=766–75 |year=2007 |month=August |pmid=17709709 |doi=10.1212/01.wnl.0000267640.03300.6b}}</ref> |
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===Long-term outcomes=== |
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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% of people who have suffered a subarachnoid hemorrhage have cognitive impairment that affects their quality of life.<ref name=Suarez/> Over 60% report frequent headaches.<ref>{{cite journal |author=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 |year=2002 |month=June |pmid=12023423 | pmc=1737916 |url=http://jnnp.bmj.com/cgi/content/full/72/6/772 |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 hormones such as [[growth hormone]], [[luteinizing hormone]] or [[follicle-stimulating hormone]]).<ref>{{cite journal |author=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=Journal of the American Medical Association |volume=298 |issue=12 |pages=1429–38 |year=2007 |month=September |pmid=17895459 |doi=10.1001/jama.298.12.1429 |url=http://jama.ama-assn.org/cgi/content/full/298/12/1429}}</ref> |
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==Epidemiology== |
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[[Image:SAH incidence graph.svg|right|thumb|300px|Average number of people with SAH per 100,000 person-years, broken down by age.<ref name=DeRooij2007/>]] |
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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 America|South]] and Central America, in contrast, have a rate of 4.2 per 100,000 on average.<ref name=DeRooij2007>{{cite journal |author=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 |year=2007 |month=December |pmid=17470467 |doi=10.1136/jnnp.2007.117655}}</ref> |
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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 much less likely than middle-aged people (risk ratio 0.1, or 10%) to suffer a subarachnoid hemorrhage.<ref name=DeRooij2007/> The risk continues to rise with age and is 60% higher in the very elderly (over 85) than in those between 45 and 55.<ref name=DeRooij2007/> Risk of SAH is about 25% 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/> |
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Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people who have suffered a subarachnoid hemorrhage.<ref name="oxford"/> However, 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 [[alcoholic beverage|alcohol]] intake.<ref name="Teunissen96">{{cite journal |author=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 |year=1996 |pmid=8610327 |url=http://stroke.ahajournals.org/cgi/content/full/27/3/544 |date=03/01/1996}}</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]], [[diabetes mellitus]] and higher than normal levels of [[cholesterol]].<ref name=Feigin05/> Approximately 4% of aneurysmal bleeds occur after [[sexual intercourse]] and 10% of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.<ref name=oxford2/> |
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Overall, about 1% of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture.<ref name=ISUIA>{{cite journal |author=International Study of Unruptured Intracranial Aneurysms Investigators |title=Unruptured intracranial aneurysms—risk of rupture and risks of surgical intervention |journal=New England Journal of Medicine |volume=339 |issue=24 |pages=1725–33 |year=1998 |month=December |pmid=9867550 | url=http://content.nejm.org/cgi/content/full/339/24/1725 |doi=10.1056/NEJM199812103392401}}</ref> |
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==Screening and prevention== |
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[[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]]. If someone has two or more first-degree relatives who have suffered an aneurysmal subarachnoid hemorrhage, screening may be worthwhile.<ref name=vanGijn/><ref name=WhiteWardlaw>{{cite journal |author=White PM, Wardlaw JM |title=Unruptured intracranial aneurysms |journal=Journal of Neuroradiology |volume=30 |issue=5 |pages=336–50 |year=2003 |month=December |pmid=14752379 |url=http://www.em-consulte.com/article/126528}}</ref> |
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[[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% 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 suffered a ruptured aneurysm.<ref>{{cite journal |author=Gibbs GF, Huston J, Qian Q, ''et al'' |title=Follow-up of intracranial aneurysms in autosomal-dominant polycystic kidney disease |journal=Kidney International |volume=65 |issue=5 |pages=1621–7 |year=2004 |month=May |pmid=15086900 |doi=10.1111/j.1523-1755.2004.00572.x}}</ref> |
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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 who had previously suffered a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those who had previously suffered SAH were more likely to bleed from other aneurysms. In contrast, those who had never bled and had small aneurysms (smaller than 10 mm) were very unlikely to suffer 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 only considered for [[Preventative medicine|preventative treatment]] if they have a reasonable [[life expectancy]] and have aneurysms that are highly likely to rupture.<ref name=WhiteWardlaw/> |
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==History== |
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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 century.<ref name=Longstreth>{{cite journal |author=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 |url=http://stroke.ahajournals.org/cgi/reprint/16/3/377.pdf}}</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 | pages=101}}</ref> In 1924, London [[neurologist]] Sir Dr [[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=Longstreth/><ref>{{cite journal | author=Symonds CP | title=Spontaneous subarachnoid hemorrhage | journal=Quarterly Journal of Medicine | year=1924 | volume=18 | pages=93–122}}</ref><ref name=Todd>{{cite journal |author=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 |year=1990 |month=June |pmid=2199609 | pmc=1014202}}</ref> Symonds also described the use of lumbar puncture and xanthochromia in diagnosis.<ref>{{cite journal | author=Symonds CP | title=Spontaneous sub-arachnoid hæmorrhage | journal=Proceedings of the Royal Society of Medicine | year=1924 | volume=17 | pages=39–52 | pmc=2201441}}</ref> |
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The first surgical intervention was performed by Mr Norman Dott, who was a pupil of Dr [[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 |author=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 |year=1972 |month=December |pmid=4654697}}</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/> in an attempt to prevent this complication. The Italian neurosurgeon Dr Guido Guiglielmi introduced his endovascular coil treatment in 1991.<ref name=Guiglielmi1991/><ref>{{cite journal |author=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 |year=2001 |month=May |pmid=11337350 |url=http://www.ajnr.org/cgi/content/full/22/5/1011 |date=05/01/2001}}</ref> |
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==References== |
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{{Reflist|2}} |
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==External links== |
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{{Spoken Wikipedia|Subarachnoid Haemorrhage.ogg|2008-08-09}} |
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* [http://neuroland.com/cvd/sah.htm Neuroland] SAH page |
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{{Cerebrovascular diseases}} |
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{{Neurotrauma}} |
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{{featured article}} |
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[[Category:Neurotrauma]] |
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[[Category:Neurosurgery]] |
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[[Category:Intensive care medicine]] |
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{{Link FA|de}} |
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[[de:Subarachnoidalblutung]] |
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[[es:Hemorragia subaracnoidea]] |
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[[fr:Hémorragie méningée]] |
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[[nl:Subarachnoïdale bloeding]] |
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[[ja:クモ膜下出血]] |
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[[no:Hjernehinneblødning]] |
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[[pl:Krwotok podpajęczynówkowy]] |
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[[sv:Akut subarachnoidalblödning]] |
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