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| | | [[File:Siren.gif|30px|link=Subarachnoid hemorrhage resident survival guide]]|| <br> || <br> |
| | | [[Subarachnoid hemorrhage resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
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| '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' | | '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' |
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| {{Infobox_Disease | | | {{Infobox_Disease | |
| Name = Subarachnoid hemorrhage | | | Name = Subarachnoid hemorrhage | |
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| {{Subarachnoid hemorrhage}} | | {{Subarachnoid hemorrhage}} |
| {{CMG}}; '''Associate Editor(s)-In-Chief:''' {{CZ}} | | {{CMG}}; {{AE}} {{SAH}} {{SaraM}} |
| {{SK}} Subarachnoid haemorrhage | |
| ==Overview==
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| '''Subarachnoid hemorrhage''' ('''SAH''') is [[bleeding]] into the [[subarachnoid space]] surrounding the brain, i.e., the area between the [[arachnoid (brain)|arachnoid membrane]] and the [[pia mater]]. It may arise due to [[Physical trauma|trauma]] or spontaneously, and is a [[medical emergency]] which can lead to death or severe disability even if recognized and treated in an early stage. Treatment is with close observation, medication and early [[neurosurgery|neurosurgical]] investigations and treatments. Subarachnoid hemorrhage causes 5% of all [[stroke]]s. 10-15% die before arriving in hospital, and average survival is 50%.<ref name=vanGijn>Van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. ''[[The Lancet|Lancet]]'' 2007;369:306-18. PMID 17258671.</ref>
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| ==Signs and symptoms==
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| The classic symptom of subarachnoid hemorrhage is [[thunderclap headache]] ("most severe ever" headache developing over seconds to minutes). This headache is often described 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 Clinicial Medicine | publisher = Oxford | date = 2007 | pages = 841 | isbn = 0-19-856837-1 }}</ref> 10% of all people with this symptom turn out to have a subarachnoid hemorrhage, and is the only symptom in about a third of all SAH patients. Other presenting features may be [[vomiting]] (non-specific), [[seizure]]s (1 in 14) and [[meningism]]. [[Confusion]], decreased level of consciousness or [[coma]] may be present. Intraocular hemorrhage (bleeding into the eyeball) may occur. Subhyaloid hemorrhages may be visible on fundoscopy (the hyaloid membrane envelopes the [[vitreous body]]).<ref name=vanGijn/>
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| In a patient with thunderclap headache, none of the signs mentioned are helpful in confirming or ruling out hemorrhage, although a seizure makes bleeding from an [[aneurysm]] more likely. [[Oculomotor nerve]] abnormalities (affected eye looking downward and outward, [[pupil]] widened and less responsive to light) may indicate a bleed at the [[posterior inferior cerebellar artery]].<ref name=vanGijn/>
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| As a result of the bleeding, [[blood pressure]] often rises rapidly, together with a release of [[adrenaline]] and similar hormones. As a result, substantial strain is put on the [[heart]], and neurogenic [[pulmonary edema]], [[cardiac arrhythmia]]s, [[electrocardiogram|electrocardiographic changes]] (some resembling a [[myocardial infarction|heart attack]]) and [[cardiac arrest]] (3%) may occur rapidly after the onset of hemorrhage.<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><ref name=vanGijn/>
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| Bleeding into the subarachnoid space may occur as a result of injury or trauma. SAH in a trauma patient is often detected when a patient who has been involved in an accident becomes less responsive or develops [[hemiparesis]] (one-sided weakness) or changed pupillary reflexes, and [[Glasgow Coma Score]] calculations deteriorate. Headache is not necessarily present.
| | {{SK}} Subarachnoid haemorrhage; Traumatic subarachnoid haemorrhage , Aneurysmal subarachnoid haemorrhage; Nonaeurysmal subarachnoid hemorrhage; Perimesencephalic nonaneurysmal subarachnoid hemorrhage; Perimesencephalic subarachnoid hemorrhage |
| | ==[[Subarachnoid hemorrhage overview|Overview]]== |
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| Risk factors for subarachnoid hemorrhage are [[tobacco smoking|smoking]], [[hypertension]] (high blood pressure) and excessive [[alcoholic beverage|alcohol]] intake; all are associated with a doubled risk for SAH. Some protection of uncertain significance is conferred by Caucasian ethnicity, [[hormone replacement therapy]], a higher than normal [[cholesterol]] and the presence of [[diabetes mellitus]].<ref>{{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}}</ref>
| | ==[[Subarachnoid hemorrhage classification|Classification]]== |
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| ==Diagnosis== | | ==[[Subarachnoid hemorrhage pathophysiology|Pathophysiology]]== |
| The initial steps in a case of possible subarachnoid hemorrhage are obtaining a [[medical history]] and performing a [[physical examination]]; these are aimed at assessing the likelihood of the condition, and identifying other potential causes of the symptoms. ''Neck stiffness'' and other signs of [[meningism]] may be present, as well as a reduced level of consciousness. Only 25% of admitted patients to the emergency department with a thunderclap headache are suffering from a SAH, and as such carefully consideration of differentials should be completed (e.g. evaluation of [[meningitis]], [[migraine]] headaches and/or central venous [[thrombosis]]).<ref name="oxford"/>
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| The diagnosis of subarachnoid hemorrhage cannot be made on clinical grounds alone. [[Medical imaging]] is usually required to confirm or exclude bleeding. The modality of choice is [[computed tomography]] (CT/CAT) of the brain. This has a high [[Sensitivity (tests)|sensitivity]] (it will correctly identify >95% of the cases), especially on the first day after the onset of bleeding. Some data suggests that [[magnetic resonance imaging]] (MRI) may be more sensitive after several days. In those where the CT/MRI scan is normal, [[lumbar puncture]] (removal of [[cerebrospinal fluid]]/CSF with a needle from the lumbar sac under [[local anesthetic]]) will identify another 3% of the cases by demonstrating ''xanthochromia'' (yellow appearance of centrifugated fluid) or [[bilirubin]] (a breakdown product of [[hemoglobin]]) in the CSF.<ref name=vanGijn/>
| | ==[[Subarachnoid hemorrhage causes|Causes]]== |
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| Once a subarachnoid hemorrhage is confirmed, the next question is about its origin. CT angiography (using [[radiocontrast]]) to identify aneurysms is generally the first step, as invasive [[angiography]] (injecting radiocontrast through a catheter advanced to the brain arteries) has a small rate of complications but is useful if there are plans to obliterate the source of bleeding, such as an aneurysm, at the same time.<ref name=vanGijn/>
| | ==[[Subarachnoid hemorrhage differential diagnosis|Differentiating Subarachnoid Hemorrhage from other Diseases]]== |
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| ==Causes== | | ==[[Subarachnoid hemorrhage epidemiology and demographics|Epidemiology and Demographics]]== |
| Spontaneous SAH is most often due to rupture of [[cerebral aneurysm]]s (85%), weaknesses in the wall of the [[artery|arteries]] of the brain that enlarge. While most cases of SAH are due to bleeding from small aneurysms, there is evidence from research that larger aneurysms (which are rarer) are still more likely to rupture. A further 10% of cases is due to ''non-aneurysmal perimesencephalic hemorrhage'', in which the blood is limited to the area of the midbrain. No aneurysms are generally found. The remaining 5% are due to [[vasculitis|vasculitic]] damage to arteries, other disorders affecting the vessels, disorders of the spinal cord blood vessels, and bleeding into various [[tumor]]s.<ref name=vanGijn/>
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| ==Classification== | | ==[[Subarachnoid hemorrhage risk factors|Risk Factors]]== |
| There are several grading scales available for subarachnoid hemorrhage. These have been derived by retrospectively matching characteristics of patients with their outcomes. In addition to the ubiquitously used [[Glasgow Coma Scale]], three other specialized scores are in use.<ref>{{cite journal |author=Rosen D, Macdonald R |title=Subarachnoid hemorrhage grading scales: a systematic review |journal=Neurocrit Care |volume=2 |issue=2 |pages=110-8 |year=2005 |pmid=16159052}}</ref>
| | ==[[Subarachnoid hemorrhage natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| ;Hunt and Hess scale
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| The first scale of severity, described by Hunt and Hess in 1968:<ref>{{cite journal |author=Hunt W, Hess R |title=Surgical risk as related to time of intervention in the repair of intracranial aneurysms |journal=J Neurosurg |volume=28 |issue=1 |pages=14-20 |year=1968 |pmid=5635959}}</ref>
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| *Grade 1: Asymptomatic; or minimal [[headache]] and slight [[nuchal rigidity]]. Approximate survival rate 70%.
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| *Grade 2: Moderate to severe headache; nuchal rigidity; no [[neurology|neurologic]] deficit except [[cranial nerve]] [[palsy]]. 60%.
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| *Grade 3: Drowsy; minimal neurologic deficit. 50%.
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| *Grade 4: Stuporous; moderate to severe [[hemiparesis]]; possibly early [[decerebrate rigidity]] and vegetative disturbances. 20%.
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| *Grade 5: Deep [[coma]]; decerebrate rigidity; moribund. 10%.
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| ;Fisher grade
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| The Fisher Grade classifies the appearance of subarachnoid hemorrhage on [[CT scan]]:<ref>{{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}}</ref>
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| * Grade 1= No hemorrhage evident
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| * Grade 2= Subarachnoid hemorrhage less than 1 mm thick
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| * Grade 3= Subarachnoid hemorrhage more than 1 mm thick
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| * Grade 4= Subarachnoid hemorrhage of any thickness with intra-ventricular hemorrhage (IVH) or parenchymal extension
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| ;World Federation of Neurosurgeons
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| The World Federation of Neurosurgeons classification:<ref>{{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=J Neurol Neurosurg Psychiatry |volume=51 |issue=11 |pages=1457 |year=1988 |pmid=3236024}}</ref>
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| * Class 1 - GCS (Glasgow Coma Scale)15
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| * Class 2 - GCS 13-14 without focal neurological deficit
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| * Class 3 - GCS 13-14 with focal neurological deficit
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| * Class 4 - GCS 7-12 with or without focal neurological deficit
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| * Class 5 - GCS <7 with or without focal neurological deficit
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| ==Diagnosis== | | ==Diagnosis== |
| ====Computed Tomography====
| | [[Subarachnoid hemorrhage history and symptoms|History and Symptoms]] | [[Subarachnoid hemorrhage physical examination|Physical Examination]] | [[Subarachnoid hemorrhage laboratory findings|Laboratory Findings]] | [[Subarachnoid hemorrhage CT|CT]] | [[Subarachnoid hemorrhage MRI|MRI]] | [[Subarachnoid hemorrhage other imaging findings|Other Imaging Findings]] | [[Subarachnoid hemorrhage other diagnostic studies|Other Diagnostic Studies]] | [[Subarachnoid hemorrhage clinical prediction rules|Clinical prediction rules]] |
| *Subarachnoid hemorrhage appears as a high-attenuating, amorphous substance that fills the normally dark CSF-filled subarachnoid spaces.
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| *These findings are most evident in the largest subarachnoid spaces, such as the suprasellar cistern and Sylvian fissures.
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| *Acute Subarachnoid hemorrhage is typically 50-60 HU.
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| *When CT scanning is performed several days to weeks after the initial bleed, the findings are more subtle.
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| **The initial high-attenuation of blood and clot tend to decrease, and these appear as intermediate gray.
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| **These findings can be isointense relative to normal brain parenchyma.
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| *In addition to detecting Subarachnoid hemorrhage, CT is useful in localizing the source of bleeding.
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| [http://www.radswiki.net Images courtesy of RadsWiki] | |
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| <gallery>
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| Image:Subarachnoid hemorrhage 001.jpg|CT: Diffuse subarachnoid hemorrhage
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| Image:Subarachnoid hemorrhage 002.jpg|CT: Diffuse subarachnoid hemorrhage
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| Image:Subarachnoid hemorrhage 003.jpg|CT: Diffuse subarachnoid hemorrhage
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| Image:Subarachnoid hemorrhage 004.jpg|CT: Diffuse subarachnoid hemorrhage
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| </gallery>
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| === MRI ===
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| *Fluid-attenuated inversion recovery (FLAIR) is the most sensitive MRI pulse sequence for the detection of SAH. '''SAH appears as high-intensity signal in normally low signal CSF spaces.'''
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| *T2- and T2*-weighted images can potentially demonstrate SAH as low signal intensity in normally high-signal subarachnoid spaces.
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| *On T1-weighted images, acute SAH may appear as intermediate- or high-intensity signal in the subarachnoid space.
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| *MR angiography may be useful in the evaluation of aneurysms and other vascular lesions that cause SAH.
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| ==Treatment== | | ==Treatment== |
| ===General measures===
| | [[Subarachnoid hemorrhage medical therapy|Medical Therapy]] | [[Subarachnoid hemorrhage surgery|Surgery]] | [[Subarachnoid hemorrhage primary prevention|Primary Prevention]] | [[Subarachnoid hemorrhage secondary prevention|Secondary Prevention]] | [[Subarachnoid hemorrhage cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Subarachnoid hemorrhage future or investigational therapies|Future or Investigational Therapies]] |
| The first priority is stabilization of the patient. In those with a depressed level of consciousness, [[intubation]] and [[mechanical ventilation]] may be required. Blood pressure, pulse, respiratory rate and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an [[intensive care unit]] (ICU) may be considered preferable, especially given that 15% have a further episode (rebleeding) in the first hours after admission. Nutrition is an early priority, with oral or [[Nasogastric intubation|nasogastric tube]] feeding being preferable over parenteral routes. [[Analgesia]] (pain control) is generally restricted to non-sedating agents, as sedation would interfere with the monitoring of the level of consciousness. There is emphasis on the prevention of complications; for instance, [[deep vein thrombosis]] is prevented with [[compression stockings]] and/or intermittent pneumatic compression.<ref name=vanGijn/>
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| ===Prevention of rebleeding===
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| Those patients with a large hematoma, depressed level of consciousness or focal neurology may be candidates for urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are admitted and stabilized more extensively, and undergo an [[Cerebral angiography|transfemoral angiogram]] or CT angiogram at a later stage. In those where the bleeding is from an aneurysm (as opposed to non-aneurysmal perimesencephalic hemorrhage), most neurosurgical centers use either coiling or clipping of the aneurysm to prevent rebleeding. After the first 24 hours, rebleeding risk is about 40% over four weeks, suggesting that interventions should be aimed at reducing this risk.<ref name=vanGijn/>
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| Currently there are two treatment options for brain aneurysms: surgical clipping or endovascular coiling. Surgical clipping was introduced by [[Walter Dandy]] of the [[Johns Hopkins Hospital]] in 1937. It consists of performing a [[craniotomy]], exposing the aneurysm, and closing the base of the aneurysm with a clip.<ref>{{cite journal |author=Dandy WE |title=Intracranial aneurysm of the internal carotid artery: cured by operation |journal=Ann. Surg. |volume=107 |issue=5 |pages=654–9 |year=1938 |pmid=17857170}} {{PMC|1386933}}</ref> The surgical technique has been modified and improved over the years. Surgical clipping remains the best method to permanently eliminate aneurysms. Endovascular coiling was introduced by Guido Guglielmi at UCLA in 1991.<ref>{{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=J. Neurosurg. |volume=75 |issue=1 |pages=8-14 |year=1991 |pmid=2045924 |doi=}}</ref> It consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. Once the catheter is in the aneurysm, platinum coils are pushed into the aneurysm and released. These coils initiate a clotting or thrombotic reaction within the aneurysm that, if successful, will eliminate the aneurysm. In the case of broad-based aneurysms, a stent is passed first into the parent artery to serve as a scaffold for the coils ("stent-assisted coiling").
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| Presently it appears that the risks associated with surgical clipping and endovascular coiling, in terms of stroke or death from the procedure, are the same. The major problem associated with endovascular coiling, however, is the high recurrence rate and subsequent bleeding of the aneurysms. For instance, a major French study reported in 2007 indicates that 28.6% of aneurysms recurred within one year of coiling, and that the recurrence rate increased with time.<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://stroke.ahajournals.org/cgi/content/full/38/5/1538}}</ref> These results are similar to those previously reported by other endovascular groups; a series from Canada reported in 2003 found that 33.6% of aneurysms recurred within one year of coiling.<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}}</ref> The long-term coiling results of one of the two prospective randomized studies comparing surgical clipping versus endovascular coiling (the International Subarachnoid Aneurysm Trial or ISAT), too, suggest that the need for late retreatment of aneurysms is 6.9 times more likely for endovascular coiling as compared to surgical clipping.<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}}</ref>
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| Therefore it appears that although endovascular coiling is associated with a shorter recovery period as compared to surgical clipping, it is also associated with a significantly higher recurrence and bleeding rate after treatment. Patients who undergo endovascular coiling need to have annual studies (such as MRI/MRA, CTA, or angiography) indefinitely to detect early recurrences. If a recurrence is identified, the aneurysm needs to be retreated with either surgery or further coiling. The risks associated with surgical clipping of previously-coiled aneurysms are very high.Ultimately, the decision to treat with surgical clipping versus endovascular coiling should be made by a cerebrovascular team with extensive experience in both modalities. At present it appears that only older patients with aneurysms that are difficult to reach surgically are more likely to benefit from endovascular coiling. These generalizations, however, are difficult to apply to every case, which is reflected in the wide variabilty internationally in the use of surgical clipping versus endovascular coiling.
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| Medical treatment is available to both reduce the risk of repeat bleeding, and to treat a serious complication of SAH called vasospasm. In the case of spontaneous SAH from an aneurysm, there is a significant risk of repeat bleeding until definitive surgical intervention can be performed. During this waiting period medical treatments to control blood pressure, [[bed rest]], and a quiet environment reduce the risk of rebleed.
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| ===Prevention of vasospasm===
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| [[Vasospasm]] is a serious complication of SAH. It may be seen in 50% of SAH patients studied with angiography, and is symptomatic roughly 30% of the time. This condition can be verified by [[transcranial doppler]] or [[cerebral angiography]], and can cause ischemic brain injury that can cause permanent brain damage, and if severe can be fatal. [[Nimodipine]], an oral [[calcium channel blocker]], has been shown to reduce the chance of a bad outcome, even if it does not significantly reduce the amount of angiographic vasospasm.<ref name="pmid6338383">{{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=N. Engl. J. Med. |volume=308 |issue=11 |pages=619-24 |year=1983 |pmid=6338383 |doi=}}</ref><ref name="pmid17636626">{{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) |volume= |issue=3 |pages=CD000277 |year=2007 |pmid=17636626 |doi=10.1002/14651858.CD000277.pub3}}</ref>
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| ===Follow-up===
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| A patient who recovers without immediate intervention may receive follow-up [[angiography]] to identify [[aneurysm]]s which may be amenable to either surgical clipping or endovascular coiling to prevent recurrent episodes of SAH.
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| ==Complications==
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| Complications of SAH can be acute, subacute, or chronic.
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| * Acute:
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| ** [[Coma]] and [[Brain herniation|brainstem herniation]] due to increased [[intracranial pressure]] (ICP)
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| ** [[Pulmonary edema]] ("neurogenic pulmonary edema") as a result of the suddenly increased ICP
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| ** [[Cardiac arrhythmia]]s and [[myocardial]] damage
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| ** [[Hydrocephalus]], which may also happen in the subacute time frame
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| * Subacute:
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| ** [[Vasospasm]], leading to [[ischemia]] of the brain
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| ** [[Hyponatremia]] (low [[sodium]] levels) - due to [[SIADH]] or [[cerebral salt wasting syndrome]]
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| * Chronic:
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| ** Long-term immobility
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| ** [[Pneumonia]] and [[pulmonary embolism]] (due to immobility)
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| ** SAH recurrence (20% within two weeks if the aneurysm is not secured by clipping or coiling)
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| ** Persistent neurologic deficits
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| ==Prognosis==
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| Nearly half the cases of SAH are either dead or moribund before they reach a hospital. Of the remainder, a further 10-20% die in the early weeks in hospital from rebleeding. Delay in diagnosis of minor SAH without coma (or mistaking the sudden headache for [[migraine]]) contributes to this mortality. Patients who remain comatose or with persistent severe deficits have a poor prognosis.
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| After the SAH is treated the patients can experience prolonged, even permanently reoccurring headaches.
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| ==References== | | == Case Studies == |
| {{Reflist|2}}
| | [[Subarachnoid hemorrhage case study one|Case #1]] |
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| | ==Related Chapters== |
| | * [[Syphilis]] |
| | * [[TORCH complex]] |
| {{Cerebral hemorrhage}} | | {{Cerebral hemorrhage}} |
| {{Injuries, other than fractures, dislocations, sprains and strains}} | | {{Injuries, other than fractures, dislocations, sprains and strains}} |
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| {{WS}} | | {{WS}} |
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| [[Category:Neurotrauma]] | | [[Category:Cardiology]] |
| [[Category:Neurosurgery]]
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| [[Category:Intensive care medicine]]
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| [[Category:Neurology]] | | [[Category:Neurology]] |
| [[Category:Emergency medicine]] | | [[Category:Emergency medicine]] |
| [[Category:Mature chapter]]
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| [[Category:Disease]]
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