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Subarachnoid

haemorrhage
The right clinical information, right where it's needed

Last updated: Aug 08, 2016

Table of Contents
Summary 3

Basics 4

Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 4

Prevention 6

Primary prevention 6
Screening 6
Secondary prevention 6

Diagnosis 7

Case history 7
Step-by-step diagnostic approach 7
Risk factors 8
History & examination factors 9
Diagnostic tests 10
Differential diagnosis 12
Diagnostic criteria 13

Treatment 15

Step-by-step treatment approach 15
Treatment details overview 16
Treatment options 18
Emerging 21

Follow up 22

Recommendations 22
Complications 22
Prognosis 26

Guidelines 28

Diagnostic guidelines 28
Treatment guidelines 28

Evidence scores 29

References 30

Images 44

Disclaimer 48

Summary

◊ Presents as a sudden severe headache, often described as 'the worst headache of life', with nausea, vomiting,
and photophobia.

◊ Examination can be normal or may reveal altered consciousness, meningismus, intraocular haemorrhages, or
focal findings.

◊ CT indicated if subarachnoid haemorrhage is clinically suspected. Lumbar puncture (LP) is indicated if CT is
unrevealing. Cerebral angiography confirms the presence of aneurysms.

◊ Initial stabilisation followed by surgical clipping or endovascular coil embolisation is standard therapy.

◊ Complications are common and include rebleeding, acute hydrocephalus, and vasospasm.

Subarachnoid haemorrhage Basics

Definition

Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space and is an emergency. The most common
BASICS

cause of non-traumatic SAH is intracranial aneurysm.[1] Aneurysmal SAH causes substantial morbidity and mortality.
When a cerebral aneurysm ruptures, blood flows into the subarachnoid space, sometimes seeping into brain parenchyma
and/or ventricles. The sudden increase in intracranial pressure, as well as the destructive and toxic effects of blood on
brain parenchyma and cerebral vessels, accounts for most complications.

Epidemiology

The incidence of SAH in most populations is between 6 and 8 cases out of 100,000 per year.[5] In the UK, just over 9000
cases were reported in 2012-2013.[6] Unlike other types of stroke, this has not changed over the past three decades.
The incidence is higher in Finland (21.4 cases/100,000 per year) and Japan.[5] A higher incidence in Hispanic populations
compared with in non-Hispanic populations has also been noted in some areas of the US.[7] Incidence also increases
with age. The average age at onset is between 50 and 55 years.[1] [8] [9] It is 1.6 times more common in women than in
men,[5] and 2.1 times more common in black people than in white people.[10]

SAH accounts for about 5% of all strokes.[11]

Aetiology

Rupture of an intracranial saccular aneurysm is the leading cause of non-traumatic SAH, accounting for approximately
80% of cases. The remaining 20% are attributed to non-aneurysmal perimesencephalic SAH, arteriovenous malformations,
arterial dissections, use of anticoagulants and other rare conditions.[12] This distinction is crucial, as aneurysmal SAH
has a different spectrum of complications and outcome, requiring more specific treatment and management.

Cerebral saccular aneurysm formation is an acquired process. Very little is known about this process, but evidence
suggests structural abnormalities are acquired in the intimal and medial layers of cerebral vessels,[13] [14] and could
result from an inflammatory process occuring within these layers.[15] Structural abnormalities may be influenced by
smoking, hypertension, and alcohol abuse.[12] Patients with previous SAH are at substantial risk for new aneurysm
formation and enlargement of previously diagnosed and untreated aneurysms. This suggests that aneurysm formation
is a dynamic, continuous process.[16] Hereditary and genetic factors may also contribute. Patients with Ehlers-Danlos
syndrome, Marfan syndrome, pseudoxanthoma elasticum, adult polycystic kidney disease, and neurofibromatosis type
I are at increased risk of aneurysm formation and SAH.

Pathophysiology

Cerebral aneurysms arise at the bifurcation of major arteries that form the circle of Willis. The majority are located at the
anterior communicating/anterior cerebral artery junction (Acom/ACA), distal internal carotid artery/posterior
communicating artery junction (ICA/Pcom), and middle cerebral artery bifurcation (MCA). Less than 10% arise from the
vertebral or basilar arteries. Up to 19% of patients are found to have multiple aneurysms.[8] [9] Greater pressures at the
apexes of arterial bifurcation, pulsatile flow patterns, and turbulence have been suggested as explanations for the
predilection of aneurysm growth at these sites.[14]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08, 2016.
4 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.bmj.com . Use
of this content is subject to our disclaimer. © BMJ Publishing Group Ltd 2016. All rights reserved.

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.5% when located on Pcom or posterior cerebral. asymptomatic aneurysms (<7 mm) are less prone to rupture than bigger ones that exert mass effect on surrounding structures.bmj. vertebral.[24] An unruptured aneurysm discovered during work-up for SAH (caused by a different aneurysm) has a higher annual incidence of rupture than a single unruptured aneurysm. and whether previous aneurysms have ruptured. in the vertebrobasilar.4% for aneurysms between 7 mm and 24 mm.6% and 18. the presence of multiple aneurysms. 2016. or MCA and 2. or posterior part of the circle of Willis are more likely to rupture compared with aneurysms in other locations. . © BMJ Publishing Group Ltd 2016. posterior cerebral BASICS distribution. Small. location. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.5% and 3.[14] [17] [18] [19] [20] [21] [22] [23] Patient-related predictors of rupture are age and smoking. Acom. Use 5 of this content is subject to our disclaimer.[14] [20] [21] In this case.Subarachnoid haemorrhage Basics The risk of aneurysm rupture depends on its size.[18] [19] [24] The 5-year cumulative rupture rate of an aneurysm <7 mm in diameter is 0% when located on ICA.com .4% for aneurysms <7 mm and between 2. Aneurysms located at the basilar tip. the 5-year cumulative rupture rate ranges between 1. or basilar arteries. All rights reserved. the presence of symptoms.

com . Use of this content is subject to our disclaimer.[25] [50] Secondary prevention Smoking cessation advice should be given and hypertension corrected. Because of the theoretical risk of rebleeding with a seizure.[25] Because of the possible hereditary aspects of SAH. patients who have survived SAH are at higher risk for another. However. due to a newly formed aneurysm. it is uncertain that widely applied screening programmes are cost-effective given PREVENTION the low prevalence of cerebral aneurysms in the general population and risk of rupture. Patients who have two or more first-degree relatives with SAH or those with autosomal dominant polycystic kidney disease are potential candidates for aneurysm screening. prophylactic anticonvulsants are recommended in the immediate post-haemorrhage period. as this is one of the most important modifiable risk factors. 2016. In addition. However.[25] Hypertension should be corrected. and 2% to 8% of patients with aneurysms have ADPKD.[60] A short course of anticonvulsant treatment may be adequate prophylaxis and better tolerated than longer periods of treatment. Subarachnoid haemorrhage Prevention Primary prevention One quarter of patients with autosomal dominant polycystic kidney disease (ADPKD) have aneurysms at autopsy. 6 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. In addition. All rights reserved. Screening provides a major opportunity to treat intracranial aneurysms before catastrophic rupture. All patients should be encouraged not to smoke. © BMJ Publishing Group Ltd 2016. patients who have two or more first-degree relatives with SAH are potential candidates for aneurysm screening.bmj.[62] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. . there are controversies about when and how to treat unruptured intracranial aneurysms. Screening SAH is associated with high mortality and morbidity.[31] Individuals with ADPKD are potential candidates for aneurysm screening. whether this subgroup will benefit from screening and how it should be performed is undecided.

All rights reserved. It is the most important clue to diagnosis and is often described as 'the worst-ever headache'. connective tissue disorders. or there can be altered level of consciousness. She loses consciousness following onset of the headache and is on the floor for less than 1 minute. and ST segment/T wave abnormalities.[3] Patients who experience sentinel headache might have an increased risk of rebleeding.[32] History-taking (from the patient and/or relatives) may reveal risk factors of smoking. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. and respiratory rate. and prominent neck pain. There are no sensory deficits or weakness. Around 10% to 43% of patients experience a sentinel headache during the 3 months prior to SAH. agitation. Use 7 of this content is subject to our disclaimer.[37] Serum tests and ECG FBC. A poor neurological status on admission seems to predict cardiac abnormalities thought to be secondary to overwhelming sympathetic activation.[4] Step-by-step diagnostic approach Occurrence of a sudden. A poor level of awareness and seizures on presentation are risk factors for aspiration.[33] [34] [35] [36] Close monitoring of vital signs should be instituted. excruciating headache while sitting at work. A full neurological examination should be performed with special attention to pupillary reaction. 2016. CT and LP Suspicion of SAH based on a history of sudden. . Half of patients have an abnormal ECG on admission. Isolated dilation of one pupil and loss of the pupillary light reflex may indicate brain herniation as a result of rising intracranial pressure. bilateral subhyaloid haemorrhages. which CT is unreliable in detecting. family history of SAH. headaches accompanied by vomiting and low-grade fever. Other presentations An atypical history of SAH includes less severe headaches. This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. nausea. meningismus.[2] Some of these headaches are caused by minor leaks from the aneurysm. The headache is diffuse. intense. © BMJ Publishing Group Ltd 2016.bmj. Physical examination DIAGNOSIS can be normal. Brain CT reveals diffuse subarachnoid blood in basal cisterns and sulci.[38] Abnormalities include arrhythmias.Subarachnoid haemorrhage Diagnosis Case history Case history #1 A 53-year-old black woman complains of a sudden. History and examination The first priority should be an urgent assessment of level of consciousness and need for cardiopulmonary resuscitation and/or ventilatory support. and focal findings. She is being treated for hypertension and is a smoker. and right third cranial nerve palsy. altered mental state. heart rate and rhythm. Consciousness level should be assessed using the Glasgow Coma Scale (GCS). On examination she has a normal mental state.com . prolonged QTc. and clotting profile should be ordered in the initial work-up in addition to serum troponin I. Photophobia. or autosomal dominant polycystic kidney diseases. Intraocular haemorrhages and cranial nerve palsies may be present. serum electrolytes. severe headache is characteristic of SAH. severe headaches is sufficient to order an emergency non-contrast brain CT as the first test. She describes the headache as the worst headache of her life. cocaine use. and accompanied by nausea and vomiting. and vomiting are common symptoms. hypertension. including blood pressure. meningismus.

reaching 100% when performed within 6 hours of headache onset and read by experienced neuroradiologists.[25] • Having two or more first-degree relatives with SAH has a relative risk of SAH of 6.7% and specificity of 77. Therefore.[21] [26] [27] [28] [29] [30] smoking • Smoking is one of the most important potentially modifiable risk factors. meta-analysis has shown that MRA has a sensitivity of 95% and specificity of 89%.[8] family history • First-degree relatives of patients with SAH have a 4% prevalence of harbouring cerebral aneurysms[30] and a 3-fold to 7-fold increased risk of having SAH than the general population. Subarachnoid haemorrhage Diagnosis Thin cuts should be ordered (3-5 mm).[12] The risk is highest when the affected relative is a sibling. © BMJ Publishing Group Ltd 2016.[12] Patients who have two or more first-degree relatives with SAH are potential candidates for aneurysm screening. especially when newer-generation multidetector scanners were used.bmj.9. Lysed RBCs will impart a xanthochromic (faint. and timing of CT from ictus.6. quantity of SAH.[44] RBCs in the subarachnoid space start lysing approximately 12 hours after the bleed. Spectrophotometric analysis of haemoglobin degradation products is most reliable. the morbidity associated with a missed or delayed diagnosis of aneurysmal SAH is unacceptably high. small.[47] but neither CTA nor MRA has widely replaced DSA yet. Digital subtraction angiography (DSA) is the most accurate imaging technique used to diagnose aneurysms.[45] Further imaging After SAH is confirmed by CT or LP. otherwise. All rights reserved. though inconsistently. major fissures. yellow tinge) appearance to the CSF. and blood with haemoglobin below 100g/L (10 g/dL) may not be visible. Visual inspection for xanthochromia is unreliable.[39] [Fig-1] [Fig-2] Detection of SAH on CT depends on density of blood.[46] [47] [48] [49] CTA has been used as the only method for diagnosing aneurysms. Use of this content is subject to our disclaimer. 2016. A small quantity of blood in the subarachnoid space may be missed. many physicians still advocate for a lumbar puncture if the CT scan fails to reveal SAH or if the patient seeks medical attention 24 hours or more after symptom onset with inconclusive CT findings.com . A serial count of RBCs in tubes 1 to 4 is not sufficiently accurate to distinguish SAH from a traumatic LP.[51] Similarly.[46] [50] though another reported sensitivity and specificity surpassing 95%. A meta-analysis reported CTA to have a sensitivity of 92. thin collections of blood might be missed.[52] DIAGNOSIS Risk factors Strong hypertension • Hypertension is an important risk factor (relative risk is 2.[25] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.[39] Nonetheless.[40] [41] [42]The aneurysm rupture site can be predicted.[21] [26] [27] [28] [29] [30] Relative risk is 1.8)[25] and is potentially modifiable. and sulci. . from patterns of blood accumulation on CT (thick collection in fissures) or parenchymal haematoma. Four tubes of CSF should be collected and examined for gross blood. Subarachnoid blood will appear hyperdense (white) in the basal cisterns. Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) are non-invasive imaging methods that have been compared with DSA. high protein content in CSF or contamination with iodine used for disinfection can cause CSF to look xanthochromic. further imaging tests should be ordered. the advent of third-generation CT scanners has dramatically improved the sensitivity of detecting subarachnoid blood. 8 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. However.[43] Despite the higher sensitivity of newer CT scanners.2%.

[31] History & examination factors Key diagnostic factors DIAGNOSIS presence of risk factors (common) • Key factors include hypertension. headache (common) • Most important clue to diagnosis when described as sudden. Marfan's syndrome • Connective tissue disorder with an increased risk for aneurysmal formation and SAH. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Use 9 of this content is subject to our disclaimer.com .[25] One quarter of patients with ADPKD have aneurysms at autopsy. and 2% to 8% of patients with aneurysms have ADPKD.bmj.[25] Weak alcohol use • The relationship of SAH to excessive alcohol use is less robust than hypertension (HTN) or smoking.Subarachnoid haemorrhage Diagnosis autosomal dominant polycystic kidney disease (ADPKD) • ADPKD is an important risk factor (relative risk is 4. 2016. This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.[31] Ehlers-Danlos syndrome • Connective tissue disorder with an increased risk for aneurysmal formation and SAH. third cranial nerve palsy (uncommon) • The presence of third cranial nerve palsy can be very useful and specific as it signals the presence of a posterior communicating artery aneurysm compressing the ipsilateral third cranial nerve.[31] neurofibromatosis type I • Connective tissue disorder with an increased risk for aneurysmal formation and SAH. .[31] • Individuals with ADPKD are potential candidates for aneurysm screening.[26] [27] [30] cocaine use • The relationship of SAH to cocaine use is less robust than HTN or smoking.[31] pseudoxanthoma elasticum • Connective tissue disorder with an increased risk for aneurysmal formation and SAH. Around 10% to 43% of patients experience a sentinel headache in the 3 months prior to SAH. All rights reserved.4). positive family history. © BMJ Publishing Group Ltd 2016. severe or 'worst ever'. and autosomal dominant polycystic kidney disease (ADPKD). smoking. loss of consciousness (common) • Seen in up to half of patients.[2] photophobia (common) • Eye pain with exposure to light.

com .6 times more than men.1 times higher than in white people. 2016. This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. hydrocephalus.[8] [9] CT may also show subdural or parenchymal haematoma. unilateral or bilateral sixth cranial nerve palsies (uncommon) • This indicates increased intracranial pressure. altered mental status (common) • Common but non-specific. hypodensities. and sometimes the aneurysm(s) if large or thrombosed. major fissures.[39] FBC leukocytosis • This is a non-specific test. Subarachnoid haemorrhage Diagnosis Other diagnostic factors age >50 years (common) • Average age between 50 and 55 years. nausea/vomiting (common) • Seen in majority of patients with SAH but non-specific. Use of this content is subject to our disclaimer. intraocular haemorrhage (uncommon) • Intraocular haemorrhages are seen in 10% to 40% of patients with SAH. third-generation scanners will detect SAH in 93% of cases if done in first 24 hours after the bleed. 10 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. prolonged PTT • Coagulopathy may be present. clotting profile elevated INR. . © BMJ Publishing Group Ltd 2016. Non-specific. • Modern. meningismus (uncommon) • A clue to diagnosis only when associated with sudden. female sex (common) • Women are affected 1. black people (common) • Incidence in black people is 2. severe headache.bmj.[54] and in 100% of cases when performed within 6 hours of onset of headache and interpreted by experienced neuroradiologists. All rights reserved. and • This is the standard diagnostic test for SAH and should be ordered if SAH is sulci suspected.[40] [41] [42] The sensitivity of CT in detecting SAH declines after the first 24 hours to 68% on day 3 and 58% on day 5.[53] focal neurological deficits (uncommon) • Focal neurological deficits reflect presence of mass effect from subdural or parenchymal haematomas. Diagnostic tests DIAGNOSIS 1st test to order Test Result CT head hyperdense areas in the basal cisterns.

Visual inspection for xanthochromia is unreliable. • CSF opening pressure should be measured and CSF should be visually inspected for gross blood and xanthochromia. if the suspicion of an aneurysm still remains. However.[52] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Many physicians still advocate for a LP if the CT scan fails to reveal SAH or if the patient seeks medical attention 24 hours or more after symptom onset with inconclusive CT findings.[37] troponin I elevated • Elevated in 20% to 28% of cases during the first 24 hours. computed tomography angiography (CTA) aneurysm • Non-invasive.2%). it has not widely replaced DSA though meta-analysis has shown that MRA has a sensitivity of 95% and specificity of 89%.[56] ECG arrhythmias. within the 15 days following SAH. Use 11 of this content is subject to our disclaimer. digital subtraction angiography (DSA) aneurysm • DSA is the most accurate test for visualising aneurysms and should be carried out once the diagnosis of SAH is made based on CT and/or LP results. ST segment.[38] abnormalities Abnormalities include arrhythmias.7% and specificity of 77. Four tubes of CSF should be collected and examined for gross blood. or T wave • Fifty percent of patients with SAH have an abnormal ECG on admission. CTA has been used as the only method for diagnosing aneurysms.[44] • Xanthochromia is an indicator of the presence of blood in the subarachnoid space. © BMJ Publishing Group Ltd 2016.[47] however. and ST segment/T wave abnormalities. Spectrophotometric analysis of haemoglobin degradation products is most reliable. All rights reserved.[55] [33] This elevation in troponin I is an order of magnitude less than what is usually seen in the setting of myocardial infarction. It also needs to be performed if suspicion is still high despite inconclusive CT and/or LP results or repeated. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. primarily because of sensitivity and specificity issues (a meta-analysis reported CTA to have a sensitivity of 92.Subarachnoid haemorrhage Diagnosis Test Result serum electrolytes electrolyte abnormalities • Hyponatraemia may occur due to salt wasting.com . which is the DIAGNOSIS time necessary for red blood cells to start lysing. Xanthochromia is absent in the first 12 hours after SAH. prolonged QTc. in the absence of coronary artery disease. despite the high sensitivity of newer CT scanners because of the high morbidity associated with a missed or delayed diagnosis of aneurysmal SAH. prolonged QT. 2016.[46] magnetic resonance angiography (MRA) aneurysm • Non-invasive. Other tests to consider Test Result LP bloody CSF (xanthochromia) • Should be performed if CT is unrevealing. it has not widely replaced DSA. A serial count of RBCs in tubes 1 to 4 is not sufficiently accurate to distinguish SAH from a traumatic LP.bmj. .

Axial T1 and T2 neck region. This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Cerebral and cervical • Symptoms and signs are similar • Arteriovenous malformations arteriovenous malformation to aneurysmal SAH.com . however. might be more prominent. include a Horner’s sign and/or neurological deficits related to stroke secondary to dissection. Saccular aneurysms of spinal • Pain localised to posterior • Spinal angiography visualises the arteries neck/occipital area. CT usually reveals differentiate this condition from subarachnoid blood in front and aneurysmal SAH.bmj. MRA. Subarachnoid haemorrhage Diagnosis Differential diagnosis Condition Differentiating signs / Differentiating tests symptoms Non-aneurysmal • There are no features in the • No aneurysms are found on perimesencephalic SAH history or on examination that angiography. around the pons (perimesencephalic or pontine cistern). . © BMJ Publishing Group Ltd 2016. Meningismus aneurysm(s).[45] Overall. as it may also be seen with a ruptured aneurysm located in the posterior circulation. Angiography with corresponding abnormalities might disclose beading of on examination. or CTA. All rights reserved. arteries. Headache is medium and small intracranial usually less severe. Dull neck pain might fat-suppressed neck MRI images precede a more severe pain. MRA. Use of this content is subject to our disclaimer. DIAGNOSIS Dural arteriovenous fistulae • Symptoms and signs are similar • Arteriovenous fistulae visualised (AVF) to aneurysmal SAH. MRA. it has a better outcome than aneurysmal SAH. A sciatica-like picture due to blood in the lumbar thecal sac can be seen. or accompanied by findings related to mass effect caused by the AVM. may be present. might visualise the characteristic occurring at the time of SAH. or localised to anterior or posterior CTA. Arterial dissection • Pain is less severe and is • Dissected arteries are visualised frequently felt behind the eye or on cerebral angiography. the diagnostic standard for this condition. or CTA. on cerebral angiography. Caution is required when this blood distribution pattern is seen. 12 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Vasculitis • A subacute to chronic history of • Cerebrospinal fluid pleocytosis recurrent neurological deficits. 2016. intramural haemorrhage Examination findings might associated with dissection. Brain and meningeal biopsy is. Subarachnoid visualised on cerebral (AVM) haemorrhage could be preceded angiography.

cisterns. Sickle cell disease • There is a history of sickle cell • Computed angiography might disease. focal. typically in the distribution of the middle cerebral artery (MCA). show an elevated ESR and Ischaemia may occur in the bowel peripheral leukocytosis. Coagulation studies are abnormal (prolonged PTT and/or elevated INR). Intracerebral haematomas are likely to be seen on CT. Haemoglobin S is identified upon testing. associated with subarachnoid blood. © BMJ Publishing Group Ltd 2016. blood and possible intracerebral haematomas. previous strokes. This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. fissures. Osler's nodes. Echocardiography might reveal valvular vegetations. not widely distributed in skin petechiae. Cerebral and spleen. or choice for diagnosis. Blood cultures haemorrhages under the nails.com . All rights reserved. Cocaine abuse • There is a history of drug abuse • Urine drug screen is positive for preceding the event. angiography reveals aneurysms located distally. 2016.bmj.Subarachnoid haemorrhage Diagnosis Condition Differentiating signs / Differentiating tests symptoms Cardiac myxoma • Age between 30 and 60 years. obstructive. CT might also reveal intracerebral haematomas. Diagnostic criteria Hunt and Hess Grading Scale[57] Grade I: asymptomatic or minimal headache and slight nuchal rigidity (survival 70%). The headache is less severe. Subarachnoid blood is headache is usually less severe. may be positive. Visual loss is haemorrhage or infarction. Acute the pituitary gland. and sulci as in Janeway lesions. or reveal intracerebral haematomas sickling episodes. constitutional symptoms precede SAH. adrenal insufficiency develops in two-thirds of patients. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. . heart murmur. Blood tests may and Roth spots in optic fundi. DIAGNOSIS Anticoagulants • There is a history of anticoagulant • A CT shows minimal subarachnoid use. The cocaine. Use 13 of this content is subject to our disclaimer. splinter aneurysmal SAH. Pituitary apoplexy • Patients have a known history of • MRI with contrast shows pituitary pituitary adenoma. seen in up to half of patients with Subarachnoid blood is minimal pituitary apoplexy (not a feature and confined to the region around of aneurysmal SAH). usually minimal and focal in sulci. Septic (mycotic) aneurysm • On physical examination there • Subarachnoid blood is usually may be a fever. • Echocardiography is method of Cardiac.

localised clot and/or vertical layer ≥1 mm. 2016.intracerebral or intraventricular clot with diffuse or no SAH. All rights reserved. and no neurological deficits other than cranial nerve palsy (survival 60%). decerebrate rigidity. moderate to severe haemiparesis. CT Fisher Scale[58] Grade I: distribution of blood . Grade IV: distribution of blood .none. . Grade V: GCS score 6-3. Use of this content is subject to our disclaimer. World Federation of Neurological Surgeons Grading Scale (adapted from Suarez et al)[1] Grade I: Glasgow Coma Scale (GCS) score 15. Grade III: GCS score 14-13. Motor deficit absent. Grade II: distribution of blood . and moribund appearance (survival 10%). Grade III: distribution of blood . confusion. Subarachnoid haemorrhage Diagnosis Grade II: moderate to severe headache. Motor deficit present or absent.bmj.minimal diffuse subarachnoid blood or vertical layers <1 mm. 14 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. nuchal rigidity. Grade III: drowsiness. Grade II: GCS score 14-13. Motor deficit present. or mild focal deficits (survival 50%). Grade IV: GCS score 12-7. Grade IV: stupor. and vegetative disturbances (survival 20%). DIAGNOSIS This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Motor deficit absent. possibly early decerebrate rigidity.com . Grade V: deep coma. © BMJ Publishing Group Ltd 2016. Motor deficit present or absent.

as straining to defecate can potentially cause rebleeding. BP. heart rate and rhythm. If present. Isolated dilation of one pupil and loss of the pupillary light reflex may indicate brain herniation as a result of rising intracranial pressure. A poor level of awareness and seizures on presentation are risk factors for aspiration.[59] [60] When patients are evaluated in rural or community settings. hyponatraemia) are common and should be corrected.. strong consideration should be made for expedited referral to a tertiary care centre. coagulopathy should be treated aggressively using fresh frozen plasma and vitamin K.[61] These units significantly reduce in-hospital mortality and length of stay.[32] Consciousness level should be assessed using the Glasgow Coma Scale (GCS).com . hypertension-related rebleeding. it helps to predict the potential risk of vasospasm.g. and maintenance of cerebral perfusion pressure.[37] Blood pressure should be monitored and controlled to balance the risk of stroke. All rights reserved. however. 3[B]Evidence Post stabilisation The patient should be admitted to an ICU. Judicious use of analgesia is therefore recommended. TREATMENT Antitussives and stool softeners Cough should be suppressed with antitussives to prevent potential rebleeding. neurological status should be graded using scales such as the Hunt and Hess Scale or the World Federation of Neurological Surgeons Scale. They reduce risk of poor outcome and secondary ischaemia after aneurysmal SAH. mental status also needs be closely followed. It is essential to establish the need for endotracheal intubation and mechanical ventilation as the first priority. and respiratory rate). especially in patients monitored for acute hydrocephalus or vasospasm. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. . in addition to airway adequacy and cardiovascular function. Use 15 of this content is subject to our disclaimer.[63] On admission to ICU.bmj. 2016. Analgesia Headache should be treated with opioid analgesics.. Stool softeners are used routinely.g. which is a serious complication.Subarachnoid haemorrhage Treatment Step-by-step treatment approach SAH requires emergency treatment and early referral to the intensive care unit (ICU). once stabilised. This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. the poorer the outcome. © BMJ Publishing Group Ltd 2016. The higher the grade.[64] The Fisher Scale can be used to document and grade the quantity and distribution of subarachnoid blood on admission CT.[58] Although not definitive. ideally a neurological and neurosurgical ICU. Despite widespread use in the US.[60] Electrolytes and coagulation Electrolyte imbalances (e. A full neurological examination should be performed with special attention to pupillary reaction.[61] Stabilisation Stabilisation of patients simultaneously with work-up is vital to prevent unwanted early complications. Anticonvulsants The effect of convulsions on patients with SAH is unknown.[62] Calcium-channel blockers Calcium-channel blockers should be started on admission for vasospasm prophylaxis. A poor neurological status on admission seems to predict cardiac abnormalities thought to be secondary to overwhelming sympathetic activation.[33] [34] [35] [36] Close monitoring of vital signs should be instituted (e. A retrospective study suggested that a short course of perioperative phenytoin is associated with fewer side effects without increasing the risk of seizures. the practice of prophylactic anticonvulsants is unsettled.

[70] Surgical clipping or endovascular coil embolisation are needed to secure the aneurysm. 2016. All rights reserved. 1[C]Evidence The results of a major international prospective and randomised trial have sparked major controversies.[66] [67] [68] The International Subarachnoid Aneurysm Trial (ISAT) included over 1000 patients in each treatment group. and a clip is placed on its neck to exclude it from the circulation. At 1 year. An arterial catheter is advanced to the aneurysm lumen where titanium coils are deposited. a craniotomy is performed to expose the aneurysm. and alternative dosing.[8] [9] Controversy exists over the choice between surgical clipping and endovascular coil embolisation. drug interactions.[71] Yet there remain drawbacks to coil embolisation. Treatment details overview Consult your local pharmaceutical database for comprehensive drug information including contraindications. differing levels of expertise among the interventionists and surgeons. but these characteristics are widely accepted in the neurosurgical and endovascular community in the US. Most surgeons operate on patients with good neurological status during the first 72 hours to prevent rebleeding. and dissection. as well as wide-neck aneurysms. and small aneurysms with small necks located in the anterior communicating artery.[69] Another publication assessing long-term follow-up (10 years and beyond) after ISAT concluded that despite a higher risk of rebleeding. Middle cerebral artery and posterior communicating artery aneurysms. making it a therapeutic option for complex aneurysms that were only amenable to surgical clipping in the past. a practice that also seems to be associated with improved outcome.[67] Criticisms of the study included uneven distribution of enrolled patients (almost all came from Europe). 23.[66] Long-term follow-up of patients enrolled in ISAT has revealed that despite an increased risk of recurrent bleeding in the coiling group. Coiling may be a better option in older patients with comorbid diseases and high surgical risks (though there is some evidence to suggest that coiling confers a greater clinical outcome benefit in patients with a better pre-operative grade[76]). mainly incomplete embolisation and recurrences requiring reintervention.6% in the clipping group.com .7% of patients were dead or dependent following coiling compared with 30. There are no guidelines or official recommendations. In surgical clipping. Subarachnoid haemorrhage Treatment Surgery and coil embolisation A neurosurgeon and interventional neuroradiologist should be involved in the decision about how to treat an aneurysm.[65] 2[C]Evidence Young age and normal pre-operative level of consciousness are associated with favourable operative results and better recovery. excluding the aneurysm from the circulation. . A thrombus forms in the lumen. Ongoing technological advances have refined coil embolisation of aneurysms. vessel rupture. A craniotomy is not needed for endovascular coil embolisation. the probability of disability-free survival was significantly greater in the endovascular group than in the neurosurgical group.bmj. ( see Disclaimer ) Acute ( summary ) Patient group Tx line Treatment all patients 1st cardiopulmonary support TREATMENT plus surgical clipping or coil embolisation plus calcium-channel blockers plus stool softeners This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. and enrolment criteria that aneurysms be considered suitable for either surgical or endovascular repair.[72] [73] [74] [75] [76] Potential adverse events of the procedure itself are stroke. basilar tip aneurysms. the 5-year death risk remained significant compared with the clipping group. © BMJ Publishing Group Ltd 2016. Use of this content is subject to our disclaimer. are better suited for surgical clipping. 16 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.

bmj. 2016.Subarachnoid haemorrhage Treatment Acute ( summary ) cough adjunct antitussives headache adjunct analgesia altered coagulation adjunct coagulopathy correction hyponatraemia adjunct sodium replacement TREATMENT This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Use 17 of this content is subject to our disclaimer. All rights reserved.com . . BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. © BMJ Publishing Group Ltd 2016.

© BMJ Publishing Group Ltd 2016. » Complications of clipping include aneurysm rupture. and clipping of arterial perforators. All rights reserved. neurological status on admission. and need for endotracheal intubation and mechanical ventilation should be established. and maintenance of cerebral perfusion pressure. comorbid conditions. postoperative stroke. and recurrences requiring reintervention.[60] plus surgical clipping or coil embolisation » A neurosurgeon and interventional neuroradiologist should be involved. Blood pressure should be monitored and controlled to balance the risk of stroke. 2016. heart rate. Subarachnoid haemorrhage Treatment Treatment options Acute Patient group Tx line Treatment all patients 1st cardiopulmonary support » Patients should be admitted to ICU. Primary options » surgical clipping: may be more suitable for aneurysms associated with large parenchymal haematomas OR » endovascular coil embolisation: may be more suitable for older people or patients in poor medical condition. Blood pressure.com .1[C]Evidence Patient factors that should be taken into account include age. Controversy exists over the choice between clipping and coil embolisation. incomplete embolisation. 18 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Calcium-channel This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. » Consciousness level should be assessed using the Glasgow Coma Scale. .bmj. intraprocedural rupture of aneurysm or parent vessel. dissection of extracranial or intracranial arteries. Use of this content is subject to our disclaimer. vertebrobasilar aneurysms and TREATMENT aneurysms deep in the skull base may be more easily accessed plus calcium-channel blockers » Calcium-channel blockers should be started on admission for vasospasm prophylaxis. injury to vascular structures. and respiratory function should be closely monitored. hypertension-related rebleeding. vasospasm of the parent vessel. and size and location of the aneurysm. » Complications of coiling include haematoma at entry site. though there is some evidence to suggest that coiling confers a greater clinical outcome benefit in patients with a better pre-operative grade.

. Primary options » codeine phosphate: 10-20 mg orally every 4-6 hours when required. 2016. » Fluid overload should be avoided. maximum 120 mg/day headache adjunct analgesia » Mental status also needs be closely monitored. All rights reserved. May be associated with TREATMENT transfusion related lung injury.Subarachnoid haemorrhage Treatment Acute Patient group Tx line Treatment blockers reduce risk of poor outcome and secondary ischaemia after aneurysmal SAH.bmj. There are many available. © BMJ Publishing Group Ltd 2016. especially in older people and patients with CHF. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. cough adjunct antitussives » Cough suppression can help prevent rebleeding. coagulopathy should be treated aggressively using fresh frozen plasma and vitamin K. Primary options » oxycodone: 5-10 mg orally (immediate-release) every 4 hours when required OR » morphine sulphate: 2-4 mg intravenously every 30 minutes when required OR » fentanyl: 25-100 micrograms intravenously every 1-2 hours when required altered coagulation adjunct coagulopathy correction » If present. including docusate and senna.com . An antitussive agent such as codeine should be given. Use 19 of this content is subject to our disclaimer.[78] [79] 3[B]Evidence Primary options » nimodipine: 60 mg orally every 4 hours for 21 days plus stool softeners » Stool softeners to prevent straining can reduce the risk of rebleeding. Primary options » fresh frozen plasma: 15 mL/kg intravenously. repeated to normalise INR This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.

bmj. .25% saline. 20 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. © BMJ Publishing Group Ltd 2016. Sodium levels should be monitored for response. A correction rate of 12 millimols/L/24 hours (12 mEq/24 hours) should not be exceeded. Use of this content is subject to our disclaimer.[77] » Central pontine myelinolysis can occur with rapid correction of hyponatraemia. All rights reserved. and the rate and composition of the hypertonic solution adjusted accordingly. hypertonic solutions can be used (1.5% or 2% or 3%). 1. refer to consultant for guidance on dosage hyponatraemia adjunct sodium replacement » Electrolyte imbalances (e.. Subarachnoid haemorrhage Treatment Acute Patient group Tx line Treatment -and- » phytomenadione: doses of 10 mg orally/intravenously once daily for 3 days have been reported. Depending on how low the sodium is and the rate of drop.com . 2016. TREATMENT This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. hyponatraemia) are common and should be corrected.g. however.

although there was no effect on outcome. ETA and ETB. many reviews have questioned the conclusions of small studies and cautioned against the widespread use of statins.[82] Researchers evaluated the incidence of transcranial Doppler-defined vasospasm.8. ETA receptors are found on vascular smooth muscle cells and mediate vasoconstriction of small and large blood vessels.Subarachnoid haemorrhage Treatment Emerging Statins Statins.bmj. large controlled trials of continuous Mg++ infusion found no conclusive effects on DID or outcome. The lack of effect on overall outcome persisted when only patients undergoing coil-embolisation were analysed. however.[105] Moderate to severe angiographic spasm was significantly reduced.com . whether it independently predicts the development of DID is controversial. and kidney vascular endothelial cells. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. ET receptor antagonists failed to show an impact on overall outcome. where they modulate vasoconstriction in response to ET-1 through the production of vasodilator substances.[104] Delayed ischaemic deficits occurred in 29. Four small randomised. DID.[82] [83] [84] [85] Three trials used simvastatin at a dose of 80 mg.or long-term benefit.[87] [88] [89] In a pilot randomised. and their use is accompanied by adverse events.61 to 1.[99] [100] A small study described direct continuous cisternal magnesium sulfate infusion in patients with SAH. leading to dilation of cerebral vessels and improved cerebral blood flow. Use 21 of this content is subject to our disclaimer. The role of ETA antagonists in the prevention of vasospasm was tested in a phase III clinical trial. appeared to have a promising role in vasospasm prevention. are found in brain. aorta. However. 2016.[93] [94] [95] [96] [97] [98] A meta-analysis suggested that evidence to support a beneficial effect of magnesium sulfate on incidence of vasospasm and DID is still lacking.[108] A Cochrane review concluded that despite reduction of DID and angiographic vasospasm. on the other hand. and overall outcome. and treatment impact on outcome.[109] TREATMENT This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. All rights reserved.[91] [92] Other randomised controlled trials have only added to the controversies regarding magnesium’s effect on the risk of vasospasm.6% of patients on placebo (RR 0. Another such agent.[80] A more recent multi-centre randomised phase III trial enrolling 803 patients studied the effect of 40 mg of simvastatin for 21 days after SAH and found no short.06). TAK-044. 95% CI 0.[102] A phase IIa trial of clazosentan (an ETA antagonist) demonstrated reduction in the incidence and severity of angiographic vasospasm. single-centre studies investigated the safety and feasibility of statins in SAH. placebo-controlled. It is a 21 amino acid peptide generated in the endothelium of blood vessels and has an important role in vascular tone regulation.[86] Magnesium sulfate Hypomagnesaemia on admission is common in individuals with SAH. DID. © BMJ Publishing Group Ltd 2016.[103] Another ETA/B antagonist. ETB receptors.[90] However. double-blind study comparing Mg++ with saline. lung. or 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors. clazosentan. The results were at best mixed and did not allow meaningful conclusions regarding statins' current place in prevention of vasospasm. was also tested in a phase II trial.5% of patients receiving active treatment and 36. there was a trend towards less symptomatic vasospasm with Mg++. They are also found on vascular smooth muscle cells where they can mediate vasoconstriction.[84] [83] [85] and in one trial 40 mg of pravastatin was administered. ET-1 exerts its effects through 2 receptor subtypes.[80] [81] The proposed mechanism of neuroprotection in vasospasm is related to induction of the nitric oxide synthase pathway. . Endothelin-1 antagonists Endothelin-1 (ET-1) was identified in 1988.[101] The intervention had no effect on risk of cerebral infarction nor a beneficial effect on overall outcome 3 months after SAH.[106] [107] Clazosentan failed to show a significant effect on mortality and vasopsasm-related morbidity or functional outcome. was tested in a controlled clinical trial enrolling 413 patients with SAH. such as prostacyclin and nitric oxide.

If untreated aneurysms are still present. numbness on one side of the body. and straining. and in whom only one or some were treated (and some are left without treatment.bmj. In patients with multiple aneurysms.[131] [132] A systematic review suggested that short-term use of these agents would still reduce the incidence of rebleeding while mitigating the risk of ischaemia. 22 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. in order to avoid blood pressure swings.[8] [9] [38] Although antifibrinolytic agents reduce the risk of rebleeding. Subarachnoid haemorrhage Follow up Recommendations Monitoring FOLLOW UP Patients with single treated (with clipping) aneurysms need no monitoring after leaving the hospital. severe headache or weakness. angiography needs to be repeated at regular intervals because coils compact and the need for recoiling arises. until the aneurysm(s) is treated. The use of prophylactic antibiotics with EVD is not established but is commonly adopted. angiography may need to be repeated unless treatment of other aneurysms is imminent. Angiography is repeated at 6 months and then yearly thereafter (until it is decided that it is not needed any more by the interventional neuroradiologist). The patient is told to seek urgent medical attention if he or she experiences sudden. Complications Complications Timeframe Likelihood rebleeding short term high Rebleeding is an important complication. Use of this content is subject to our disclaimer.[8] [9] Patients with modified Fisher grade bleeding of III and IV[58] are more likely to rebleed. thick cisternal blood collection. All rights reserved. regardless of the treatment being clipping or coiling).[8] [9] [134] [Fig-3] Its occurrence is related to presence of intraventricular blood and.[130] Rebleeding is responsible for 8% to 22% of mortality and is significantly associated with poor outcome.[134] Treatment consists of placing a temporary ventricular catheter (EVD) or shunt to drain CSF.[45] It is unclear whether microsurgical fenestration of the lamina terminalis during surgical clipping of the aneurysm protects against the need for a permanent shunt in patients with hydrocephalus.7% during the first 72 hours. double vision. vision loss. Patient instructions The patient is instructed to take it easy for 2 to 4 weeks after discharge (in particular. After coiling (if single aneurysm).[133] Aneurysm treatment prevents rebleeding and thus early mortality.[136] vasospasm short term high This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. 2016. slurred speech. The incidence is 5. acute hydrocephalus short term high Acute hydrocephalus (HCP) occurs in 15% to 20% of patients during the first 72 hours and is an obstructive HCP. no lifting) and slowly return to normal life pace.com . they are not in common use because of increased risk of cerebral ischaemia and no effect on overall outcome. to a lesser extent. and cumulative risk approaches 22% at 1 month after SAH. . lifting. © BMJ Publishing Group Ltd 2016. the patient should abstain from sexual activity. or difficulty swallowing.[134] [135] The mortality rate in SAH patients with HCP is higher than in those without it.

BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. © BMJ Publishing Group Ltd 2016.Subarachnoid haemorrhage Follow up Complications Timeframe Likelihood FOLLOW UP This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. . All rights reserved.bmj. Use 23 of this content is subject to our disclaimer.com . 2016.

and hypovolaemia. surgical clipping. a fact compounded by the use of varying nomenclature and definitions.[Fig-4] [Fig-5] Half of these patients develop delayed ischaemic deficits (DID) secondary to reduced regional or overall cerebral blood flow (CBF). It reduces risk of poor outcome and secondary ischaemia after aneurysmal SAH. Triple H (hypertension. is safe. Xenon-CT (XeCT).[153] [154] The use of perfusion CT (PCT). This is believed to be due.[171] Studies investigating the use of antiplatelet agents in SAH. does not seem to carry a lesser risk of vasospasm than endovascular coiling.[78] [79] Despite their wide use. . patients develop alteration of consciousness or acute to subacute fluctuating focal neurological deficits. also known as hyperdynamic or hypervolaemic hypertensive therapy (HHT). a calcium-channel antagonist. intraventricular blood.[159] A systematic review of uncontrolled studies has suggested that hypertension seems to be more effective in increasing cerebral blood flow (CBF) than haemodilution or hypervolaemia. focal. until clinical improvement or adverse effects occur. Endovascular techniques such as transluminal balloon angioplasty and intra-arterial vasodilators will reverse arterial narrowing. Hypertension should be titrated to a mean arterial pressure (MAP) of at least 15% higher than the patient's average MAP. Subarachnoid haemorrhage Follow up Complications Timeframe Likelihood Vasospasm is a delayed.[160] Randomised controlled studies are difficult to conduct.[38] The pathophysiology of vasospasm is poorly understood.[161] [162] There is some evidence to support early angioplasty (within 2 hours of symptom onset) in providing sustained clinical improvement.[157] though a study has suggested that early goal-directed fluid therapy reduced the incidence of DID and cerebral infarcts. but large prospective outcome studies of HHT are lacking. culminating in a global or regional reduction of cerebral perfusion. even in patients with prior cardiac disease.[131] [135] [148] [149] [150] Although the presence of blood in the subarachnoid space is necessary to the development of vasospasm.g. during which most of the subarachnoid blood is washed out. © BMJ Publishing Group Ltd 2016.[158] However.[165] Tirilazad. given the multiplicity of factors that affect outcome in SAH. and other metabolic disturbances.[172] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. was studied in several controlled trials for prevention of vasospasm.[164] Nimodipine. These techniques are non-invasive and. is given for vasospasm prophylaxis. not merely arterial diameter or flow velocities. 24 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.. and duration of unconsciousness.com . It was well tolerated but had inconsistent effect on overall outcome across the different studies. to altered autoregulation of distal cerebral vessels.[163] Increased age and poor neurological status at presentation are predictive of poor clinical outcome after angioplasty. impaired autoregulatory function.[155] CT angiography (CTA) and PCT have shown excellent accuracy in diagnosing vasospasm. seizures.[147] Clinical improvement can be dramatic. Isotonic fluids are used. thick blood collections in cisterns and fissures. further compounding this problem. The benefit of prophylactic hypervolaemia is questionable.[166] [167] [168] [169] [170] Studies have investigated the use of simvastatin and pravastatin in SAH with mixed results. and improved functional outcome especially in poor grade patients. In addition. in part. Risk factors for DID are a poor clinical condition on admission. have yielded conflicting results on the risk of DID and overall outcome. have resulted in less than universal adoption of this practice. symptomatic patients should be kept hypervolaemic (central venous pressure ≥8 cm H2O) and hypertension induced using vasopressors.[145] [102] [146] Vasospasm develops between days 4 and 14 after SAH and is seen on angiography in 50% to 70% of cases. Clinically.[156] but these CT imaging techniques do not allow for therapeutic intervention (e. It accounts for FOLLOW UP 23% of deaths related to SAH. hypervolaemia. which when below a certain threshold causes ischaemia.[147] If untreated. 2016. together with an increased risk of haemorrhagic complications. HCP.[83] [82] [85] [84] Wide use of statins in SAH is awaiting larger confirmatory studies. and single photon emission computed tomography (SPECT) in detecting vasospasm is becoming more common.[151] [152] The diagnosis of vasospasm is a clinical one made after excluding rebleeding.[140] [141] [142] [143] [144] Presence of oxyhaemoglobin in the subarachnoid space seems to be necessary. Use of this content is subject to our disclaimer. measure perfusion. All rights reserved.[139] however. quantity and duration of exposure to subarachnoid blood. and an inflammatory response is implicated in the pathogenesis. especially following endovascular coiling. a non-glucocorticoid 21 amino-steroid free-radical scavenger. although TCD is less reliable. electrolyte imbalances.[Fig-4] [Fig-5] though clinical improvement is not consistent. Those conflicting findings. and haemodilution).bmj. most importantly. it is believed to result from a delayed and reversible vasculopathy. studies of corticosteroids in SAH have failed to show positive effects on DID or overall outcome. DID progresses to permanent cerebral infarction in 50% of cases. or diffuse narrowing of large capacitance vessels of the circle of Willis. transluminal balloon angioplasty and intra-arterial vasodilators) in the same way that angiography permits.[Fig-6] Ischaemic deficits may also be seen in the absence of discrete angiographic vasospasm.[8] [9] [145] Angiography or transcranial Doppler (TCD) confirms the diagnosis. low haemoglobin may impair oxygen delivery to brain regions with precarious perfusion.

[128] Prophylactic use of anticonvulsants in SAH has not been comprehensively studied.Subarachnoid haemorrhage Follow up Complications Timeframe Likelihood The effect on vasospasm of pharmacological compounds with controlled-release forms has drawn much interest. All rights reserved. controlled-release system include papaverine.[178] Another intervention that rids the subarachnoid space of blood is lumbar drainage (LD) of CSF.com . The use of thrombolytic agents instilled during surgery and/or after securing the aneurysm into the intrathecal space could potentially be beneficial.[173] [174] [175] A multi-centre cooperative study is ongoing in Japan. It is debated whether it is an independent predictor of outcome or is merely associated with severity of SAH. continuous insulin infusion) as used in critically ill patients.[179] It is unknown whether angiographic.[180] Except for 1 retrospective study using albumin. A prospective trial of LD showed a benefit on the incidence of DID. Use 25 of this content is subject to our disclaimer.[129] However. Small case series and a randomised double-blind trial using such implants have reported a lower than expected incidence of DID. The cumulative incidence of epilepsy (defined as 2 or more unprovoked seizures) is 12% at 5 years.[62] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. An apex-sparing pattern is seen in half of affected patients.bmj. These abnormalities rarely cause cardiac failure and are almost always reversible.[177] Larger controlled trials are needed before widespread use of this technique.[176] Other drugs used in an intracranial. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.[181] prophylactic volume expansion in asymptomatic patients has failed to show an impact on outcome. there is no evidence in support of this practice. one should refrain from such aggressive management (i. prophylactic anticonvulsants are recommended in the immediate post-haemorrhage period. however. including considerable risk of bias.[55] [33] [56] [38] [Fig-7] [Fig-8] Ventricular wall motion abnormalities occur in 27% of patients.[125] Furthermore.[60] Short course treatment may be adequate prophylaxis and better tolerated than longer periods of treatment. Beta-blockers can be administered for ischaemic-type ECG changes accompanied by troponin leaks. hyperglycaemia short term high Hyperglycaemia on admission is common even in non-diabetic patients. a middle cerebral artery location of aneurysm might impart an increased risk. because of the theoretical risk of rebleeding with a seizure. FOLLOW UP Nicardipine prolonged-release implants (NPRIs) are placed in the subarachnoid space at the time of surgical clipping of aneurysm. 2016.. and nitric oxide donors. Pulmonary oedema is severe.[125] It is independently associated with poor functional recovery and quality of life. but no effect on 6-month outcome.[183] [184] [36] Treatment of cardiac failure is supportive. requiring ventilatory support in 6% of cases. © BMJ Publishing Group Ltd 2016.[126] [127] The risk of seizures is significantly lower after coil embolisation than following surgical clipping of aneurysm.e. .[182] [159] cardiac abnormalities short term high Arrhythmias and non-specific ECG changes are common. pulmonary oedema short term high Pulmonary oedema occurs in up to 23% of patients. asymptomatic vasospasm needs to be treated.[185] [186] [187] [188] Until more robust evidence exists for treating hyperglycaemia in SAH.[189] seizure short term medium Seizures occur in 11% to 19% of patients with SAH. A meta-analysis concluded that while such compounds could improve outcome. The presence of intracerebral haemorrhage is associated with an increased risk of epilepsy. the analysed studies had limitations. They rid the subarachnoid space of blood necessary for the development of vasospasm. fasudil.

If fever occurs.[33] Forty percent of patients will have at least one medical complication during the first 3 months after SAH. © BMJ Publishing Group Ltd 2016. SAH increases the risk of developing infectious and unexplained fever. randomised controlled trial is needed to strongly demonstrate its effectiveness.[8] [9] [38] [114] Cardiac and respiratory complications are most frequent.[8] [9] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.[190] Intraventricular catheterisation is a risk factor for unexplained fever in the NICU. Use of this content is subject to our disclaimer. Causes of mortality are initial haemorrhage (19%).. aggressive treatment should be commenced with paracetamol. multi-centre. thrombophlebitis (1. Although the overall literature supports this technique.[116] [117] death long term high At 6 months after SAH.[1] and volume of subarachnoid blood are powerful predictors of 30-day mortality. which could be associated with a worse outcome. . shunt placement is necessary to avoid cerebral injury due to ventricular dilation. perioperative and immediate postoperative neurological injury could account for a percentage of poor outcomes in those with good admission WFNS grades.g.[112] Mortality is slightly greater in black patients and women. If fever persists above 38. and quality of life. Blood. 26 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. sputum. vasospasm (23%).5°C (101. and medical complications (23%).com . The presence of cardiac wall motion abnormality seem to portend a worse overall outcome after SAH. and CSF (if applicable) samples should be obtained for Gram staining and culture. emotional health.[112] Mortality rate for SAH is around 3 in 100.000 per year.[38] Old age. rebleeding (22%). more than 25% of patients are dead. overall outcome in SAH is still poor. level of responsiveness on admission (measured by the World Federation of Neurological Surgeons [WFNS] Scale).[113] Medical complications account for one quarter of deaths in SAH. occurring in > 20% of patients. ibuprofen.[191] [192] An infectious aetiology should always be sought. a well-designed.[115] Some degree of hepatic dysfunction is seen in 24% (4% with severe hepatic dysfunction).[8] [9] chronic hydrocephalus long term medium Chronic hydrocephalus is a well-known complication after aneurysmal SAH.4% of cerebrovascular deaths.3°F). The technique can be accomplished when a craniotomy is performed for aneurysm clipping.4%). Lamina terminalis fenestration plays a crucial role in chronic hydrocephalus prevention.8%) are also complications encountered during hospitalisation. However. 2016. All rights reserved. resulting in a negative impact on functional status.bmj. and pulmonary embolism (0.[137] On diagnosis of this disorder. neuropsychiatric problems long term high Over 50% of survivors report cognitive impairment (e. antibiotics should be withheld until there is clear evidence of an infection.[110] [111] SAH is responsible for about one third of premature deaths related to stroke.[38] Renal failure (1. and surface or intravascular cooling devices.[64] In patients undergoing clipping. Subarachnoid haemorrhage Follow up Complications Timeframe Likelihood fever short term medium FOLLOW UP Fever in the neurological intensive care unit (NICU) appears to be an independent predictor of poor outcome.4%). mood and memory problems).[138] Prognosis Advances in operative and endovascular techniques and postoperative critical care have led to a decrease in case-fatality rate over the past 3 decades. accounting for 4. anaemia (5%). It is associated with longer ICU stay and overall length of hospital stay. . urine.

Use 27 of this content is subject to our disclaimer. © BMJ Publishing Group Ltd 2016.[123] Apolipoprotein E (APOE) appears to have some influence on outcome. 2016. and quality of life. emotional health.bmj. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. and other cognitive impairment.[8] [9] Over 50% of survivors report problems with memory. . which is an independent predictor of outcome.[124] This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.[120] [121] [122] This led some to justify regionalisation of SAH treatment. patients with the apoE4 isoform have a relatively higher risk of poor outcome following SAH.[116] [117] At 6 months.Subarachnoid haemorrhage Follow up At 6 months after SAH. 75% of patients who were alert on admission had a good recovery.[118] [119] This identifies organ system dysfunction. Because the neuroprotective effectiveness of the apoE4 isoform is less than that of the others. resulting in negative impact on functional status. apoE4). mood. whereas only 11% of those comatose on admission survived. The product of the APOE genotype is a polymorphic protein existing as 3 common isoforms (apoE2. apoE3. other than the brain. ApoE is produced by astrocytes and is a complex multifunctional protein involved in neuroprotection.[8] [9] FOLLOW UP More than 40% of patients who die after SAH have extracerebral organ system dysfunction. All rights reserved. more than 25% of patients are dead and up to half of the survivors are moderately to severely disabled. The frequency of aneurysm repairs in a hospital (more than 30 craniotomies for aneurysm repair per year) and the presence and use of endovascular therapy are independently associated with better outcome after SAH.com . as a potential therapeutic target that might have a positive effect on outcome.

MRI and MRA are both established techniques for screening for cerebral aneurysm. MRI is superior to CT for depicting acute and chronic areas of intracerebral haemorrhage. All rights reserved. © BMJ Publishing Group Ltd 2016. GUIDELINES Expert meeting: hypopituitarism after traumatic brain injury and subarachnoid haemorrhage Published by: Acta Neurochirurgica Last published: 2006 Summary: This provides expert consensus on the diagnosis of hypopituitarism following SAH. Transcranial Doppler imaging can be used to monitor vasospasm following SAH. It examines the endocrine changes that accompany the acute and chronic phases after traumatic brain injury and provides possible pathophysiological explanations for the condition.bmj. 28 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Use of this content is subject to our disclaimer. American Stroke Association Last published: 2012 Treatment guidelines Europe Early management of patients with a head injury: a national clinical guideline Published by: Scottish Intercollegiate Guidelines Network Last published: 2009 North America Guidelines for the management of aneurysmal subarachnoid hemorrhage : a guideline for healthcare professionals from the American Heart Association/American Stroke Association Published by: American Heart Association. American Stroke Association Last published: 2012 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Subarachnoid haemorrhage Guidelines Diagnostic guidelines Europe Early management of patients with a head injury: a national clinical guideline Published by: Scottish Intercollegiate Guidelines Network Last published: 2009 EFNS guideline on neuroimaging in acute stroke Published by: European Federation of Neurological Societies Last published: 2006 Summary: Non-contrast CT scan is the established imaging procedure for the initial evaluation of stroke. . 2016.com . North America Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association Published by: American Heart Association.

methodologically flawed systematic reviews (SRs) or good quality observational (cohort) studies. © BMJ Publishing Group Ltd 2016. More info from BMJ Clinical Evidence 2. methodologically flawed RCTs of >200 participants. . More info from BMJ Clinical Evidence 3. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Mortality and disability: there is medium-quality clinical evidence to suggest that compared with placebo. 2016. Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized controlled trials (RCTs) of <200 participants. All rights reserved. oral nimodipine seems more effective at 3 months at reducing the proportion of people with poor outcome (death or dependence) and at reducing the proportion of people with cerebral infarction (measured by CT/MRI scan) after aneurysmal subarachnoid haemorrhage (SAH). Mortality and disability: there is poor-quality clinical evidence to suggest that endovascular coiling may be more effective at reducing the proportion of people with poor outcome (death or dependence) at 1 year. and reducing the risk of epilepsy in people with aneurysmal subarachnoid haemorrhage (SAH) in whom the aneurysm anatomy is considered suitable for both endovascular coiling and surgical clipping.com . Mortality and disability: there is poor-quality clinical evidence to suggest that early surgery (day 0-3 after aneurysmal subarachnoid haemorrhage [SAH]) may be more effective than intermediate surgery (days 4-7 after aneurysmal SAH) at improving the proportion of people with poor outcome (death or dependency) at 3 months in people with good clinical grades having surgical clipping.bmj. Use 29 of this content is subject to our disclaimer. Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized controlled trials (RCTs) of <200 participants.Subarachnoid haemorrhage Evidence scores Evidence scores 1. More info from BMJ Clinical Evidence EVIDENCE SCORES This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Evidence level B: Randomized controlled trials (RCTs) of <200 participants.

Selman WR. Stroke. Kistler JP. Abstract • Bederson JB. Stroke. J Neurosurg. Algra A. Full text Abstract References 1. 2012. Full text Abstract • Molyneux A. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. et al. Randomized trial of clazosentan in patients with aneurysmal subarachnoid hemorrhage undergoing endovascular coiling. 30 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Higashida RT. Rinkel GJ.354:387-396.366:809-817. et al. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Abstract • Connolly ES Jr. Yang K.(8):CD001245. The International Cooperative Study on the Timing of Aneurysm Surgery. seizures. Carhuapoma JR. Abstract • Molyneux AJ. Wiebers DO. and aneurysm occlusion. Lancet. 1996. Rabinstein AA. Full text Abstract • Guo J.84:405-414. Recommendations for the management of patients with unruptured intracranial aneurysms. Keller E. et al. 2013. rebleeding. Circulation.73:18-36. N Engl J Med. et al. Aneurysmal subarachnoid hemorrhage. Davis JM. Endothelin receptor antagonists for subarachnoid hemorrhage. Use of this content is subject to our disclaimer. Abstract • Barker FG 2nd. Cochrane Database Syst Rev. Jane JA. 2012. J Neurosurg.73:37-47.(4):CD000483. 2016. A statement for healthcare professionals from the Stroke Council of the American Heart Association. Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. © BMJ Publishing Group Ltd 2016. Circulatory volume expansion therapy for aneurysmal subarachnoid haemorrhage. et al. Kerr RS. Part 2: Surgical results. Part 1: Overall management results. 2005.43:1463-1469.43:1711-1737. Ogilvy CS. Kerr R. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. J Neurosurg. 2000:108:2300-2308. et al. Stratton I. Abstract • Macdonald RL. The International Cooperative Study on the Timing of Aneurysm Surgery. Lancet. Germans MR. Abstract • Kassell NF. 1990. Full text Abstract • Fisher CM. Full text Abstract • Baharoglu MI. Shi Z. Cochrane Database Syst.bmj. 2012. Haley EC Jr. et al.6:1-9. All rights reserved. subgroups. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis.360:1267-1274. Full text Abstract • Rinkel GJ. Torner JC. Neurosurgery. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. et al. 1980. Feigin VL. Suarez JI. 2006. Subarachnoid haemorrhage References Key articles REFERENCES • Kassell NF.(9):CD008354. 2002.com . 2004. et al. Awad IA. 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. et al. .Rev. 1990. Torner JC. Cochrane Database Syst Rev. Tarr RW. Yu LM. dependency.

van Gijn J. Stroke: pathophysiology. Meyer FB. et al. Sentinel headaches in aneurysmal subarachnoid haemorrhage: what is the true incidence? A systematic review. et al. Raabe A. van der Schaaf IC. 2010. Adams HP. J Neurosurg. 2006. Rinkel GJ. Tomsick T. Wermer MJ. Torner JC. 1992. Incidence of subarachnoid hemorrhage: role of region. Leblanc R. Linn FH. Cephalalgia. Jane JA. Wiebers DO. Abstract 10. year. 2000. et al. Grotta J. Beck J. Algra A. Abstract 14. Abstract REFERENCES 3. Brisman JL. 1990. et al. J Neurosurg. In: Mohr JP. Brain. Stroke. Abstract 17. Philadelphia. Winn HR. Brott T. 1990. N Engl J Med. Velthuis BK. Cerebral aneurysms. 2004.79:1572-1583. Polmear A.23:935-941. Abstract 5. Unruptured intracranial aneurysms . © BMJ Publishing Group Ltd 2016.bmj.hscic.37:2733-2737. Abstract 11. Bruno A. Broderick JP. 2003.27:625-629. 2001. Torner JC. 1998. Newell DW. 2004:271-285. J Neurosurg. Targeting chronic inflammation in cerebral aneurysms: focusing on NF-kappaB as a putative target of medical therapy. Kassell NF.326:733-736. Part 1: Overall management results. Aoki T. Abstract 4. Mayo Clin Proc.Subarachnoid haemorrhage References 2. Solomon RA. In: Le Roux PD. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. 2006. 1987. N Engl J Med. eds.com .uk/hes (last accessed 2 August 2016). Newell DW.73:18-36. 2004:377-396. 1996. and rate of computed tomography: a meta-analysis. London: Churchill Livingstone.124:249-278. Abstract 8. Kassell NF. Management of unruptured aneurysms. Health and Social Care Information Centre. Abstract 9. Pathogenesis. et al. 2016. Szelenyi A. Davis P. Choi D. Aneurysmal subarachnoid hemorrhage. eds. Qualls C. et al.19:227-232. Piepgras DG.339:1725-1733. Sentinel headache and the risk of rebleeding after aneurysmal subarachnoid hemorrhage. 18.66:35-39. Full text Abstract 13. PA: Saunders. The International Cooperative Study on the Timing of Aneurysm Surgery. http://www.73:37-47. Stroke..gov.2012-2013. Brain. Risk factors for intracerebral and subarachnoid hemorrhage among Hispanics and non-Hispanic whites in a New Mexico community.128:2421-2429. Abstract 15. Abstract 6.risk of rupture and risks of surgical intervention. Haley EC Jr.14:265-273. . Neuroepidemiology. et al. Full text 7. diagnosis and management. The minor leak preceding subarachnoid hemorrhage. Expert Opin Ther Targets. Follow-up screening after subarachnoid haemorrhage: frequency and determinants of new aneurysms and enlargement of existing aneurysms. Abstract 16. Use 31 of this content is subject to our disclaimer. Connolly ES. 12. All rights reserved. et al. causes and management. Subarachnoid haemorrhage: diagnosis. The risk of subarachnoid and intracerebral hemorrhages in blacks as compared with whites. Nishimura M. The International Cooperative Study on the Timing of Aneurysm Surgery. Management of cerebral aneurysms. Part 2: Surgical results. Song JK. natural history. 2005. N Engl J Med. International Study of Unruptured Intracranial Aneurysms Investigators. Hospital episode statistics . and treatment of unruptured intracranial aneurysms. Full text Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.355:928-939. Rinkel GJ.

Broderick JP. N Engl J Med. et al. Abstract 22. Whisnant JP. et al.. Full text Abstract 21. et al. 2000:108:2300-2308. 2003. Lancet. Poussa K. Juvela S. Neurosurgery. Awad IA. Stroke. Abstract 30. Neurosurgery.27:544-549. Ueki K. et al. 2000. Schievink WI. 2000. Rinkel GJ. et al. 1999. Piepgras DG. Circulation.93:379-387. Major risk factors for aneurysmal subarachnoid hemorrhage in the young are modifiable. 1981. . A statement for healthcare professionals from the Stroke Council of the American Heart Association. 2016. Newell JB. Abstract REFERENCES 20. Juvela S. 2003. Stroke.25:889-903. 2001. Kopelnik A.44:34-39. Subarachnoid haemorrhage References 19. Prehemorrhage risk factors for fatal intracranial aneurysm rupture. Recommendations for the management of patients with unruptured intracranial aneurysms. Acute stroke: bench to bedside. Tung P. Use of this content is subject to our disclaimer. Rinkel GJ. 1996. 33. N Engl J Med. Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies. Medical management of subarachnoid hemorrhage.35:548-551. Abstract 29. © BMJ Publishing Group Ltd 2016. Lancet Neurol.49:607-612.4:122-128. New York.34:1375-1381. Abstract 23. Porras M. et al. Bederson JB. Abstract 28. In: Bhardwaj A. Full text Abstract 31. Risk factors for subarachnoid hemorrhage. Suri MF. Lawes CM. et al. Stroke. 1999.com .93:550-553. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities.36:2773-2780.340:744.bmj. Diringer MN. Qureshi AI. 2004. 2005. Wiebers DO. Whisnant JP. A review. et al. Stroke. J Neurosurg. Abstract 26. clinical outcome. Abstract 32. 2003. 32 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Abstract 24. Risk of rupture from incidental cerebral aneurysms. Neurovascular manifestations of heritable connective tissue disorders. Abstract 34. O'Fallon WM. Rordorf GA. Yahia AM. Feigin VL. Correction: unruptured intracranial aneurysms risk of rupture and risks of surgical intervention. Abstract 25. et al. NY: Informa Healthcare. et al.304:696-698. Alkayed NJ. eds. Michels VV. The natural history of unruptured intracranial aneurysms. Wiebers DO. Rinkel GJ. Banki N. 1994. and risks of surgical and endovascular treatment. Stroke. Morita A. Axelrod KA. All rights reserved. Stroke. 2005. Risk factors for subarachnoid hemorrhage: a systematic review. Huston J 3rd. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Teunissen LL.362:103-110. Abstract 27.34:1852-1857. Intracranial aneurysm screening: indications and advice for practice. Natural history of unruptured intracranial aneurysms: probability of and risk factors for aneurysm rupture. Viscoli CM. Kirsch JR. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. J Neurosurg. Algra A. Tsutsumi K. Brott T. Zaroff JG. Unruptured intracranial aneurysms: natural history. Wiebers DO. 2006.

2004. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter.13:774-779. Crit Care Med. Abstract REFERENCES 36. Perry JJ. et al. Use 33 of this content is subject to our disclaimer. 2016. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.80:550-559. et al. Hoh BL. . Chappell ET. Sensitivity of early brain computed tomography to exclude aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. Participants of the Multicenter Cooperative Aneurysm Study. Ann Clin Biochem.54:1329-1340. Silva P. Rabinstein AA. BMJ. Neurology. Giavroglou C. Abstract 47. Beetham R. Tung GA. Falcone SF. Latchaw RE. Jain R. et al. Solenski NJ. Sivilotti ML. Bellolio MF. Rordorf GA. 1995. All rights reserved. Full text 45. Neuroimaging Clin N Am. Charitanti A.230:510-518.7:693-708. Clinical review: subarachnoid haemorrhage. Good MC. Hasan D. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.com . 2006. Mayo Clin Proc. et al. 2004. Cruickshank A. Kassell NF. Abstract 49. Abstract 46. Intracranial aneurysms: evaluation using CTA and MRA. Neurosurgery. Bijvoet HW. Correlation with DSA and intraoperative findings. Abstract 43.46:842-850. Zaroff JG. et al. © BMJ Publishing Group Ltd 2016. Time-dependent test characteristics of head computed tomography in patients suspected of nontraumatic subarachnoid hemorrhage. UK NEQAS Specialist Advisory Group for EQA of CSF Proteins and Biochemistry. Manno EM. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. Results of a prospective protocol of computed tomographic angiography in place of catheter angiography as the only diagnostic and pretreatment planning study for cerebral aneurysms by a combined neurovascular team. Stroke.45:238-244. 2004.343:d4277. 2016. White PM. et al. Stiell IG. Jayaraman MV. van der Jagt M. Abstract 44. cooperative aneurysm study. Regional patterns of left ventricular systolic dysfunction after subarachnoid hemorrhage: evidence for neurally mediated cardiac injury. et al. Cheung AC.47:750-755. 2004. Full text Abstract 42. et al. Detection of intracranial aneurysms: multi-detector row CT angiography compared with DSA. Abstract 37. 1999. Abstract 40. 1997. J Am Soc Echocardiogr.25:126-129. Subarachnoid hemorrhage: neurointensive care and aneurysm repair.333:235-240. Kouskouras C.52:624-631. Kemperman H. Stroke. 2008.43:2115-2119. Deveikis J. 2012. Backes D. et al. et al. Neuroradiology. Comparison of computed tomographic angiography with digital subtraction angiography in the diagnosis of cerebral aneurysms: a meta-analysis. 2011. Davenport RJ. Dubosh NM. Auld P. Haley EC Jr. 2003. Ogilvy CS. et al. Mayo-Smith WW. Revised national guidelines for analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage. Management of patients with stunned myocardium associated with subarachnoid hemorrhage. AJNR Am J Neuroradiol. Rabinov JD. Validity of prediction of the site of ruptured intracranial aneurysms with CT. Rinkel GJ. Al-Shahi R. Wijdicks EF. Abstract 48. Full text Abstract 41. 2000. The role of CT following aneurysmal rupture. Radiology.23:1007-1017. Abstract 38.bmj. Abstract 39. Thompson BG. 2005.Subarachnoid haemorrhage References 35. Kallmes DF. et al. Neurosurgery. BMJ.52:34-39. Moure FC.

Kim DH. Storrow AB. Stroke.6:1-9. © BMJ Publishing Group Ltd 2016. Diagnosing cerebral aneurysms by computed tomographic angiography: meta-analysis. Kistler JP. Crit Care Med. Duldner JE. Abstract REFERENCES 51. and likelihood ratios. Abstract 64. Neurosurgery. A systematic review of Terson's syndrome: frequency and prognosis after subarachnoid haemorrhage. Neurosurgery. Abstract 53. 2007. Abstract 56. Clinical significance of elevated troponin I levels in patients with nontraumatic subarachnoid hemorrhage.43:1711-1737. Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team. Stroke. Zaidat OO. Deibert E. 2016. Abstract 63. Sensitivity of new-generation computed tomography in subarachnoid hemorrhage. Hunt WE. Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage. Nelemans PJ.28:14-20. Abstract 52. Full text Abstract 61. Bleck TP. Bulsara KR. Larsen J. Dunn IF.98:524-528. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society's Multidisciplinary Consensus Conference. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Abstract 58.75:491-493. Ann Neurol. Subarachnoid haemorrhage References 50. et al. McCarron MO. Abstract 57. 2011. Sames TA. Full text Abstract 54. Davis JM.bmj. et al. Abstract 55. Finkelstein JA. et al. 34 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Menke J. . 2011. et al. Wagemans BA.98:741-746. Use of this content is subject to our disclaimer. Connolly ES Jr. et al. Three-day phenytoin prophylaxis is adequate after subarachnoid hemorrhage.69:646-654.15:211-240.32:2311-2317.60:99-102.com . et al. 2009. Diringer MN. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. Carhuapoma JR. Diringer MN. 2003.3:16-20. J Neurol Neurosurg Psychiatry. Claude Hemphill J 3rd. et al. Chumnanvej S. Kallenberg K. 2003. specificity. van Gelder JM. 2003. McCarron P. Sailer AM. 1996. Barzilai B. Abstract 62. All rights reserved. Rabinstein AA. Neurosurgery. Broderick JP. J Neurosurg. et al.25:1342-1347. Diagnosing intracranial aneurysms with MR angiography: systematic review and meta-analysis. 2004.37:432-440. Braverman AC. J Neurosurg. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Computed tomographic angiography for detecting cerebral aneurysms: implications of aneurysm size distribution for the sensitivity. Suarez JI. 1980. Brott TG. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Crit Care Med. Suri MF. Fisher CM. McGirt MJ. Alberts MJ. Liao L. 2012.53:597-605. Abstract 59. Stroke. Hess RM. 2014. Abstract 60. 2004. Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage. Management of aneurysmal subarachnoid hemorrhage. J Neurosurg. 1968. Neurocrit Care.45:119-126. 1994. Acad Emerg Med.

Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. Abstract 73. et al. Lozier AP. Birks J.8:427-433. Use 35 of this content is subject to our disclaimer.15:354-360. Diringer MN. Clipping versus coiling for ruptured intracranial aneurysms: a systematic review and meta-analysis. National Institute for Health and Care Excellence. Management of hyponatremia and volume contraction.33:2509-2518. Molyneux AJ. et al. 2012. 1996. 2003. 2009.com . BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. 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.54:268-280. 2005. et al. 2003. Endovascular coil occlusion of 1811 intracranial aneurysms: early angiographic and clinical results. http://www. Abstract 74. Stratton I. et al. Abstract REFERENCES 66. et al. Kerr RS. © BMJ Publishing Group Ltd 2016. Yu LM. Molyneux A. 2015. Henkes H. et al. Molyneux AJ. Timing of aneurysm treatment after subarachnoid hemorrhage: relationship with delayed cerebral ischemia and poor outcome. Raymond J. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. 2002. et al. To clip or to coil acutely ruptured intracranial aneurysms: update on the debate. 2013. Lancet Neurol.84:405-414.43:2126-2129. Stroke. Full text Abstract 71. or dependence and standardised mortality ratios after clipping or coiling of an intracranial aneurysm in the International Subarachnoid Aneurysm Trial (ISAT): long-term follow-up. Abstract 78. Stroke.Subarachnoid haemorrhage References 65. Duckwiler G. et al. and aneurysm occlusion. Lavine SD. Guglielmi detachable coil embolization of cerebral aneurysms: 11 years' experience. . May 2012. Pan R. Pipeline embolisation device for the treatment of complex intracranial aneurysms. Kerr RS. Clarke A. J Neurosurg. Lancet.34:1398-1403. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils. Dorhout Mees SM. rebleeding. Li H. Full text Abstract 70. Molyneux AJ.385:691-697. Lancet.nice.98:959-966. J Neurosurg. Ogilvy CS. Stroke. Nien YL. 2005. Full text Abstract 76. Fischer S. Risk of recurrent subarachnoid haemorrhage. Molyneux AJ. Guglielmi detachable coil embolization of posterior circulation aneurysms: a systematic review of the literature. dependency. Bruder N. ISAT Collaborators.bmj. Kerr RS. Neurocrit Care.366:809-817. Kerr R. The durability of endovascular coiling versus neurosurgical clipping of ruptured cerebral aneurysms: 18 year follow-up of the UK cohort of the International Subarachnoid Aneurysm Trial (ISAT). Abstract 69. Full text 72. Rabinstein AA. Stroke. 2002. seizures. Lancet. Weber W. Connolly ES Jr. Abstract 68. death. Abstract 75.org/ (last accessed 2 August 2016). Birks J. subgroups. Guilbert F. Barker FG 2nd. et al.44:29-37. Weill A. 2016. Curr Opin Crit Care. et al. Neurosurgery. Wang H. Murayama Y. Abstract 67. 2011.360:1267-1274. 2004.11:121-125. Full text Abstract 77. All rights reserved.

et al. autoregulation. 2005. 2007. Wang H. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Piepgras DG. et al. All rights reserved. et al. Sandercock P. Plasma magnesium concentrations and clinical outcomes in aneurysmal subarachnoid hemorrhage patients: post hoc analysis of intravenous magnesium sulphate for aneurysmal subarachnoid hemorrhage trial. Full text Abstract 92. Neurosurgery. Chan MT. Effects of acute treatment with pravastatin on cerebral vasospasm. Hypomagnesemia after aneurysmal subarachnoid hemorrhage. et al. Full text Abstract 82.bmj. Lynch JR. J Cereb Blood Flow Metab. and death? A cautionary tale of 2 meta-analyses. et al.1:441-448. et al. 2013. Badjatia N. Stroke. et al. et al. Magnesium sulfate in aneurysmal subarachnoid hemorrhage: a randomized controlled trial. vasospasm.(4):CD008184. Liu L. Stroke. 2005. Abstract 91. placebo-controlled pilot study of simvastatin in aneurysmal subarachnoid hemorrhage. Abstract REFERENCES 80. Lancet Neurol. Chan MT. placebo-controlled randomized trial. double-blind. Boet R. Full text Abstract 81. et al.18:142-148. van den Bergh WM. Geskus RB. Feigin VL. .39:2891-2893. et al. Abstract 89. Vandertop WP. Smith EE. et al.41:e1-2. 2014. Intravenous magnesium versus nimodipine in the treatment of patients with aneurysmal subarachnoid hemorrhage: a randomized study.58:1054-1065. Abstract 87.36:1627-1632. Kirkpatrick PJ. © BMJ Publishing Group Ltd 2016. Wong GK. Stroke.41:1841-1844. Simvastatin reduces vasospasm after aneurysmal subarachnoid hemorrhage: results of a pilot randomized clinical trial.52:276-281. 2012. Zhang Z. Cochrane Database Syst Rev. 2009. et al. Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial. 2003. Friedman JA. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. 2016. Czosnyka M.com . MASH Study Group.36:1011-1015. Algra A. Kunz M. Turner CL. 2008. Meijers JC. van den Bergh WM. Abstract 83. Abstract 85. A randomized. Liu Z. and delayed ischemic deficits after aneurysmal subarachnoid hemorrhage: a phase II randomized placebo-controlled trial. Stroke.380:44-49. Full text Abstract 86. Chou SH. Algra A. Simvastatin in aneurysmal subarachnoid haemorrhage (STASH): a multicentre randomised phase 3 trial. Poon WS. Dorhout Mees SM. van Kooten F. Schmid-Elsaesser R.(3):CD000277. Wong GK. Rinkel GJ. Dorhout Mees SM. Zausinger S. 2005.Rev. J Neurosurg Anesthesiol. Neurosurgery. Lancet. Neurocrit Care. Richards H. 2010. Subarachnoid haemorrhage References 79. Use of this content is subject to our disclaimer. Abstract 90. Serum magnesium levels as related to symptomatic vasospasm and outcome following aneurysmal subarachnoid hemorrhage. et al. McGirt MJ. Collignon FP. 2004. 36 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Tseng MY.29:1444-1453. Algra A. van der Sprenkel JW. Biologic effects of simvastatin in patients with aneurysmal subarachnoid hemorrhage: a double-blind. Full text Abstract 93.36:2024-2026. Stroke. 2006. et al. Cholesterol-reducing agents for aneurysmal subarachnoid haemorrhage. 2006. Cochrane Database Syst.13:666-675. Stroke. Vergouwen MD. 2010. Abstract 84. Intravenous magnesium sulfate after aneurysmal subarachnoid hemorrhage: a prospective randomized pilot study. Smith C. 'Yes' or 'no' to routine statins after subarachnoid hemorrhage to prevent delayed cerebral ischaemia. Abstract 88.

Abstract 103. multicenter phase IIa study. Murray GD.38:1284-1290. et al. Clazosentan to overcome neurological ischemia and infarction occurring after subarachnoid hemorrhage (CONSCIOUS-1): randomized.103:9-17.93:992-997. placebo-controlled.com .Subarachnoid haemorrhage References 94. Full text Abstract 106. et al. 2001.39:3015-3021. Abstract 96. placebo-controlled. Abstract 102. Clinical review: prevention and therapy of vasospasm in subarachnoid hemorrhage. Keyrouz SG. Radiology. Prevedello DM. et al. 2011. Intracranial aneurysms in patients with subarachnoid hemorrhage: CT angiography as a primary examination tool for diagnosis: systematic review and meta-analysis. Meyer B.13:202-206. Use 37 of this content is subject to our disclaimer. Neurocrit Care. Wong GK. © BMJ Publishing Group Ltd 2016. Cordeiro JG. Preventive effect of continuous cisternal irrigation with magnesium sulfate solution on angiographic cerebral vasospasms associated with aneurysmal subarachnoid hemorrhages: a randomized controlled trial. Parra A.16:1394-1397. Westerlaan HE. Full text Abstract 101. Westermaier T. placebo-controlled.258:134-145. et al. receptor antagonist TAK-044 in treating subarachnoid hemorrhage: a report by the Steering Committee on behalf of the UK/Netherlands/Eire TAK-044 Subarachnoid Haemorrhage Study Group. Mori K. J Neurosurg. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. 2010. Preventing vasospasm improves outcome after aneurysmal subarachnoid hemorrhage: rationale and design of CONSCIOUS-2 and CONSCIOUS-3 trials.124:18-26. J Clin Neurosci. Clazosentan (AXV-034343). 2011. Boet R. Surg Neurol. A meta analysis of treating subarachnoid hemorrhage with magnesium sulfate. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Crit Care. double-blind.65 Suppl 1:S1:14-1:20. 2007. Mayer S. Jansen-van der Weide MC. J Neurosurg. Lynch J. Zhao XD. Macdonald RL. 2016. a selective endothelin A receptor antagonist. Poon WS. Kassell NF. van Dijk JM. double-blinded. et al. Poon WS.bmj. Abstract 105. Full text Abstract 98. 2008. Zhang X. . Stetter C. et al. Brewer RP. Prophylactic intravenous magnesium sulfate for treatment of aneurysmal subarachnoid hemorrhage: a randomized. clinical study. Magnesium sulfate: role as possible attenuating factor in vasospasm morbidity. Shaw MD. Stroke. Diringer MN. Abstract REFERENCES 95. et al. 2010. 2009. de Morais AL.15:R52. Esaki T. 2000. Crit Care. Vermeulen M.11:220. Abstract 99. 2005. Weidauer S. Intravenous magnesium sulphate for aneurysmal subarachnoid hemorrhage (IMASH): a randomized. in the prevention of cerebral vasospasm following severe aneurysmal subarachnoid hemorrhage: results of a randomized. Wong GK. Intravenous magnesium sulphate for aneurysmal subarachnoid hemorrhage: an updated systemic review and meta-analysis. Macdonald RL. Higashida RT. Zhou YT. Cerebral blood flow velocity response to magnesium sulfate in patients after subarachnoid hemorrhage. 2016. et al. 2006. multicenter phase III trial. et al. J Neurosurg. placebo-controlled phase 2 dose-finding trial. Stroke.41:921-926. Chan MT. double-blind. et al. J Neurosurg Anesthesiol. IMASH Investigators. Full text Abstract 100. All rights reserved. Vince GH. Abstract 97. 2010. Abstract 104.13:416-424. et al. CONSCIOUS-1 Investigators. Vajkoczy P. Yamamoto T. et al. Crit Care Med. Keller E. Efficacy and safety of the endothelin.

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Cochrane Database Syst. Lanterna LA. et al. Huttunen J. 2009. et al. and therapeutic perspectives . Use 39 of this content is subject to our disclaimer. van Donkelaar CE. Tarmey JJ. Neurology. rebleeding. Sneade M. Kassell NF. Predictive factors for rebleeding after aneurysmal subarachnoid hemorrhage: rebleeding aneurysmal subarachnoid hemorrhage study. 1987. Abstract 136. Elkins JS. Abstract 128. Significance of apolipoprotein E in subarachnoid hemorrhage: neuronal injury. Claassen J. 2003. Mayer SA. Epilepsy after subarachnoid hemorrhage: the frequency of seizures after clip occlusion or coil embolization of a ruptured cerebral aneurysm: results from the International Subarachnoid Aneurysm Trial. Efficacy of lamina terminalis fenestration in reducing shunt-dependent hydrocephalus following aneurysmal subarachnoid hemorrhage: a systematic review. Baharoglu MI.154:1-9. 1985. 62:1743-1748. Regionalization of treatment for subarachnoid hemorrhage: a cost-utility analysis. Predicting cerebral ischemia after aneurysmal subarachnoid hemorrhage: influences of clinical condition. . Circulation. Abstract 131. et al.a review. et al. Kim GH. et al. 2004. Hijdra A. Abstract 125. Claassen J. et al.bmj. 2010. Stroke. Kowalski RG. Stroke.com . Germans MR. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Birks J. von Und Zu Fraunberg M. Abstract 135. Abstract 132.111:147-154. Adams HP Jr. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Prediction of delayed cerebral ischemia.46:2100-2106. Clinical article. 2009. Bakker NA. Wijdicks EF. 2012. and antifibrinolytic therapy. Gaberel T. et al. Abstract 124. Veeger NJ. van Gijn J. 2011. Acta Neurochir (Wien). Abstract 129. A report of the Cooperative Aneurysm Study.Rev.(8):CD001245. repair. Hart Y. All rights reserved. Abstract 126. Solomon RA. Riordan KC. Detection of electrographic seizures with continuous EEG monitoring in critically ill patients. J Neurosurg. 2004. Magheru C. Torner JC.115:1159-1168. Biroli F.Subarachnoid haemorrhage References 122. Wellik KE. J Neurosurg. Predictors and clinical impact of epilepsy after subarachnoid hemorrhage. Neurologist. et al. Wingerchuk DM. et al. long-term follow-up study. Antifibrinolytic therapy in the management of aneurismal subarachnoid hemorrhage revisited: a meta-analysis.109:2207-2212. Relationship between the volume of craniotomies for cerebral aneurysm performed at New York state hospitals and in-hospital mortality.19:1250-1256.84:2229-2237. Hahn DK. Epilepsy after aneurysmal subarachnoid hemorrhage: a population-based. 1988. Bardach NS.37:1586-1591. 2015. Peery S. Komotar RJ. Kreiter KT. Mayer SA.60:208-214. Abstract 127. Neurology. Rinkel GJ. 2015. Stroke. et al. Anticonvulsant drug therapy after aneurysmal subarachnoid hemorrhage: a critically appraised topic. et al.27:13-17. 1996. et al. Neurology. J Neurosurg. Abstract 130.18:116-123. Nagelkerke NJ. CT results. et al.16:397-399. Neurology. 2016. Kurki MI. J Stroke Cerebrovasc Dis. Full text Abstract 133. Emery E. Hijdra A. Olson SJ. © BMJ Publishing Group Ltd 2016. and outcome after aneurysmal subarachnoid hemorrhage. Abstract 134. van Gijn J.63:355-362. 2013. Acute hydrocephalus after aneurysmal subarachnoid hemorrhage. Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. Abstract REFERENCES 123.

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1999. et al.55:112-123. Thomas JE. Use 41 of this content is subject to our disclaimer. J Neurosurg. et al. . Rinkel GJ. 2005. Ackery A. 1998.bmj. Lad SP.44:975-979. Gold R. Reichman M. Abstract 159. 2009. Corticosteroids for aneurysmal subarachnoid haemorrhage and primary intracerebral haemorrhage. 2011. Dankbaar JW. Kassell NF.25:1778-1782. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a systematic review. Abstract 166. Rigamonti A. van den Bergh WM. 2010. Early intensive versus minimally invasive approach to postoperative hemodynamic management after subarachnoid hemorrhage. AJNR Am J Neuroradiol. Schwamm LH. Kazumata K. Manno EM. Mutoh T.31:1853-1860. et al.15:275-280.Subarachnoid haemorrhage References 152. Gress DR. et al. Full text Abstract REFERENCES 153. Full text Abstract 161. 2004.(4):CD000483. Cerebral perfusion imaging in vasospasm. et al. Feigin VL. Efficacy of transluminal angioplasty for the management of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Hansen CA. et al.29:422-428. 2004. 2010. Wolf S. Cochrane Database Syst Rev. Abstract 163. Full text Abstract 160. Predictors of outcome after endovascular treatment of cerebral vasospasm. Abstract 162. Feigin VL. double-blind. J Neurosurg. Neurosurg Focus. Guzman R. Abstract 158. et al. © BMJ Publishing Group Ltd 2016. Cochrane Database Syst Rev. Armonda RA. Kerr RS. Neurocrit Care. Algra A. Greenberg ED. Rosenwasser RH. Rinkel GJ. Baker AJ. et al. Therapeutic modalities for the management of cerebral vasospasm: timing of endovascular options. Yang BP. Kelly ME. Circulatory volume expansion therapy for aneurysmal subarachnoid haemorrhage. Stroke. Abstract 165. Endovascular treatment strategies for cerebral vasospasm. Schaaf IC. Nichols DA. Diagnostic accuracy of CT angiography and CT perfusion for cerebral vasospasm: a meta-analysis. Anderson N.14:R23.(3):CD004583. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.92:284-290. Routine management of volume status after aneurysmal subarachnoid hemorrhage. vehicle-controlled trial of tirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study in North America. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Full text Abstract 157. Coenen VA. Neurosurg Focus.45:1280-1284. Polin RS. Slooter AJ. Can J Anaesth. 2006. Transcranial Doppler monitoring in subarachnoid hemorrhage: a critical tool in critical care. Mindea SA. Effect of antiplatelet therapy for endovascular coiling in aneurysmal subarachnoid hemorrhage. Stroke.86:467-474. Rabinstein AA. Haley EC Jr. et al. Bendok BR.40:1969-1972. Friedman JA. 1997. Crit Care. Abstract 154. International Subarachnoid Aneurysm Trial (ISAT) Collaborative Group. 2006. Algra A.com . 2000. Apperson-Hansen C. 2016. AJNR Am J Neuroradiol. 2008. et al. et al. Participants in the International Multi-Disciplinary Consensus Conference on the Critical Care Management of Subarachnoid Hemorrhage. Effects of induced hypertension on transcranial Doppler ultrasound velocities in patients after subarachnoid hemorrhage. Rinkel GJ. Abstract 164. et al. Abstract 155.21:E7. Abstract 156. Stroke. Neurosurgery. Terasaka S.21:E13. All rights reserved. 2014. A randomized.

Australia. Lumbar drainage of cerebrospinal fluid after aneurysmal subarachnoid hemorrhage: a prospective. et al. Richards H. A cooperative study in North America. Kassell NF. Stroke. van den Bergh WM. Lanzino G.bmj. Efficacy and safety of nicardipine prolonged-release implants for preventing vasospasm in humans. Neurosurgery. Neurocrit Care. Randomized. Haley EC Jr. Effect of human albumin administration on clinical outcome and hospital cost in patients with subarachnoid hemorrhage. Abstract 169. Abrahams JM.110(Pt 2):165-167. Al-Tamimi YZ. Abstract 179. controlled trial (LUMAS). Kasuya H. 42 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Neil JA.56:895-902.38:330-336. Neurosurg Focus. Full text Abstract 176.21:E10. J Neurosurg.14:489-499. Kassell NF. Cochrane Database Syst Rev. Double-blind. Clinical trial of nicardipine prolonged-release implants for preventing cerebral vasospasm: multicenter cooperative study in Tokyo. Treatment of cerebral vasospasm with biocompatible controlled-release systems for intracranial drug delivery. Application of nicardipine prolonged-release implants: analysis of 97 consecutive patients with acute subarachnoid hemorrhage. Wang L. Abstract 177.90:1011-1017. Dorsch NW. randomized. Onda H. Nolan CP. J Neurosurg. Abstract 172. J Neurosurg. Kasuya H. Effect of nicardipine prolonged-release implants on cerebral vasospasm and clinical outcome after severe aneurysmal subarachnoid hemorrhage: a prospective. 2016. Sasahara A. Effects of acute treatment with statins on cerebral autoregulation in patients after aneurysmal subarachnoid hemorrhage. et al. Zhang S. Macdonald RL. vehicle-controlled trial of tirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study in Europe. Wu B. Zaidat OO.(2):CD006778. All rights reserved. Abstract 175. Part II. Apperson-Hansen C. A cooperative study in Europe. Lanzino G. 2010. double-blind.6:1011-1019. 2005. Part I. Australia. Abstract 180. Abstract REFERENCES 168. randomized. Abstract 173. Barth M. Czosnyka M. Shannon L. Use of this content is subject to our disclaimer. Bhargava D. Feltbower RG. and South Africa. Tirilazad for aneurysmal subarachnoid haemorrhage. double-blind phase IIa study.21:E1. Abstract 170. Stroke. Abstract 178. Suarez JI.com . 2007. Kramer AH. Full text Abstract 171. Cochrane Database Syst Rev. Neurosurgery. randomized. 2008. 2011. vehicle-controlled study of high-dose tirilazad mesylate in women with aneurysmal subarachnoid hemorrhage. et al. Weidauer S. Liu M. Murali R. et al.(4):CD006184. Double-blind. randomized. 2004. Kassell NF. New Zealand. Fletcher JJ. Algra A. et al. Acta Neurochir Suppl. et al. 1996. 1999. 2012. 2006. Kasuya H. J Neurosurg. and New Zealand. 2006. Stroke. Abstract 181. Rinkel GJ.84:221-228. 2007.43:677-682.90:1018-1024. et al. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Onda H.100:585-590. et al. Takeshita M. Subarachnoid haemorrhage References 167. 2011. Capelle HH. Full text Abstract 174. Dorhout Mees SM. 1999. Locally-administered intrathecal thrombolytics following aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. 2002. Tseng MY. Omeis I. Antiplatelet therapy for aneurysmal subarachnoid haemorrhage. © BMJ Publishing Group Ltd 2016. . Can angiographic vasospasm be used as a surrogate marker in evaluating therapeutic interventions for cerebral vasospasm? Neurosurg Focus.33:1011-1015. vehicle-controlled study of high-dose tirilazad mesylate in women with aneurysmal subarachnoid hemorrhage.

Kruyt ND. Diringer MN. Effect of hypervolemic therapy on cerebral blood flow after subarachnoid hemorrhage: a randomized controlled trial.bmj. et al. Use 43 of this content is subject to our disclaimer. Risk factors for fever in the neurologic intensive care unit. Effect of acute physiologic derangements on outcome after subarachnoid hemorrhage. et al.Subarachnoid haemorrhage References 182. Hyperglycemia. Kuhmonen J. J Am Soc Echocardiogr. Deibert E. Abstract 189. Neurology. 2004. Wilmer A. Stroke. Van den Berghe G. 2004. Abstract 187.com . Mayer SA. © BMJ Publishing Group Ltd 2016. Stroke. Kreiter KT. Claassen J.102:998-1003. Vu A. Hindman BJ. Heart. 2006. 2005. Crit Care Med.31:383-391.61:1132-1133. et al. Hyperglycemia and clinical outcome in aneurysmal subarachnoid hemorrhage: a meta-analysis. Intensive insulin therapy in the medical ICU. Reversible left ventricular dysfunction associated with raised troponin I after subarachnoid haemorrhage does not preclude successful heart transplantation. et al. Fink ME. Dorhout Mees SM. Glucose levels and outcome after subarachnoid hemorrhage. Abstract 184. IHAST Investigators. Juvela S. et al. Full text Abstract 190. 2009.60:837-841. 2005.40:e424-430. Abstract 188. et al. Perioperative fever and outcome in surgical patients with aneurysmal subarachnoid hemorrhage. Algra A. 2016. Reaven NL. Elevated body temperature independently contributes to increased length of stay in neurologic intensive care unit patients. Neurology. 2003. All rights reserved. Abstract REFERENCES 183.84:205-207.18:168-174. 2009. Clarke WR. Tung P. 2000. de Haan RJ. 2000. van Dijk GW. J Neurosurg. et al. Diringer MN. and history of hypertension as risk factors for poor outcome and cerebral infarction after aneurysmal subarachnoid hemorrhage. Abstract 192.32:1489-1495. Abstract This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. N Engl J Med. Lennihan L. Abstract 186. Neurosurgery. . Commichau C. Age and aneurysm position predict patterns of left ventricular dysfunction after subarachnoid hemorrhage. Abstract 191.354:449-461.64:897-908. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. Abstract 185. Siironen J. Crit Care Med. Todd MM.32:832-838. Aiyagari V. Funk SE. Mayer SA. excess weight. Khush K. Biessels GJ. 2003. et al. Kopelnik A. Scarmeas N. Hermans G.

used with permission IMAGES Figure 2: CT brain showing subarachnoid haemorrhage from a ruptured posterior cerebral artery aneurysm (2 of 2) Courtesy of Dr Salah Keyrouz. Subarachnoid haemorrhage Images Images Figure 1: CT brain showing subarachnoid haemorrhage from a ruptured posterior cerebral artery aneurysm (1 of 2) Courtesy of Dr Salah Keyrouz. used with permission This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.bmj. © BMJ Publishing Group Ltd 2016. 44 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.com . . 2016. All rights reserved. Use of this content is subject to our disclaimer.

used with permission This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. Use 45 of this content is subject to our disclaimer. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice.com .Subarachnoid haemorrhage Images IMAGES Figure 3: Communicating hydrocephalus in the setting of subarachnoid haemorrhage. used with permission Figure 4: Severe vasospasm of distal left internal carotid artery and proximal middle and anterior cerebral arteries before (A) and after (B) intra-arterial infusion of nicardipine and transluminal balloon angioplasty Courtesy of Dr Salah Keyrouz.bmj. note dilatation of fourth and temporal horns of lateral ventricles Courtesy of Dr Salah Keyrouz. . © BMJ Publishing Group Ltd 2016. 2016. All rights reserved.

46 BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. All rights reserved. 2016. Subarachnoid haemorrhage Images Figure 5: Distal left vertebral and basilar arteries spasm before (left) and after (right) intra-arterial Infusion of nicardipine Courtesy of Dr Salah Keyrouz.com . Use of this content is subject to our disclaimer. note peaked.bmj. used with permission IMAGES Figure 6: Left frontal infarct (arrows) in a patient with subarachnoid haemorrhage-related vasospasm Courtesy of Dr Salah Keyrouz. tall T waves (1 of 2) This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08. © BMJ Publishing Group Ltd 2016. used with permission Figure 7: ECG done on admission of a patient with subarachnoid haemorrhage. .

used with permission This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Aug 08.com . note normalisation of T waves (2 of 2) IMAGES Courtesy of Dr Salah Keyrouz. BMJ Best Practice topics are regularly updated and the most recent version of the topics can be found on bestpractice. 24 hours later.Subarachnoid haemorrhage Images Courtesy of Dr Salah Keyrouz.bmj. All rights reserved. © BMJ Publishing Group Ltd 2016. Use 47 of this content is subject to our disclaimer. . used with permission Figure 8: Same patient. 2016.

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FRCP Consultant Neurologist Addenbrookes Hospital. MA. MD. UK DISCLOSURES: PM declares that he has no competing interests. a previous contributor to this monograph. IL DISCLOSURES: VA declares that he has no competing interests. PhD Aggregate Professor of Neurosurgery Neurosurgical Clinic . Peter Martin. MO DISCLOSURES: SK is an author of a reference cited in this monograph. // Peer Reviewers: Venkatesh Aiyagari. MD Associate Professor Department of Neurology and Rehabilitation. Diringer. Palermo. Chicago. MD..D. Giovanni Grasso. Department of Clinical Neuroscience . Louis. University of Illinois at Chicago. Cambridge. St. BM BCh. University of Palermo. M. Italy DISCLOSURES: GG declares that he has no competing interests. Washington University School of Medicine. DISCLOSURES: MND is an author of a number of references cited in this monograph. . // Acknowledgements: Dr Salah Keyrouz would like to gratefully acknowledge Dr Michael N.Contributors: // Authors: Salah Keyrouz. FAHA Associate Professor Neurology and Neurosurgery.