eMedicine Specialties > Radiology > Brain/Spine

Subarachnoid Hemorrhage

Author: Abner Gershon, MD, Director of Interventional Neuroradiology, St Francis Hospital and Medical Center; Assistant Clinical Professor, Department of Radiology, University of Connecticut School of Medicine
Coauthor(s): Robert S Feld, MD, Consulting Staff, Department of Radiology, Radiology Associates of Hartford, PC, Saint Francis Hospital and Medical Center; Michael T Twohig, MD, Clinical Instructor, Yale University; Assistant Clinical Professor, University of Connecticut School of Medicine; President and Chief, Radiology Associates of Hartford, PC; Chair, Department of Radiology, Saint Francis Hospital and Medical Center
Contributor Information and Disclosures

Updated: May 21, 2009

Introduction

Background

Subarachnoid hemorrhage (SAH) is a condition in which there is bleeding into the subarachnoid space around the brain and spinal cord. This space is normally filled with clear, colorless cerebrospinal fluid (CSF). The most common causes of subarachnoid hemorrhage are head trauma and rupture of an intracranial aneurysm. Atraumatic subarachnoid hemorrhage accompanied by the sudden onset of neurologic symptoms has been termed hemorrhagic stroke. Radiologic evaluation is essential for determining the prognosis and treatment of subarachnoid hemorrhage. Radiologic interventional procedures have become increasingly important for the management of this condition.

Subarachnoid hemorrhage (SAH). A nonenhanced CT s...

Subarachnoid hemorrhage (SAH). A nonenhanced CT scan of the brain that demonstrates an extensive SAH filling the basilar cisterns in a patient with a ruptured intracranial aneurysm.

Subarachnoid hemorrhage (SAH). A nonenhanced CT s...

Subarachnoid hemorrhage (SAH). A nonenhanced CT scan of the brain that demonstrates an extensive SAH filling the basilar cisterns in a patient with a ruptured intracranial aneurysm.



An angiogram showing a bilobed aneurysm of a post...

An angiogram showing a bilobed aneurysm of a posteroinferior cerebellar artery immediately before rupturing.

An angiogram showing a bilobed aneurysm of a post...

An angiogram showing a bilobed aneurysm of a posteroinferior cerebellar artery immediately before rupturing.



An angiogram showing the onset of an aneurysmal r...

An angiogram showing the onset of an aneurysmal rupture, with extravasation of contrast material into the subarachnoid space from the anterosuperior aspect of a bilobed aneurysm in a posteroinferior cerebellar artery.

An angiogram showing the onset of an aneurysmal r...

An angiogram showing the onset of an aneurysmal rupture, with extravasation of contrast material into the subarachnoid space from the anterosuperior aspect of a bilobed aneurysm in a posteroinferior cerebellar artery.



A later-phase angiogram of a rupturing bilobed an...

A later-phase angiogram of a rupturing bilobed aneurysm of a posteroinferior cerebellar artery shows progressive opacification of the subarachnoid space in the posterior fossa.

A later-phase angiogram of a rupturing bilobed an...

A later-phase angiogram of a rupturing bilobed aneurysm of a posteroinferior cerebellar artery shows progressive opacification of the subarachnoid space in the posterior fossa.



A late angiogram demonstrating contrast medium fi...

A late angiogram demonstrating contrast medium filling the posterior fossa subarachnoid spaces, including the ambient, prepontine, and perimedullary cisterns.

A late angiogram demonstrating contrast medium fi...

A late angiogram demonstrating contrast medium filling the posterior fossa subarachnoid spaces, including the ambient, prepontine, and perimedullary cisterns.



A CT scan obtained after angiography of a rupturi...

A CT scan obtained after angiography of a rupturing bilobed aneurysm of the posteroanterior cerebellar artery (see Images 2-5 in Multimedia) showing a subarachnoid hemorrhage and contrast medium filling the right sylvian fissure, the interhemispheric fissure, and the lateral and third ventricles.

A CT scan obtained after angiography of a rupturi...

A CT scan obtained after angiography of a rupturing bilobed aneurysm of the posteroanterior cerebellar artery (see Images 2-5 in Multimedia) showing a subarachnoid hemorrhage and contrast medium filling the right sylvian fissure, the interhemispheric fissure, and the lateral and third ventricles.




In January 2009, the American Heart Association published recommendations for treatment of patients with aneurysmal SAH.1,2 They note the following:
  • Current standard of practice calls for microsurgical clipping or endovascular coiling of the aneurysm neck whenever possible.
  • Treatment morbidity is determined by various factors, including factors relating particularly to the patient, to the aneurysm itself, and to the institution performing the treatment.
  • More favorable outcomes are more likely in institutions that treat high volumes of patients with SAH, in institutions that offer endovascular services, and in selected patients whose aneurysms are coiled rather than clipped.
  • Optimal treatment requires availability of both experienced cerebrovascular surgeons and endovascular surgeons working in a collaborative effort to evaluate each case of SAH.

For excellent patient education resources, visit eMedicine's Brain and Nervous System Center and Stroke Center. Also, see eMedicine's patient education article Aneurysm, Brain.

Presentation

Demographics

Age

From ages 25-64 years, the incidence of nontraumatic subarachnoid hemorrhage increases in a linear relationship with age.

Sex

Epidemiologic studies have found gender differences in the incidence of subarachnoid hemorrhage in certain populations; however, these gender differences are not clinically useful with regard to screening or diagnosis.

  • In Sweden and Denmark, women were found to have a higher rate of subarachnoid hemorrhage; conversely, in Russia and Finland, men have been found to have a higher subarachnoid hemorrhage rate.3 At least 50% of the populations studied demonstrated no significant differences in subarachnoid hemorrhage rates between men and women.
  • In the United States, the overall prevalence of cerebral aneurysms is slightly higher in women than in men; however, in persons younger than 40 years, cerebral aneurysms are more common in men.4

Race

In the United States, no racial differences exist in the incidence of subarachnoid hemorrhage or the prevalence of aneurysms. No studies have demonstrated racial differences within a given geographic population. A multinational study sponsored by the World Health Organization (WHO) has demonstrated a relatively lower incidence of subarachnoid hemorrhage in China compared with Europe and Scandinavia. The lower incidence of subarachnoid hemorrhage in China may reflect a lower incidence of reporting of this disease.3

Frequency

In the United States, the incidence of nontraumatic subarachnoid hemorrhage in the general population is approximately 10 cases per 100,000 per year.3 Approximately 30,000 new cases of subarachnoid hemorrhage are diagnosed per year. Of these cases, 80% are caused by aneurysmal subarachnoid hemorrhage.5

Internationally, there is wide geographic and regional variation in the incidence of nontraumatic subarachnoid hemorrhage.6 At the low end of the spectrum, China has an annual subarachnoid hemorrhage rate of 2 cases per 100,000 population. Finland has the highest annual incidence, with 22.5 cases per 100,000 population. Between these extremes, the following annual subarachnoid hemorrhage cases (per 100,000 population) have been reported1,3 :

  • East Germany: 4.9
  • Yugoslavia: 6.1
  • Russia: 6.7
  • Italy: 7.6
  • Lithuania: 9.75
  • Sweden: 9.9
  • Poland: 10
  • Denmark: 10.55


Mortality

  • Approximately 10-30% of patients with subarachnoid hemorrhage die before reaching medical attention. For those reaching a hospital alive, mortality rates for nontraumatic subarachnoid hemorrhage have been reported in the 30-60% range. In-hospital mortality has been shown to be lower at facilities with interventional neuroradiology.7
  • Aneurysmal subarachnoid hemorrhage is associated with a poor prognosis. Only 30% of patients survive without major disability. Patient outcome is closely associated with neurologic status at the time of presentation8 ; however, even for patients presenting in good clinical condition, only 55% have good outcomes at 90 days.9
  • The prognosis varies with the etiology of the hemorrhage. Patients with benign perimesencephalic hemorrhage typically have excellent clinical outcomes. Subarachnoid hemorrhage secondary to bleeding from an arteriovenous malformation appears to be associated with a better prognosis than aneurysmal subarachnoid hemorrhage.10



Presentation and natural history

Three layers of meninges surround the brain and spinal cord; these are called the pia mater, the arachnoid, and the dura mater. The subarachnoid space exists between the pia mater and the arachnoid. It is normally filled with clear, colorless CSF, and it contains fine trabeculae of connective tissue. Distal to the cavernous sinus, the internal carotid arteries and branches are in this space. Hemorrhage into the subarachnoid space causes immediate elevation of intracranial pressure and decreasing cerebral perfusion, and it often results in a transient loss of consciousness. Delayed effects of subarachnoid hemorrhage include vasospasm, which can lead to brain infarctions and communicating hydrocephalus.9

Causes of subarachnoid hemorrhage

Common causes of subarachnoid hemorrhage include the following:

Less frequent causes of subarachnoid hemorrhage include the following:

Rupture of a saccular intracranial aneurysm causes approximately 80% of nontraumatic subarachnoid hemorrhage. Intracranial aneurysms develop predominantly at vessel bifurcation or branching points. Saccular aneurysms are acquired lesions that rarely present before the third decade of life. Theories for the pathogenesis of these aneurysms include underlying congenital weakness in the arterial wall, degenerative weakening in the arterial wall from atherosclerosis, and the stress of arterial pulsations on the arterial wall at turning or branching points. It is likely that a combination of these factors is involved in the formation of intracranial aneurysms.

Other problems to consider

Traumatic subarachnoid hemorrhage must be distinguished from spontaneous subarachnoid hemorrhage. Cerebral angiography may sometimes be avoided if it can be confidently established that the hemorrhage is caused by trauma. This distinction can be difficult to make because the traumatic event may not have been witnessed and the patient may be unable to provide a reliable history. There is often a question as to whether a spontaneous subarachnoid hemorrhage has caused a traumatic event or the trauma caused the hemorrhage. When in doubt, it is usually best to obtain a cerebral angiogram to exclude an underlying aneurysm or vascular malformation; such angiograms can sometimes be limited to the location of the hemorrhage, if no pathology is detected.

Most intracranial aneurysms occur at typical locations within or near the circle of Willis. The most common specific locations of intracranial aneurysms are at the middle cerebral artery bifurcation and along the anterior communicating artery. These 2 locations account for approximately 60% of all intracranial aneurysms.

Other common sites of aneurysm formation in the anterior circulation are at the origins of the posterior communicating and ophthalmic arteries. Approximately 10-20% of aneurysms arise from the vertebral and basilar arteries.

The tip of the basilar artery is the most common location of aneurysm formation in the posterior circulation. The origins of the posterior inferior cerebellar arteries also are common sites of aneurysm formation. AVMs occur throughout the brain without predisposition for a particular anatomic area.

Headache is the most common complaint in patients presenting with nontraumatic subarachnoid hemorrhage. Headache is also one of the most common symptoms reported by all patients seeking medical attention. Severe headache of an abrupt onset that reaches maximal intensity within seconds is particularly suggestive of subarachnoid hemorrhage. The classic description by the patient is, "It's the worst headache of my life." Nausea, vomiting, altered alertness, and altered level of consciousness are frequently associated symptoms.1,12

About 23-37% of subarachnoid hemorrhages are initially misdiagnosed because of the nonspecific nature of the clinical symptoms. Of patients who complain of "the worst headache of my life" and who have normal neurologic findings, 12% are ultimately found to have subarachnoid hemorrhage. If patients with neurologic symptoms are included, this number increases to 25%. About 1-4% of emergency department patients with headache are found to have subarachnoid hemorrhage. Headache is the most common symptom reported by patients to their primary care physicians.1

Twenty percent of all lumbar spinal taps are traumatic. It is important to distinguish between a traumatic tap and bloody cerebrospinal fluid from a subarachnoid hemorrhage. Subarachnoid hemorrhage is frequently accompanied by xanthochromia. In a traumatic tap, it may be possible to obtain clear fluid from a second puncture at a higher level in the spine.

Treatment

The endovascular treatment of intracranial aneurysms has evolved rapidly. The initial experience in the treatment of intracranial aneurysm with catheter-based techniques relied predominantly on parent-vessel occlusion by various mechanisms, including endovascular detachable balloons and coils. With widespread physician acceptance and approval of the Guglielmi detachable coil (GDC) by the US Food and Drug Administration (FDA), the emphasis of endovascular management has changed to aneurysm occlusion with the preservation of patency of the parent.13,14

Although the primary indication for GDC embolization of an intracranial aneurysm is for patients with surgically high-risk aneurysms, a growing body of evidence indicates that endovascular treatment should be considered as a primary option for aneurysm in certain anatomic locations. Specifically, patients with basilar tip aneurysms appear to have better outcomes with endovascular therapy than with open craniotomy and surgical aneurysm clipping. The technical expertise and experience of the local treating physicians may determine the optimal treatment for aneurysms at other locations.

Improvements in small-vessel angioplasty balloon catheters and promising initial therapeutic results have led to increased use of intracranial angioplasty for the treatment of subarachnoid hemorrhage–induced vasospasm. In general, intracranial angioplasty may be performed in the internal carotid, proximal middle or anterior cerebral, and vertebral and basilar arteries. Selective intra-arterial papaverine infusion has also been used in the treatment of intracranial vasospasm.1

Preferred Examination

Computed tomography (CT) scanning without intravenous contrast enhancement is the preferred initial diagnostic study, with cerebral angiography the next procedure of choice.1

Advances are being made in the noninvasive vascular imaging modalities of CT angiography and magnetic resonance angiography (MRA). At institutions with a high degree of expertise and experience, these noninvasive imaging technologies may be used in addition to or even replace catheter angiography.1

At most institutions in the United States, conventional angiography remains the standard for evaluating patients with subarachnoid hemorrhage (SAH). If a CT scan of the brain is negative and a strong clinical suggestion of SAH exists, a CSF tap may be of value for confirming this diagnosis. If the CSF reveals no evidence of SAH (ie, either overt hemorrhage or xanthochromia), cerebral angiography may not be indicated.

Limitations of Techniques

Nonenhanced CT scanning may fail to depict small subarachnoid hemorrhages (SAHs), particularly if imaging is performed several days after the onset of bleeding. Furthermore, CT scans are degraded by patient motion. If a patient cannot cooperate because of an alteration in mental status, sedation may be necessary to obtain satisfactory diagnostic images.

Cerebral angiography is an invasive procedure with a small but significant risk of complication. Without the use of a special hemostasis device, at least 6 hours of bed rest is required after the procedure to prevent bleeding at the puncture site. Additionally, because of its small false-negative rate for aneurysm, cerebral angiography must be repeated after 1-2 weeks to further improve its diagnostic sensitivity.

Differential Diagnoses

Brain, Aneurysm
Brain, Arteriovenous Malformation
Brain, Stroke

More on Subarachnoid Hemorrhage

Overview: Subarachnoid Hemorrhage
Imaging: Subarachnoid Hemorrhage
Follow-up: Subarachnoid Hemorrhage
Multimedia: Subarachnoid Hemorrhage
References
Further Reading

References

  1. Bederson JB, Connolly ES Jr, Batjer HH, Dacey RG, Dion JE, Diringer MN, et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage. A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Heart Association. Stroke. Jan 22 2009;[Medline].

  2. Bederson J B, Connolly E Jr, Batjer H H, MD, et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Heart Association. Stroke. 2009;40:994-1025. Available at http://stroke.ahajournals.org/cgi/content/full/40/3/994. Accessed May 21, 2009.

  3. Ingall T, Asplund K, Mahonen M. A multinational comparison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study. Stroke. May 2000;31(5):1054-61. [Medline].

  4. Laligam S, Heros R. Origin, growth, and rupture of saccular aneurysms: a review. Neurosurgery. 1981;8:248-60.

  5. Mayberg MR, Batjer HH, Dacey R. Guidelines for the management of aneurysmal subarachnoid hemorrhage. A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke. Nov 1994;25(11):2315-28. [Medline].

  6. Wiebers D. The International Study of Unruptured Intracranial Aneurysms Investigators: unruptured intracranial aneurysms—risk of rupture and risks of surgical intervention. N Engl J Med. 1998;339:1725-32.

  7. Johnston SC. Effect of endovascular services and hospital volume on cerebral aneurysm treatment outcomes. Stroke. Jan 2000;31(1):111-7. [Medline].

  8. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. 1968;28:14-20.

  9. Ayer RE, Zhang JH. The clinical significance of acute brain injury in subarachnoid hemorrhage and opportunity for intervention. Acta Neurochir Suppl. 2008;105:179-84. [Medline].

  10. Hirsch KG, Froehler MT, Huang J, Ziai WC. Occurrence of Perimesencephalic Subarachnoid Hemorrhage During Pregnancy. Neurocrit Care. Jan 30 2009;[Medline].

  11. Ro A, Kageyama N, Abe N, Takatsu A, Fukunaga T. Intracranial vertebral artery dissection resulting in fatal subarachnoid hemorrhage: clinical and histopathological investigations from a medicolegal perspective. J Neurosurg. Feb 6 2009;[Medline].

  12. Togha M, Sahraian MA, Khorram M, Khashayar P. Warning signs and symptoms of subarachnoid hemorrhage. South Med J. Jan 2009;102(1):21-4. [Medline].

  13. [Best Evidence] Macdonald RL, Kassell NF, Mayer S, Ruefenacht D, Schmiedek P, Weidauer S, et al. Clazosentan to overcome neurological ischemia and infarction occurring after subarachnoid hemorrhage (CONSCIOUS-1): randomized, double-blind, placebo-controlled phase 2 dose-finding trial. Stroke. Nov 2008;39(11):3015-21. [Medline].

  14. [Best Evidence] Kronvall E, Undrén P, Romner B, Säveland H, Cronqvist M, Nilsson OG. Nimodipine in aneurysmal subarachnoid hemorrhage: a randomized study of intravenous or peroral administration. J Neurosurg. Jan 2009;110(1):58-63. [Medline].

  15. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery. Jan 1980;6(1):1-9. [Medline].

  16. Latchaw RE, Silva P, Falcone SF. The role of CT following aneurysmal rupture. Neuroimaging Clin N Am. Nov 1997;7(4):693-708. [Medline].

  17. Yuzawa H, Higano S, Mugikura S, Umetsu A, Murata T, Nakagawa A. Pseudo-subarachnoid hemorrhage found in patients with postresuscitation encephalopathy: characteristics of CT findings and clinical importance. AJNR Am J Neuroradiol. Sep 2008;29(8):1544-9. [Medline].

  18. Stuckey SL, Goh TD, Heffernan T, Rowan D. Hyperintensity in the subarachnoid space on FLAIR MRI. AJR Am J Roentgenol. Oct 2007;189(4):913-21. [Medline].

  19. Morris JM, Miller GM. Increased signal in the subarachnoid space on fluid-attenuated inversion recovery imaging associated with the clearance dynamics of gadolinium chelate: a potential diagnostic pitfall. AJNR Am J Neuroradiol. Nov-Dec 2007;28(10):1964-7. [Medline].

  20. Rajendran JG, Lewis DH, Newell DW, Winn HR. Brain SPECT used to evaluate vasospasm after subarachnoid hemorrhage: correlation with angiography and transcranial Doppler. Clin Nucl Med. Feb 2001;26(2):125-30. [Medline].

  21. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med. Jan 6 2000;342(1):29-36. [Medline].

Further Reading

Related eMedicine topics

Subarachnoid Hemorrhage: Neurology

Subarachnoid Hemorrhage: Emergency Medicine

Subarachnoid Hemorrhage: Neurosurgery

Clinical guidelines

Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. American College of Emergency Physicians - Medical Specialty Society.  2008 Nov 25.  35 pages.  NGC:006720

Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. American College of Emergency Physicians - Medical Specialty Society.  2002 (revised 2008 Oct).  30 pages.  NGC:006719

Diagnosis and initial treatment of ischemic stroke. Institute for Clinical Systems Improvement - Private Nonprofit Organization.  2001 Oct (revised 2008 Jun).  57 pages.  NGC:006681

Guidelines for the early management of adults with ischemic stroke. A guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups. American Heart Association - Professional Association
American Stroke Association - Disease Specific Society.  2007 Apr 12.  58 pages.  NGC:005693

Clinical trials

Treating Patients With Aneurysmal SubArachnoid Hemorrhage (SAH) With Epoetin Alfa (EPO)

Treatment of Subarachnoid Hemorrhage With Human Albumin

Serial Echocardiography After Subarachnoid Hemorrhage (SEAS)

Hypothalamo-, Pituitary-, Adrenal Axis Dysfunction in Subarachnoid Hemorrhage (SAHENDO)

Evaluation of Cerebral Spinal Fluid and Blood in Patients With Subarachnoid Hemorrhage

Keywords

subarachnoid hemorrhage, brain stroke, head trauma, brain hemorrhage, hemorrhagic stroke, cerebral hemorrhage, SAH, intracranial hemorrhage, subarachnoid bleeding, subarachnoid space, intracranial aneurysms, benign perimesencephalic hemorrhage, nontraumatic SAH, traumatic SAH, aneurysmal SAH

Contributor Information and Disclosures

Author

Abner Gershon, MD, Director of Interventional Neuroradiology, St Francis Hospital and Medical Center; Assistant Clinical Professor, Department of Radiology, University of Connecticut School of Medicine
Abner Gershon, MD is a member of the following medical societies: American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology, and Connecticut State Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Robert S Feld, MD, Consulting Staff, Department of Radiology, Radiology Associates of Hartford, PC, Saint Francis Hospital and Medical Center
Disclosure: Nothing to disclose.

Michael T Twohig, MD, Clinical Instructor, Yale University; Assistant Clinical Professor, University of Connecticut School of Medicine; President and Chief, Radiology Associates of Hartford, PC; Chair, Department of Radiology, Saint Francis Hospital and Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Hugh J F Robertson, MD, DMR, FRCPC, FRCR, FACR, Professor Emeritus of Radiology, Professor of Clinical Radiology, Louisiana State University Health Sciences Center, New Orleans; Clinical Professor of Radiology, Tulane University School of Medicine; Active Staff, Department of Radiology, University Hospital
Hugh J F Robertson, MD, DMR, FRCPC, FRCR, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Neuroradiology, American Society of Spine Radiology, Louisiana State Medical Society, Orleans Parish Medical Society, Radiological Society of North America, Royal College of Physicians and Surgeons of Canada, Royal College of Radiologists, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

 
 
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