eMedicine Specialties > Neurosurgery > Vascular

Subarachnoid Hemorrhage: Workup

Author: Jennifer Oman, MD, Associate Clinical Professor, Department of Emergency Medicine, University of California at Irvine
Coauthor(s): Sean David Lavine, MD, Assistant Professor of Neurosurgery and Radiology, Columbia College of Physicians and Surgeons; Adjunct Assistant Professor of Radiology and Neurological Surgery, Weill Medical College of Cornell University; Clinical Director, Neuroendovascular Services, New York Presbyterian Hospital, Columbia Presbyterian Medical Center
Contributor Information and Disclosures

Updated: Aug 3, 2009

Workup

Laboratory Studies

  • CBC count - For evaluation of possible infection or hematologic abnormality
  • Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - For evaluation of possible coagulopathy
  • Serum electrolytes - To establish a baseline for detection of future complications
  • Blood type and screen - In case intraoperative transfusion is required or in the setting of massive hemorrhage
  • Cardiac enzymes - For evaluation of possible myocardial ischemia
  • Arterial blood gas (ABG) - Assessment is necessary in cases with pulmonary compromise

Imaging Studies

  • CT scan: The diagnosis of SAH usually depends on a high index of clinical suspicion combined with radiographic confirmation via CT scan without contrast. The sensitivity decreases with respect to increased time from ictus and decreased scanner resolution (older CT scanners). CT scan has a sensitivity of 98% within the first 12 hours of the ictus and 93% within 24 hours; sensitivity decreases to approximately 80% at 72 hours and 50% at 1 week. CT scan findings are positive in 92% of patients who have SAH. Sensitivity is less on older second- or first-generation scanners. Most North American hospitals have been using third-generation scanners since the mid 1980s.


CT scan reveals subarachnoid hemorrhage in the ri...

CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of hydrocephalus is apparent.

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CT scan reveals subarachnoid hemorrhage in the ri...

CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of hydrocephalus is apparent.

    • Thin (3 mm) cuts are necessary to properly identify the presence of smaller hemorrhages.
    • CT scan findings may be falsely negative in patients with small hemorrhages and in patients with severe anemia.
    • The location of blood within the subarachnoid space correlates directly with the location of the aneurysm in 70% of cases. In general, blood localized to the basal cisterns, the sylvian fissure, or the intrahemispheric fissure indicates rupture of a saccular aneurysm. Blood found lying over the convexities or within the superficial parenchyma of the brain often is indicative of AVM or mycotic aneurysm rupture.
    • Anterior communicating artery aneurysms often are associated with interhemispheric and intraventricular hemorrhages. Middle communicating artery and posterior communicating artery aneurysms are associated with intraparenchymal hemorrhages.
    • CT scan allows for the detection of ventricular size and, thus, evaluation and surveillance of mass effect and hydrocephalus.
    • A contrast-enhanced CT scan may reveal an AVM; however, this study should not be performed before a noncontrast CT scan because the contrast may interfere with the visualization of subarachnoid blood.
  • After the diagnosis of SAH, further imaging should be performed to characterize the source of the hemorrhage. This effort can include standard angiography, CT angiography, and magnetic resonance (MR) angiography. If the diagnosis of SAH is yet unclear, lumbar puncture (LP) should be performed (see Diagnostic Procedures).
  • Cerebral angiography is particularly useful in cases of diagnostic uncertainty (after CT scan and LP) and in patients with septic endocarditis and SAH to search for the presence of mycotic aneurysms.
    • In cases where the diagnosis of SAH has been determined, the timing of cerebral angiography will depend on surgical considerations. Cerebral angiography can provide the following important surgical information in the setting of SAH:
      • Cerebrovascular anatomy
      • Aneurysm location and source of bleeding
      • Aneurysm size and shape, as well as orientation of the aneurysm dome and neck
      • Relation of the aneurysm to the parent artery and perforating arteries
      • Presence of multiple or mirror aneurysms (identically placed aneurysms in both the left and right circulations)
    • A trial balloon occlusion of the parent artery can be performed and may help to guide preoperative surgical planning. If cerebral angiography findings are negative (10-20%) a repeat test should be performed 3-4 weeks later. Patients with SAH and a negative finding on cerebral angiography may have an improved prognosis. A negative study finding can result from aneurysm obliteration secondary to clotting. Hemorrhage secondary to a ruptured AVM or spinal cord aneurysm may be present despite a negative finding on cerebral angiogram. Perimesencephalic venous hemorrhage also should be considered.
    • Follow-up angiogram also is useful postsurgically to detect the presence of aneurysmal obliteration and to evaluate for possible cerebral vasospasm.
    • The management of moribund patients with CT scan evidence of a large SAH and focal hematoma is controversial.
    • Performing angiography may result in a life-threatening delay in treatment.
  • Infusion CT scan and CT angiography: Some centers have obtained good results with infusion CT scanning. This scan employs a contrast dye and can be performed immediately after a noncontrast CT scan. Reformatted image data can be viewed and rotated in 2-dimensional displays. Infusion CT scanning has been reported to detect aneurysms larger than 3 mm with a sensitivity of 97%, which may provide sufficient anatomic detail to allow for surgical management in the absence of angiography.
  • MRI: This is not sensitive for SAH within the first 48 hours. MRI is a useful tool to diagnose AVMs that are not detected by cerebral angiography or spinal AVMs causing SAH. It can be useful for diagnosing and monitoring unruptured cerebral aneurysms. MRI can detect aneurysms 5 mm or larger with a high sensitivity and is useful for monitoring the status of small, unruptured aneurysms. MRI can be used to evaluate the degree of intramural thrombus in giant aneurysms.
  • Magnetic resonance angiography (MRA): The role of MRA in the detection of SAH currently is under investigation; however, many authors believe that MRA eventually will replace conventional transfemoral cerebral angiography. Given the current limitations of MRA (eg, failure to detect posterior inferior communicating artery and anterior communicating artery aneurysms in one series) most authors feel that the risk/benefit ratio still favors conventional angiography.
  • Transcranial Doppler studies are useful in the detection and monitoring of arterial vasospasm.
  • Chest radiograph: All patients with SAH should have a baseline chest radiograph to serve as a reference point for evaluation of possible pulmonary complications.
  • Evaluation of ventricular wall motion via echocardiogram may be necessary in cases with suspected myocardial ischemia.

Other Tests

  • All patients with SAH should have an ECG on admission. Changes noted on ECG are attributed to myocardial ischemia and/or infarction caused by high levels of circulating catecholamines. Myocardial ischemia/infarction is present in 20% of SAH cases. Electrocardiogram abnormalities frequently detected in patients with SAH include the following:
    • Nonspecific ST and T wave changes
    • Decreased PR intervals
    • Increased QRS intervals
    • Increased QT intervals
    • Presence of U waves
    • Dysrhythmias, including premature ventricular contractions (PVCs), supraventricular tachycardia (SVT), and bradyarrhythmias
  • Anticoagulation and thrombolytic therapy are contraindicated in cases of suspected SAH.

Diagnostic Procedures

  • LP should be performed when strong clinical suspicion of SAH exists with a negative finding on CT scan or when a CT scan is not available.
    • If possible, a CT scan should be performed before LP to exclude significant intracranial mass effect, elevated ICP, obstructive hydrocephalus, or obvious intracranial bleed. LP findings often are negative within 2 hours of the ictus, and LP is most sensitive 12 hours after the bleed.
    • No consensus is found in the literature on the lower limit of RBCs in the CSF, which signifies a positive tap. However, most counts range from a few hundred to a million or more cells per cubic millimeter.
    • LP should not be performed if the CT scan demonstrates an SAH because of the (small) risk of further intracranial bleeding associated with a drop in ICP.
    • SAH often can be distinguished from traumatic LP by comparing the red blood cell count of the first and last tubes of CSF. The RBC count usually will not decrease between the first and last tubes in the setting of SAH; however, case reports of this phenomenon do exist.
    • The most reliable method of differentiating SAH from a traumatic tap is to spin down the CSF and examine the supernatant fluid for the presence of xanthochromia, a pink or yellow coloration of the CSF supernatant caused by the breakdown of RBCs and subsequent release of heme pigments.
    • Spectrophotometry is much more sensitive than the naked eye in detecting xanthochromia. Xanthochromia typically will not appear until 2-4 hours after the ictus. In nearly 100% of patients with an SAH, xanthochromia is present 12 hours after the bleed and remains for approximately 2 weeks. Xanthochromia is present 3 weeks after the bleed in 70% of patients, and it is still detectable at 4 weeks in 40% of patients.
  • D-dimer assay: Some authors have suggested that the D-dimer assay can be used to discriminate SAH from traumatic LP; however, results have been conflicting, and further data are needed. Spinal fluid samples taken within 24 hours of the ictus usually show a WBC-to-RBC ratio that is consistent with the normal circulating WBC-to-RBC ratio of approximately 1:1000. After 24 hours, CSF samples may demonstrate a polymorphonuclear and mononuclear polycytosis secondary to chemical meningitis caused by the degradation products of subarachnoid blood.

More on Subarachnoid Hemorrhage

Overview: Subarachnoid Hemorrhage
Workup: Subarachnoid Hemorrhage
Treatment: Subarachnoid Hemorrhage
Follow-up: Subarachnoid Hemorrhage
Multimedia: Subarachnoid Hemorrhage
References
Further Reading
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Further Reading

Clinical guidelines

Acute stroke management. Management of subarachnoid and intracerebral hemorrhage. In: Canadian best practice recommendations for stroke care: 2006. Ottawa (ON): Canadian Stroke Network, Heart & Stroke Foundation of Canada; 2006. p. 61-3.

Edlow JA, Panagos PD, Godwin SA, Thomas TL, Decker WW, American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med 2008 Oct;52(4):407-36. 5

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Keywords

SAH, nontraumatic subarachnoid hemorrhage, nontraumatic SAH, extravasation of blood into the subarachnoid space between the pial and arachnoid membranes, spontaneous atraumatic intracranial hemorrhage, ruptured cerebral aneurysm, ruptured arteriovenous malformation

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Contributor Information and Disclosures

Author

Jennifer Oman, MD, Associate Clinical Professor, Department of Emergency Medicine, University of California at Irvine
Disclosure: Nothing to disclose.

Coauthor(s)

Sean David Lavine, MD, Assistant Professor of Neurosurgery and Radiology, Columbia College of Physicians and Surgeons; Adjunct Assistant Professor of Radiology and Neurological Surgery, Weill Medical College of Cornell University; Clinical Director, Neuroendovascular Services, New York Presbyterian Hospital, Columbia Presbyterian Medical Center
Sean David Lavine, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, and Neurosurgical Society of America
Disclosure: Nothing to disclose.

Medical Editor

Paul L Penar, MD, Professor, Department of Surgery, Division of Neurosurgery, University of Vermont School of Medicine
Paul L Penar, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, and Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.

 
 
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