Disclosure
Background: Subarachnoid hemorrhage (SAH) 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 SAH are head trauma and rupture of an intracranial aneurysm. Atraumatic SAH accompanied by sudden onset of neurologic symptoms has been termed hemorrhagic stroke. Radiologic evaluation is essential in determining the prognosis and treatment of SAH. Radiologic interventional procedures have an increasingly important role in the management of this condition. For excellent patient education resources, visit eMedicine's Brain and Nervous System Center and Stroke Center. Also, see eMedicine's patient education articles Aneurysm, Brain; Stroke; and Spinal Tap. Pathophysiology: Three layers of meninges surround the brain and spinal cord: the pia mater, the arachnoid, and dura mater. The subarachnoid space exists between the pia mater and arachnoid. It is normally filled with clear, colorless CSF and 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, decreasing cerebral perfusion and often results in a transient loss of consciousness. Delayed effects of SAH include vasospasm, which can lead to brain infarctions and communicating hydrocephalus.
Causes of SAH
Common causes of SAH include the following:
Less frequent causes of SAH include the following:
Rupture of a saccular intracranial aneurysm causes approximately 80% of nontraumatic SAH. 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 of pathogenesis include underlying congenital weakness in the arterial wall, degenerative weakening in the arterial wall from atherosclerosis, and stress of arterial pulsations on the arterial wall at turning or branching points. It is likely that a combination of these factors are involved in the formation of intracranial aneurysms.
Other problems to consider
Traumatic SAH must be distinguished from spontaneous SAH. 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. Frequently, this question arises: "Did this patient lose consciousness while driving because of spontaneous SAH and subsequently crash his car, or did the patient sustain head injury from the motor vehicle accident causing traumatic SAH?" 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. Frequency: Mortality/Morbidity:
Race: In the US, no racial differences exist in SAH rate or aneurysm prevalence. No studies have demonstrated racial differences within a given geographic population. A multinational study sponsored by the World Health Organization has demonstrated a relatively lower incidence of SAH in China in comparison to Europe and Scandinavia. The lower incidence of SAH in China may reflect a lower incidence of reporting this disease.
Sex: Epidemiologic studies have found sex differences in SAH rates in certain populations. However, these sex differences are not clinically useful with regard to screening or diagnosis.
Age: From age 25 years to age 64 years, the incidence of nontraumatic SAH increases with age in a linear relationship.
Anatomy: 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. Clinical Details: Headache is the most common complaint in patients presenting with nontraumatic SAH. Headache is also one of the most common symptoms reported by all patients seeking medical attention. Severe headache with abrupt onset that reaches maximal intensity within seconds is particularly suggestive of SAH. 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.
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 their lives 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.
Of all lumbar spinal taps, 20% are traumatic. It is important to distinguish between a traumatic tap and bloody cerebrospinal fluid from subarachnoid hemorrhage. Subarachnoid hemorrhage frequently is accompanied by xanthochromia. In traumatic tap, it may be possible to obtain clear fluid from a second puncture at a higher level in the spine. Preferred Examination: CT scanning without intravenous contrast enhancement is the preferred first diagnostic study, with cerebral angiography the next procedure of choice.
Advances are being made in the noninvasive vascular imaging modalities of CT angiography and magnetic resonance (MR) angiography. At centers with a high degree of expertise and experience, these noninvasive imaging technologies may replace or be used in addition to catheter angiography.
At most institutions in the US, conventional angiography remains the standard in the evaluation of patients with SAH. If a strong clinical suggestion of SAH exists and if the CT brain scan is negative, a CSF tap may be of value to confirm this diagnosis. If the CSF reveals no evidence of SAH, either overt hemorrhage or xanthochromia, cerebral angiography may not be indicated. Limitations of Techniques: Nonenhanced CT scanning may fail to depict small SAH, particularly if imaging is performed several days after the onset of bleeding. Furthermore, CT scans are degraded by patient motion, and if the 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.
Brain, Aneurysm
The most common underlying causes of SAH are listed in Pathophysiology above.
Findings: Plain radiographs of the skull and orbits may be used to exclude the presence of an aneurysm clip or intraorbital foreign body in an unresponsive or unreliable patient on whom it is necessary to perform MRI. Plain radiographs also may be useful in evaluating for facial or cervical spinal fractures to assess the probability of traumatic SAH versus spontaneous SAH. Some neuroradiologists use skull radiographs in their routine follow-up care of patients with aneurysm treated with coil embolization. Interval follow-up skull radiographs can be compared with baseline studies to check for coil compaction. Degree of Confidence: The degree of confidence is high for the purposes stated above. Plain radiography offers no reliable findings for detecting SAH. False Positives/Negatives: Guglielmi detachable coils (GDCs) have been observed to shift in position during the subsequent thrombosis of large- and medium-sized aneurysms. This finding does not necessarily mean that the aneurysm is patent. Cerebral angiography should be performed when any change in coil position is observed on postembolization follow-up studies. |
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Findings: On CT scans, SAH appears as a high-attenuating, amorphous substance that fills the normally dark CSF-filled subarachnoid spaces around the brain. The normally black subarachnoid cisterns and sulci may appear white in acute hemorrhage. These findings are most evident in the largest subarachnoid spaces, such as the suprasellar cistern and Sylvian fissures. Over the cerebral hemispheres, SAH is exhibited by the filling in of the normally low-attenuation (black) sulci with high-attenuating (white) subarachnoid blood. SAH is most conspicuous within 2-3 days of the onset of acute bleeding. Acute SAH is typically 50-60 HU. The protein content of the hemoglobin molecule is predominantly responsible for the attenuating effect of blood. Therefore, the absolute measurement in Hounsfield units varies somewhat with the hematocrit value. When CT scanning is performed several days to weeks after the initial bleed, the findings are more subtle. The initial high-attenuation of blood and clot tend to decrease, and these appear as intermediate gray. These findings can be isointense relative to normal brain parenchyma. If the patient presents during this subacute period, evidence of SAH includes (1) decreased visualization of the normally hypoattenuating fluid within the sulci and (2) basal cisterns and enlargement of the ventricles because of communicating hydrocephalus. In addition to detecting SAH, CT is useful in localizing the source of bleeding. This is particularly important in the patient with multiple intracranial aneurysms, which occur in 20% of patients. Localization of SAH on CT correlates with the location of the ruptured aneurysm. The presence of blood in the anterior interhemispheric fissure or the adjacent frontal lobe suggests rupture of an anterior communicating artery aneurysm. Sylvian fissure clot correlates with ipsilateral middle cerebral artery aneurysm. Blood predominantly localized to the posterior fossa suggests bleeding from a posterior circulation aneurysm. The ability to discern the location of aneurysm rupture is limited by the fact that many patients with SAH have a diffuse distribution of blood in the subarachnoid spaces and basal cisterns on CT. The effect of gravity has been suggested as a possible cause for misleading patterns of blood distribution. Published studies report a wide variation in the accuracy of CT in localizing the bleeding source. In addition to the diagnosis of SAH and the localization of the bleeding site, CT also allows some degree of prognostication, particularly in the probability of development of vasospasm. In 1980, Fisher originally demonstrated that the amount of blood and the presence of localized clots in the subarachnoid space is correlates with a higher incidence of delayed symptomatic arterial spasm; this correlation has since been well validated. A specialized CT technique involving inhalation of xenon gas allows quantitative determination of regional cerebral blood flow, which can be of value in monitoring the severity and effect of cerebral vasospasm. Degree of Confidence: Nonenhanced brain CT is the study of choice in the initial evaluation of patients with potential SAH. The sensitivity is 93-100% in patients presenting with SAH within 24 hours of symptom onset. Conversely, the detection of SAH on CT has a 0-7% false-negative rate during this period. As the time from the onset of the bleeding episode increases, the sensitivity of CT decreases. At 5 days, the sensitivity is approximately 85%, and at 1 week, it is approximately 50%. If a high clinical concern for SAH exists and if the CT brain scan is negative, lumbar puncture (LP) is indicated. Although LP is considered to have a higher sensitivity than that of CT, its specificity is lower, and LP is an invasive procedure. False Positives/Negatives: Various normally attenuating extra-axial structures may be misinterpreted as SAH, and these can lead to false-positive results. The falx cerebri, tentorium cerebelli, and intracranial blood can be confused for small amounts of SAH. Streak artifact from bone at the skull base and partial volume-averaging artifact also may lead to the false diagnosis of SAH. False-negative studies may occur from errors in interpretation or from failure of the technology itself. Perceptual errors aside, several conditions may lead to the inability of SAH to be detected on CT. An interval of days to weeks between the bleeding episode and the CT allows for the breakdown and resorption of some or all of the hemoglobin from the subarachnoid space, decreasing the contrast between the SAH and CSF. Similarly, small amounts of SAH may be masked by dilution by CSF and/or CT volume averaging with CSF. Motion artifact occurring in scans of agitated or confused patients can lead to either false-positive or false-negative SAH diagnosis.
Findings: Fluid-attenuated inversion recovery (FLAIR) is the most sensitive MRI pulse sequence for the detection of SAH. However, some studies have demonstrated false-positive rates as high as 30% with the use of this sequence. On FLAIR images, SAH appears as high-intensity signal (white) in normally low signal (black) CSF spaces. FLAIR is similar to CT in its findings in SAH. T2- and T2*-weighted images can potentially demonstrate SAH as low signal intensity in normally high-signal subarachnoid spaces. On T1-weighted images, acute SAH may appear as intermediate- or high-intensity signal in the subarachnoid space. MR angiography may be useful in the evaluation of aneurysms and other vascular lesions that cause SAH. The low sensitivity for aneurysms smaller than 5 mm, the inability to evaluate small aneurysm contour irregularities, and difficulty in obtaining high-quality images in patients who are agitated or confused limits the utility of MR in the diagnosis of acute SAH. Degree of Confidence: MRI and magnetic resonance angiography (MRA) are not as sensitive or specific as CT and conventional angiography in the evaluation of patients with SAH. However, in patients with equivocal findings on CT or angiography or in those patients who cannot undergo CT or conventional angiography, MRI and/or MRA may provide clinically useful information. False Positives/Negatives: Magnetic field inhomogeneity can lead to artifactual increase in signal intensity in sulci over the cerebral convexities on FLAIR images mimicking SAH. CSF flow artifacts can mimic the appearance of SAH on either T1- or T2-weighted images. Intracranial thrombus can appear similar in signal to flowing blood on time of flight gradient echo MRA. In uncooperative patients, motion artifact may produce images leading either to false-positive or false-negative interpretations.
Findings: Echoencephalography is useful in the diagnosis of germinal matrix and intraventricular hemorrhage in the newborn; however, ultrasound has no direct role in the diagnosis of SAH in the adult patient. Conversely, transcranial Doppler has become increasingly used in the diagnosis and management of vasospasm in patients with SAH. Serial transcranial Doppler examinations accurately detect the presence of vasospasm and allow maximization of medical therapy for vasospasm before the patient becomes symptomatic. Flow velocity increases correspond to cross-sectional diameter decrease in vessel lumen from vasospasm. The more severe the vasospasm, the higher the flow velocity. Flow is most easily measured for the middle cerebral arteries, which have been found to have flow velocities normally in the 30- to 80-cm/s range. Elevation to 120 cm/s indicates moderate vasospasm, and elevation to 200 cm/s, severe vasospasm. Single abnormal measurements are much less reliable then serial examinations performed to allow the establishment of patient baseline velocities prior to the development of vasospasm. Degree of Confidence: The sensitivity of transcranial Doppler imaging for the detection of vasospasm has been reported to be 85-90%. Because not all vasospasm is necessarily symptomatic, the finding must be correlated with clinical neurologic examination to determine the appropriate therapy. False Positives/Negatives: Elevated intracranial vascular flow from an AVM or fistula may cause high flow velocities in the absence of vasospasm. Similarly, elevation of cardiac output from any cause generally leads to systemic increase in flow velocities. Doppler measurements are highly dependent on technical factors. Inaccuracy in the angle of insonation may result in artifactual elevation or reduction in the reported velocity measurements.
Findings: Like sonography, nuclear medicine studies are not useful in the initial diagnosis of SAH, but they can play a role in the diagnosis of related vasospasm. The nuclear medicine technique studied most for this purpose is single-photon emission computed tomography (SPECT) using the radiopharmaceutical technetium-99m hexamethylpropyleneamine oxime (HMPAO). SPECT allows evaluation of qualitative or semiquantitative regional blood flow. The information provided is complementary to the transcranial Doppler findings. SPECT demonstrates perfusion of the brain tissue, whereas transcranial Doppler sonography provides information about the flow in medium and large intracranial arteries. These 2 datasets are independent variables. Perfusion of brain tissue can be maintained through collateral circulation and autoregulation despite severe vasospasm in a proximal artery. Conversely, perfusion can be persistently diminished in areas of infarction or small vessel ischemia despite successful angioplasty of a proximal intracranial artery. Degree of Confidence: The results of 99mTc HMPAO SPECT are semiquantitative and qualitative in that the cerebellum is generally considered as a control value for normal perfusion. Generalized cerebral hypoperfusion may go unrecognized but this pattern is not typical of vasospasm. Since early vasospasm is frequently asymptomatic, correlation with serial clinical examination is crucial to establish appropriate therapy. Clinical use of this study is hampered by the qualitative nature of the results. Absolute negative results are uncommon, and positive results may not be clinically relevant. False Positives/Negatives: Space-occupying lesions such as cerebral hematoma cause perfusion defects on SPECT perfusion imaging. These should be obvious from correlation with conventional CT images. Hydrocephalus can lead to global decrease in cerebral perfusion, which could go unrecognized because of the lack of absolute quantification of cerebral blood flow.
Findings: Cerebral angiography is considered the standard for the detection of intracranial aneurysms and arteriovenous malformations and fistulae. Aneurysms are detected as focal areas of outpouching or dilatation of the arterial wall. These frequently occur at arterial branching points in characteristic locations within or near the circle of Willis. Cerebral angiography should include anteroposterior (AP), lateral, and one or more oblique views of both carotid and vertebral artery contrast injection studies. A submentovertical view is sometimes useful in demonstrating the neck of a middle cerebral artery bifurcation aneurysm or anterior communicating artery aneurysm. Compression of the contralateral carotid artery should be performed during carotid cerebral angiogram to demonstrate the anterior communicating artery if it does not fill spontaneously during one of the internal carotid artery injections. Carotid artery compression should be done on a segment of the common carotid artery without atherosclerotic plaque, if possible. One vertebral arteriogram is occasionally omitted by some angiographers if there is abundant reflux proximal to the origin of the posterior inferior cerebellar artery of that vertebral artery when the contralateral vertebral artery is injected with contrast medium. However, this technique does not depict all aneurysms. The most reliable method of aneurysm detection is the invariable selective injection of contrast medium into both common or internal carotid arteries and both vertebral arteries. Cerebral angiography reliably demonstrates the presence or absence of an intracranial aneurysm or arterial venous malformation and establishes the number and locations of aneurysms. Morphologic information, such as aneurysm size and shape, helps to determine which aneurysm has bled in a patient with multiple aneurysms. Specifically, the presence of a lobulation, tit, or a daughter aneurysm is highly suggestive that the aneurysm is the one that has bled. In the absence of any distinguishing aneurysm shape features or hemorrhage localization by the CT scan, the largest aneurysm is the most likely to have bled. Features such as aneurysm location, shape, neck size, and neck-to-maximal diameter ratio are crucial in determining whether the aneurysm is better treated with open craniotomy or by an endovascular technique. Degree of Confidence: Cerebral angiography provides a high degree of accuracy and is generally considered the standard for the diagnosis of intracranial aneurysm. A small false-negative rate does occur, probably in the range of 1-2%. A repeat cerebral arteriogram in 10-14 days is indicated if the initial angiogram does not demonstrate a cause of the SAH. In a small number of patients, a follow-up angiogram will detect an aneurysm that was not demonstrated on the initial study. Bilateral selective external and internal carotid artery angiograms can be performed to exclude a dural arteriovenous fistula, a rare cause of SAH. Bilateral vertebral arteriograms of the neck (and if necessary, selective thyrocervical trunk and/or careful injections of the right superior intercostal artery) demonstrate the arterial and venous circulation of the cervical spinal cord. In rare cases, they show a spinal vascular malformation or neoplasm, such as hemangioblastoma, as the cause of SAH. Cervical spinal MRI and/or MRA may indicate the necessity of such additional arteriographic study. If thorough arteriographic studies do not demonstrate a specific cause for the SAH, a presumptive diagnosis of idiopathic perimesencephalic hemorrhage is sometimes made. False Positives/Negatives: The reason that some aneurysms are not initially diagnosed and detected only on a subsequent follow-up angiogram is not always evident. Vasospasm is believed to be the most common cause. Arteriographic double densities simulating aneurysm or apparent areas of vessel wall bulge or outpouching may be caused by arterial tortuosity and atherosclerosis or overlap of adjacent arteries on standard angiogram views. This can usually be determined by comparing all angiographic views and, if necessary, obtaining additional oblique arteriographic views.
Intervention: The endovascular treatment of intracranial aneurysms has evolved rapidly during the past decade. 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 GDC by the US Food and Drug Administration, the emphasis of endovascular management has changed to aneurysm occlusion with the preservation of patency of the parent. 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 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 SAH-induced vasospasm. In general, intracranial angioplasty may be performed in the internal carotid, proximal middle or anterior cerebral, vertebral and basilar arteries. Selective intra-arterial papaverine infusion has also been used in the treatment of intracranial vasospasm. Medical/Legal Pitfalls:
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