Subarachnoid Hemorrhage Workup

The diagnosis of subarachnoid hemorrhage (SAH) usually depends on a high index of clinical suspicion combined with radiologic confirmation via urgent computed tomography (CT) scan without contrast. Traditionally, a negative CT scan is followed with lumbar puncture (LP). However, noncontrast CT followed by CT angiography (CTA) of the brain can rule out SAH with greater than 99% sensitivity.^[1]

Compared with the traditional recommendation of CT followed by LP, CT/CTA may offer a less invasive and more informative diagnostic approach for emergency department patients complaining of acute-onset headache and with no significant risk factors for SAH. A disadvantage of foregoing LP is that spinal fluid analysis may point toward an alternative diagnosis.

After the diagnosis of SAH is established, 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.

Laboratory studies for SAH should include the following:

• Serum chemistry panel - To establish a baseline for detection of future complications
• Complete blood count - For evaluation of possible infection or hematologic abnormality
• Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - For evaluation of possible coagulopathy
• Blood typing/screening - To prepare for possible intraoperative transfusions
• Cardiac enzymes - For evaluation of possible myocardial ischemia
• Arterial blood gas (ABG) - Necessary in patients with pulmonary compromise

Serum cardiac troponin measurement is important in patients with subarachnoid hemorrhage, even in those without underlying cardiac conditions. It was initially thought to be useful only as a predictor for the occurrence of pulmonary and cardiac complications.^[11] However, correlation was subsequently found between troponin levels and neurologic complications and outcome.^[12]

All patients with SAH should have a baseline chest radiograph to serve as a reference point for evaluation of possible pulmonary complications. All patients with SAH should also have an electrocardiogram (ECG) on admission. Patients with SAH can have myocardial ischemia due to the increased level of circulating catecholamines or to autonomic stimulation from the brain. Myocardial infarction is a rare complication. However, suspicion of SAH is a contraindication to thrombolytic and anticoagulant therapy.

Because most of the ECG abnormalities that occur with SAH are benign and reversible, differentiating true myocardial ischemia from benign changes is important. Two-dimensional echocardiography often is more sensitive in detecting myocardial ischemia than is ECG and thus is useful in the setting of SAH.

Other imaging studies may be indicated. MRI is performed if no lesion is found on angiography, and transcranial Doppler studies are useful in the detection and monitoring of arterial vasospasm.

CT without contrast is the most sensitive imaging study in SAH (see the images below). When carried out within 6 hours of headache onset, CT has 100% sensitivity and specificity. Sensitivity is 93% within 24 hours of onset,^[13] 80% at 3 days, and 50% at 1 week.^[14] Sensitivity is less on older second- or first-generation scanners, but most North American hospitals have been using third-generation scanners since the mid 1980s. Thin (3 mm) cuts are necessary to properly identify the presence of smaller hemorrhages.

Findings may be negative in 10-15% of patients with SAH. A falsely negative CT scan can result from severe anemia or small-volume subarachnoid hemorrhage.

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 lying over the convexities or within the superficial parenchyma of the brain often is indicative of arteriovenous malformation (AVM) or mycotic aneurysm rupture.

Intraparenchymal hemorrhage may occur with middle communicating artery and posterior communicating artery aneurysms. Interhemispheric and intraventricular hemorrhages may occur with anterior communicating artery aneurysms.

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.

Degree and location of SAH are significant prognostic factors. The Fisher grading system is used to classify SAH, as follows:

• Grade 1 - No subarachnoid blood seen on CT scan
• Grade 2 - Diffuse or vertical layers of SAH less than 1 mm thick
• Grade 3 - Diffuse clot and/or vertical layer greater than 1 mm thick
• Grade 4 - Intracerebral or intraventricular clot with diffuse or no subarachnoid blood

CT scan allows for the detection of ventricular size and, thus, evaluation and surveillance of mass effect and hydrocephalus. On CT scan, hydrocephalus is evident as trapped temporal horns and "Mickey Mouse" appearance of the ventricular system.

Infusion CT scan

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.

LP is traditionally performed as a follow-up test when a CT scan has shown no SAH and has excluded possible contraindications to LP such as significant intracranial mass effect, elevated ICP, obstructive hydrocephalus, or obvious intracranial bleed. 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.

An LP is performed to evaluate the cerebrospinal fluid for the presence of red blood cells (RBCs) and xanthochromia. LP may be negative if performed less than 2 hours after an SAH occurs; LP is most sensitive 12 hours after onset of symptoms. CSF 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.

RBCs in the CSF can reflect a traumatic LP rather than SAH; however, SAH often can be distinguished from traumatic LP by comparing the RBC count of the first and last tubes of CSF. In traumatic LP, the RBC count in the last tube is usually lower, whereas in SAH the RBC typically remains consistently elevated. Nevertheless, cases of SAH in which the RBC count is lower have been reported.

No consensus is found in the literature on the lower limit of the RBC count in the CSF that signifies a positive tap. However, most counts range from a few hundred to a million or more cells per cubic millimeter. 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 caused by the breakdown of RBCs and subsequent release of heme pigments.

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. Spectrophotometry is much more sensitive than the naked eye in detecting xanthochromia. Nevertheless, many laboratories rely on visual inspection.

Some authors have suggested that the D-dimer assay can be used to discriminate SAH from traumatic LP. Results have been conflicting, however, and further data are needed.

Patients with negative CT and LP findings have a favorable prognosis. However, LP findings can be negative in approximately 10-15% of patients with SAH. In the past, LP findings were thought to be positive in 5-15% of all SAH presentations that are not evident on the CT scan. This number may be no longer valid with the advent of newer generations of CT scans. A small retrospective review of patients who presented to the ED and underwent fifth-generation CT scans and LP showed no cases of a positive LIP after a negative CT scan.^[15]

Digital-subtraction cerebral angiography has been the criterion standard for the detection of cerebral aneurysms (see the images below). It 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.

Negative angiographic findings do not rule out aneurysm. Approximately 10-20% of patients with clinically diagnosed SAH (on CT and/or lumbar puncture) have negative angiographic findings. A repeat angiogram is usually required in 10-21 days in such cases.

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 angiography is useful after surgical intervention. The postoperative study can confirm 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.

Although digital-subtraction cerebral angiography has been the criterion standard for the detection of cerebral aneurysms, multidetector CT angiography (MD-CTA) of the intracranial vessels is now routinely performed, and it is becoming fully integrated into the imaging and treatment algorithm of patients presenting with acute subarachnoid hemorrhage in many centers in the United Kingdom and Europe.^[16]

The popularity of MD-CTA derives from its noninvasiveness and a sensitivity and specificity comparable to that of cerebral angiography.^[17] This technique is beneficial in very unstable patients who cannot undergo angiography or in emergent settings prior to operative intervention for clot evacuation.^[17]

MRI is performed if no lesion is found on angiography. Its sensitivity in detecting blood is considered equal or inferior to that of CT scan. The higher cost, lower availability, and longer study time make it less optimal for detecting SAH. In addition, MRI 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 also 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.

One study found that cranial MRI including the brain and craniocervical region does not provide additional benefit for the detection of bleeding sources in patients with perimesencephalic and nonperimesencephalic SAH. However, MRI should be considered on a case-by-case basis because rare bleeding sources are possible in cases of nonperimesencephalic SAH.^[18]

The role of magnetic resonance angiography (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, which include lower sensitivity than cerebral angiography in the detection of small aneurysms and 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.

All patients with SAH should have a baseline chest radiograph to serve as a reference point for evaluation of possible pulmonary complications. All patients with SAH should have an electrocardiogram (ECG) on admission. Patients with SAH can have myocardial ischemia due to the increased level of circulating catecholamines or to autonomic stimulation from the brain. Myocardial infarction is a rare complication.

ECG 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