Current Management of Aneurysmal Subarachnoid Hemorrhage

Abstract

The diagnosis of aneurysmal subarachnoid hemorrhage (aSAH) is most difficult in patients who are in good clinical condition with a small hemorrhage, especially when a ruptured aneurysm might not be considered, or if a computed tomographic (CT) scan is not obtained, or if when a CT is obtained, the findings are subtle and missed by an inexperienced reviewer. All acute onset (thunderclap) headaches should be considered ruptured aneurysms until proven otherwise. Treatment begins with immediate control of pain and blood pressure, placement of an external ventricular drain (EVD) in poor-grade patients and those with acute hydrocephalus on CT scanning, administration of antifibrinolytic tranexamic acid, and then repair of the aneurysm with either surgical clipping or endovascular techniques as soon as the appropriate treatment team can be assembled. After securing the aneurysm, aSAH patient treatment is focused on maintaining euvolemia and a favorable systemic metabolic state for brain repair. A significant and aneurysm-specific threat after aSAH is delayed arterial vasospasm and resulting cerebral ischemia, which is detected by vigilant bedside examinations for new-onset focal deficits or neurological decline, assisted with daily transcranial Doppler examinations and the judicious use of vascular imaging and cerebral perfusion studies with CT. The management of diagnosed symptomatic vasospasm is the prompt induction of hypertension with vasopressors, but if this fails to reverse deficits quickly after reaching a target systolic blood pressure of 200 mmHg, endovascular angioplasty is indicated, providing CT scanning rules out an established cerebral infarction. Balloon angioplasty should be considered early for all patients found to have severe angiographic vasospasm, with or without detectable signs of ischemic neurological deterioration due to either sedation or a pre-existing deficit.

Keywords: acute hydrocephalus; cerebral aneurysm; cerebral vasospasm; subarachnoid hemorrhage.

Figure 1

CT scan through the basal subarachnoid cisterns showing thick, hyperdense (white) clots in a 52-year-old woman who was drowsy and confused after an acute onset headache (Hunt and Hess and WFNS grade III). Note the thicker clot in the right Sylvian and insular cisterns (left side of the figure).

Figure 2

CT angiogram of the same patient shows two right-sided saccular aneurysms (left side of figure), the larger at the right MCA bifurcation and the second arising from the right ICA (up to 20% of aSAH patients have more than one aneurysm). Given that the MCA aneurysm was larger and associated with thicker Sylvian and insular clots, we could be confident it was the source of the bleeding, but both aneurysms were repaired with microsurgical clipping on the day of admission.

Figure 3

CT scan showed a thin layer of hyperdense subarachnoid blood encircling the upper brainstem, typical of a peri mesencephalic SAH. The 44-year-old patient presented with a GCS of 15 following a sudden-onset headache. CT angiography was normal.

Figure 4

CT scan showing focal hyperdense subarachnoid clots near the midbrain and tentorial incisura, typical of a peri mesencephalic SAH. The 51-year-old patient presented with a GCS of 15 following a thunderclap headache. CT angiography was normal.

Figure 5

CT scan through the basal subarachnoid cisterns showing thick, hyperdense clots in a 31-year-old man who was drowsy and confused after a sudden onset headache with vomiting (Hunt and Hess and WFNS grade III). Note the thickest clot is in the left Sylvian fissure surrounding the left MCA (The following figures are all from the same patient).

Figure 6

CT scan through the lateral ventricles showing intraventricular blood, indicating a Fisher grade 4 aSAH associated with a high risk of delayed cerebral vasospasm. An EVD was inserted.

Figure 7

Catheter angiography immediately prior to coiling of a small anterior communicating aneurysm, just several millimeters in diameter. Note the normal caliber of the blood vessels to be compared with the next series of figures.

Figure 8

Seven days later, the patient became more lethargic with a new right-sided weakness. Velocities in the middle cerebral arteries on transcranial Doppler exceed 200 cm/s, indicating significant vasospasm. Hypertension was induced (see text), and after a CT ruled out cerebral infarction, a following catheter angiogram showed severe left MCA narrowing (a), where the thickest subarachnoid clot was located on the initial CT, and moderate vasospasm of the right MCA (b).

Figure 9

Post-angioplasty showing excellent reversal of the left MCA and proximal ACA vasospasm (a) the right MCA (b). All vasospastic vessels that could be reached with the balloon catheter were treated). The patient’s clinical condition improved and remained stable until full recovery.

Figure 10

An example of acute hydrocephalus following aSAH secondary to a ruptured ACommA in a clinical aSAH grade 3 28-year-old woman. The red arrows point to subarachnoid blood in the cisterns, sulci, and interhemispheric fissure, and the yellow arrows point to prominent ventricles. This degree of hydrocephalus, while not florid, was clear with visible temporal horns (normally not visible in young adults) (a), and “rounding” of the frontal horns of the lateral ventricles (b). Combined with the flattening of the cerebral sulci (c), this CT scan is indicative of dangerously raised intracranial pressure, especially in a young patient requiring early EVD insertion.