FIGURE 9.1 A) Initial head CT scan showing SAH with aneurysmal pattern and some blood layering in the lateral ventricles consistent with a modified Fisher scale grade 4. B) Follow-up CT scan nearly 4 hours later shows hydrocephalus.
Patients with an aneurysmal subarachnoid hemorrhage (aSAH) often appear deceptively stable. They may “look great” only to acutely or gradually decline into a much worse neurologic state. The very moment when changes in neurologic condition occur are sometimes difficult to pinpoint (as with cerebral vasospasm) but in other instances changes are overwhelmingly clear (as with rebleeding). When caring for a patient with aSAH with worsening neurological condition, the differential diagnosis to be considered will also depend on the time from aneurysm rupture. This is clearly demonstrated by this patient, who declined early due to hydrocephalus and later because of cerebral vasospasm.
The major risks to the patient on the first day after aneurysmal rupture are rebleeding and acute hydrocephalus. It is hard to overlook a rebleeding because the clinical changes are dramatic. The patient suddenly becomes stuporous or comatose and the altered consciousness is accompanied by severe hypertension, tachypnea (or apnea), and tachycardia (or brief asystole). Motor responses change, and extensor posturing (mimicking a seizure to the untrained observer) may occur. In comatose patients with a poor grade aSAH, rebleeding may cause loss of pupillary and corneal reflexes, and nursing staff may see fresh blood in the ventriculostomy bag. This catastrophic event is markedly different from the presentation of hydrocephalus. Instead, as hydrocephalus develops patients become progressively less interactive, then drowsier, and finally unresponsive. While this progression may be rapid, it is not sudden, and alarms do not go off as patients only are mildly hypertensive and bradycardic. While patients are still arousable the only physical sign may be restricted eye movements in the vertical plane caused by the pressure of the expanded third ventricle over the tectum of the brainstem. Given the paucity of clinical clues, the recognition of acute hydrocephalus remains a challenge for physicians outside the neurosciences and many do not appreciate the dilated ventricles on CT scan.
Delayed vasospasm occurs days later, typically starting 3 to 5 days after the hemorrhage to reach a peak around day 7 before resolving by days 10 to 12. Contrary to a common assumption of trainees, the first manifestation of vasospasm is usually not a focal deficit. Instead, diminished alertness and lucidity tend to be the presenting symptoms of this complication. Patients developing cerebral vasospasm are often febrile and have developed hyponatremia, which are factors that can also diminish alertness. Consequently the diagnosis of symptomatic cerebral vasospasm is far from straightforward, and good clinical judgment and experience are necessary to recognize it. Some patients are at higher risk for ischemic damage from cerebral vasospasm after aSAH and these risk factors are listed in Table 9.1. Useful modalities for the screening of vasospasm and diagnosis of delayed cerebral ischemia are summarized in Table 9.2.
Transcranial Doppler (TCD) is useful to monitor for cerebral vasospasm, especially when trends from serial measurements are documented. We suspect cerebral vasospasm when the mean blood flow velocity in the M1 segment of the middle cerebral artery exceeds 120 cm/s and consider it severe when this measurement is greater than 200 cm/s. We have been increasingly using a combination of CT angiogram and CT perfusion in patients with suspected vasospasm. Conventional angiography is reserved for patients who are refractory to medical therapy and might be candidates for endovascular treatment. However, all these techniques have limitations. Cerebral vasospasm is primarily caused by endothelial dysfunction and involves first and foremost the microcirculation. TCD and angiograms are very sensitive for the detection of vasospasm in the large arterial segments but much less accurate when cerebral vasospasm is more distal. Thus, patients may develop ischemic lesions, particularly in deep brain regions, despite having normal or near-normal velocities on TCD and vessel diameters on cerebral angiogram. CT perfusion scans only partially overcome this limitation because their interpretation in practice relies on side-to-side comparison, which loses value in common cases of diffuse, bilateral cerebral vasospasm. CT perfusion may show hypoperfusion much more clearly in the cortex than in the deep white matter. Since ischemia can occur in the absence of documented vasospasm (either because we do not have the right tools to identify it or because there are mechanisms other than reductions in arterial luminal diameter causing the ischemia) the term “delayed cerebral ischemia” is more appropriate than “symptomatic cerebral vasospasm.”
TABLE 9.1 Risk Factors for the Development of Delayed Cerebral Ischemia after aSAH
| Extensive clot in subarachnoid cisterns on admission CT scan* |
| Intraventricular hemorrhage on CT scan within first 24 hours* |
| Young age |
| Active smoking |
| Cocaine use |
| Poor clinical neurologic examination at onset |
*Factors considered in the modified Fisher scale: grade 0, no SAH or IVH; grade 1, thin SAH without IVH; grade 2, thin SAH with IVH; grade 3, thick SAH without IVH; grade 4, thick SAH with IVH.
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