venerdì 5 maggio 2006
Subarachnoid hemorrhage (SAH) due to left PICA aneurysm
High attenuation within basilar cisterns and subarachnoid spaces, extending to the Sylvian fissures consistent with hemorrhage. SAH was not seen to extend over the convexities (Figure 1, Figure 2 and Figure 3).
Vertebral artery injection digital subtraction angiography demonstrates an aneurysm of the Left PICA origin.
Figure 6 shows classic “teat” at site of rupture.
Differential diagnosis for subarachnoid hemorrhage (CT findings are diagnostic):
- Aneurysm rupture
- Cortical thrombosis
- Dissection from intraparenchymal hematoma
Differential diagnosis for cerebral aneurysm (angiographic findings are diagnostic)
DD for saccular aneurysms:
- Traumatic pseudoaneurysm
- Flow related
- Vasculopathy related
- Drug related)
DD for fusiform aneurysms: Atherosclerosis
DD for dissecting aneurysms:
Diagnosis: Subarachnoid hemorrhage (SAH) due to left PICA aneurysm
SAH is most commonly due to trauma. In the absence of trauma history or correlative findings, presence of SAH necessitates investigation for a cause. Nearly two thirds of these cases will be due to ruptured aneurysm. Clinically, patients experience severe headache. Patients often describe a “sentinel” headache, or prodrome indicating earlier bleeding. Less often, focal or global neurologic findings are present.
SAH is graded based on clinical presentation:
Grade 1) being mild headache
Grade 2) severe headache
Grade 3) mild mental status changes
Grade 4) obvious altered mental status or neurologic change
Grade 5) comatose or posturing
Long-term outcome directly correlates with grade at initial presentation. Of all patients with SAH, roughly 40% die within 24 hours and an additional 10% to 25% within six months. Of the survivors, half will have major long-term neurologic deficits.
Radiographically, high attenuation within subarachnoid spaces (sulci, ventricles, basal cisterns) on a noncontrast CT is the principal finding. Multidetector CT is up to 98% sensitive in the first 24 hours. Degree of SAH is also graded and has prognostic value, as does location of hemorrhage.
Complications of SAH include hydrocephalus, rebleeding, and vasospasm. Hydrocephalus is due to obstructing clot within the ventricular system and may be early or delayed. Early evidence is enlargement of the temporal horns. Rebleeding most often occurs within the first 24 hours, but can occur up to 2 weeks after initial insult. This is found in 20% to 30% of untreated patients and carries up to an 85% mortality. Vasospasm is the most feared complication, resulting in the greatest degree of morbidity and mortality, and affects nearly 40% of all patients. Peak time frame, according to the literature, is four to 12 days, although anecdotal experience from our institution suggests this is often seen earlier. Vasospasm can lead to ischemic events and progression of neurologic deficits.
As discussed, primary nontraumatic SAH is most commonly due to aneurysm rupture. Saccular aneurysms are true aneurysms and are the most common. These are thought to be congenital areas of weakening in arterial walls, which develop over many years into an aneurysm. Fusiform and dissecting are the other two major categories, and are much less common. Aneurysms have a fairly predictable distribution: 35% anterior communicating artery, 30% posterior communicating artery, 20% MCA bifurcation, and 15% vertebrobasilar system. Location of SAH is often a clue to aneurysm location. While no aneurysm is too small to exclude rupture, 4 to 7 mm appears to be the critical size. Aneurysms larger than 10 mm are at much higher risk. A patent aneurysm appears as an outpouching of contrast, while a thrombosed aneurysm may have a normal appearance. Lobulation or irregularity of aneurysm dome (“teat”) is an indication of possible rupture site, especially in the presence of multiple lesions.
Treatment of aneurysms has significantly progressed with intraarterial coil embolization. In the past, the only option was open surgical intervention. Timing of treatment is divided into two phases: early (within two to three days) and late (after ten to 14 days), avoiding the peak incidence of vasospasm. No significant outcome difference has been proven, however, proponents of early intervention for low-grade aneurysms cite the ability for aggressive treatment to lower risk of vasospasm once the aneurysm is controlled. Treatment for asymptomatic, unruptured aneurysms is even more controversial, due to postprocedural complications. Typically, lesions less than 5 mm are followed, while larger lesions are often treated.