majority of the lesions treated were in patients in good clinical grade (>90%), who harbored anterior circulation aneurysms (97.3%) and whose aneu- rysms were less than 10 mm (almost 95%). The gen- eralization of this study to all aneurysms, or even to all ruptured aneurysms, would not be valid.
A separate publication confi rmed these fi ndings at the 1 year follow-up for all randomized patients [34]. A third publication from the ISAT study inves- tigators reanalyzed the data substratifi ed for age and found that the fi ndings were not as robust for patients less than 50 years and may not be valid for patients less than 40 years old, again due to poorer durability and slightly increased rehemorrhage risk of coiling [35]. A proposed algorithm for the treat- ment of ruptured aneurysms is presented (Figure 6.9).
The example patient’s aneurysm was evaluated by an endovascular neurosurgeon who performs both clipping and coiling. It was deemed to be equally treatable using either modality. Based on the ISAT data, the patient was offered coiling as the recom- mended treatment. If the aneurysm could not be safely coiled, clipping would be recommended. The patient agreed to undergo coiling, which was per- formed uneventfully with complete occlusion (Figure 6.2e and 6.2f). She was discharged home 10 days later, neurologically intact. Her fi rst follow-up angiogram was performed 6 months later and showed no aneurysm recanalization.
IA documented by CTA/MRA/DSA Ruptured? Yes Yes Yes Yes Yes
Yes Yes Yes
Yes Yes YesYes
Yes Yes
Yes Yes Yes Yes Yes
No No
No NoNo No No
NoNo No No
No
NoNo No No
No No NoNo No
Hematoma requiring surgery? H&H Grade 4/5, Vasospasm or ≥65? Coil Coil Coil
Coil CoilNo Rx., follow serial MRA/CTA
No Rx., follow serial MRA/CTA Coil or clip CoilCoil or clip
Coil or clip
Clip Coil or clipCoil or clipCoil or clip
Surgically difficult location? Large or giant aneurysm?High-volume surgeon available?
Surgery, clip aneurysm
≤7 mm? ≤65 years?
≥3 mm?≥25 mm and symptomatic mass effect? ≥70 years, consider no Rx. Otherwise proceed Surgically difficuly location? Surgically difficult location?
High-volume surgeon available? High-volume surgeon available?
High-volume surgeon available? High-risk location? High-risk group?
High-risk group? Consider no treatment Decision to treat?Follow serial MRA/CTA Fig.6.9Algorithm for the treatment of intracranial aneurysms (IAs). For simplicity, the following categories are defi ned based on the International Study of Unruptured Intracranial Aneurysms and the International Subarachnoid Aneurysm Trial studies and the available literature: high-risk group = patients who have suffered subarachnoid hemorrhage (SAH) from another IA, patients who are very anxious about having an untreated IA, and patients who have a family history of SAH from an IA, or patients with adult polycystic kidney disease; high- risk location = posterior communicating artery aneurysm or aneurysms located on the vertebrobasilar system (i.e., posterior inferior cerebellar artery, basilar tip); surgically diffi cult location = aneurysms located on the vertebrobasilar system, paraclinoid aneurysms (i.e., ophthalmic, superior hypophyseal), or large (>12 mm)/giant (>25 mm) aneurysms. CTA, CT angiography; DSA, digital subtraction angiography; MRA, magnetic resonance angiography.
the increased intracranial pressure and to permit intracranial pressure measurements during the acute period (Table 6.1, Section 10). Asymptomatic acute hydrocephalus is usually followed conservatively as it will ultimately resolve spontaneously in many patients. Patients who are initially asymptomatic from hydrocephalus may also begin to show signs of increased intracranial pressure [3]; a CT scan should be obtained for all SAH patients who experience a neurological decline. The example patient had neither radiographic nor symptomatic hydrocepha- lus and did not require ventriculostomy placement.
Delayed hydrocephalus (generally communicating hydrocephalus) can occur at any time in the fi rst 1–4 weeks after SAH; it may spontaneously resolve or require ventriculoperitoneal shunt placement (Table 6.1, Section 10).
Vasospasm
Cerebral vasospasm, a diffuse or focal narrowing of the cerebral arteries occurring between day 3 and day 14 following SAH, is responsible for the major- ity of morbidity and mortality in patients surviving the initial bleed [36]. As many as 70% of patients will have angiographic vasospasm on day 7 after a hemorrhage (the peak incidence for vasospasm), but only 20–30% of patients develop symptomatic cere- bral ischemia (temporary or permanent) from the arterial narrowing that decreases blood fl ow to the brain [36]. The etiology of vasospasm is unknown.
Patients with symptomatic vasospasm often have signs including decreased level of arousal, confu- sion, or focal neurological defi cit, such as aphasia and/or hemiparesis. There is no good preventive therapy for vasospasm, although many agents have been tried. Avoiding hypovolemia is recommended as it may permit vasospasm treatment if it develops (see further discussion). The detection of vasos- pasm is crucial, as treatment is available. The use of the calcium-channel blocking agent nimodipine improved the outcome related to vasospasm in several prospective randomized trials [37]. Oral nimodipine (60 mg every 4 hours for 21 days) is administered beginning immediately after SAH and is continued for 21 days. Transcranial Doppler (TCD) ultrasonography is a very sensitive test to detect vasospasm and is generally performed on a daily basis or every other day after SAH during the acute period. Increasing velocities by TCD suggest
onset of vasospasm and will direct the management based on the clinical scenario [24]. DSA is generally employed to confi rm the diagnosis and may enable endovascular therapy (see further discussion). Once vasospasm has been diagnosed, medical treatment consists of the “triple H” therapy: hypertension, hypervolemia, and hemodilution (Table 6.1, Section 9). Those failing medical treatment with persistent neurological defi cit (given a trial of 1–2 hours of aggressive hypertensive therapy) are urgently taken for angiography and angioplasty of the stenotic vessels (Table 6.1, Section 9) [36]. On post-bleed day 5, the example patient developed increasing TCD velocities in the left middle cerebral artery con- sistent with mild-moderate vasospasm. There was no clinical deterioration, however, and the patient’s blood pressure was permitted to rise up to 200 mm Hg systolic. She was hydrated, and a central venous line was placed with a central venous pres- sure goal of 8–12 mm Hg. Her TCD velocities were unchanged until day 9 after the SAH, at which point the velocities normalized within the left middle cere- bral artery and the triple “H” therapy was weaned.
Medical complications
Numerous medical complications affl ict patients in the fi rst 2 weeks following aneurysmal SAH [24].
Some, such as hyponatremia, seizures, neurogenic pulmonary edema, or cardiogenic dysfunction, are caused by the intracranial insult, whereas others (deep vein thrombosis, pulmonary embolism, pneu- monia, malnutrition) are often the result of a gen- eralized debilitated state and prolonged intensive care unit stay. Hyponatremia is almost always a result of cerebral salt wasting and not SIADH (syndrome of inappropriate antidiuretic hormone secretion), although a mixed picture is possible.
Fluid restriction should not be attempted, particu- larly in the face of vasospasm where it might lead to decreased circulating volume and stroke (Table 6.1, Section 12).
Once the aneurysm is secured, blood pressure can be moderately elevated to improve cerebral perfu- sion. The utility of decadron is unsupported, although it seems to alleviate headaches in some patients and is commonly used for a short period if the patient undergoes craniotomy. Hyperglycemia and hyperthermia should be corrected as they have a negative impact on outcome [38]. Deep vein
thrombosis prophylaxis can be achieved with sequential compression devices and subcutaneous heparin can be safely administered in most cases as soon as the aneurysm is secured.
Cardiac abnormalities after SAH are common and include eclectrocardiographic changes, cardiac enzyme elevations, and left ventricular dysfunction with or without pulmonary edema [39–41]. These cardiac markers do not necessarily portend myocar- dial damage and should not delay early operative intervention to treat the aneurysm [42]. Findings of markedly decreased ejection fraction with wall motion abnormalities that do not match the electro- cardiographic vascular distribution of ischemia help make the diagnosis [39,40].