In most centers, follow-up examinations with catheter angiography are carried out after 3 months or 6 months, and then with MRA at 1-year or 2-year intervals. Secondary bleeding is unusual with coiled aneurysms, but approximately 10% of these aneurysms receive secondary treatment when there is asymptomatic recanalization, in order to ensure long-term protection against bleeding.
Surgical treatment
Definitive occlusion of the aneurysm using a vascular clip is carried out with neurosurgery in order to prevent repeat bleeding. The timing of the operation depends on the patient's condition, on the interval between the SAB and diagnosis, and on the extent of vasospasm. To forestall repeat bleeding and provide thorough treatment for vasospasm, an attempt is usually made to obliterate the aneurysm as early as possible.
Space-occupying intracranial bleeding is an absolute indication for surgical treatment of an aneurysm. Relative indications include broad-based aneurysms (usually of the middle cerebral artery) and those that can only be treated interventionally with difficulty or at high risk. In patients with broad-based aneurysms or giant aneurysms, the vessel can be reconstructed by placing multiple aneurysm clips. Concomitant medical conditions may argue in favor of surgical treatment in cases of renal insufficiency and hyperthyroidism, and poor general condition due to various comorbidities is an argument against surgical therapy.
For achieving a definitive occlusion, the surgical approach is the most effective treatment method; a surgical vascular clip is placed directly on the neck of the aneurysm above the vessel in order to permanently occlude the aneurysm without impairing blood flow in the affected vessel (Fig. 1.3-5). Particular attention should be given here to ensure that blood flow definitely remains unaffected by the clip, both in the vessel bearing the aneurysm and also in vascular branches that originate from it. Intraoperative fluorescence angiography with indocyanine green (ICG), a fluorescent dye, allows reliable checking of blood flow after clip application. Any intracranial hematoma that is present is removed in the same session. An external ventricular drain is often placed before the actual occlusion of the aneurysm in order to treat coexistent hydrocephalus and relieve intracranial pressure. In highly selected cases, surgical placement of an extracranial-intracranial bypass may be indicated in advance of the neurosurgical aneurysmal occlusion.
Fig. 1.3–5a-f (a, b) Status after surgical treatment for an aneurysm of the anterior communicating artery (see Fig. 1.3-10 for the preoperative image) and arteriovenous malformation (AVM) in the left frontal area. (c, d) Appearance after endovascular treatment of the AVM. (e, f) Appearance after surgical removal of the AVM.
The surgical mortality rate for unruptured aneurysms is approximately 2%, with a morbidity rate of around 7%. These complication rates increase dramatically with giant aneurysms. Following SAB, the outcome depends to a great extent on the patient’s initial clinical state. The poorest postoperative results can be expected in patients who start with a Hunt and Hess grade of 4 or 5. The poor clinical outcome here is due to the preoperative condition and is not necessarily specific to the surgical procedure.
The course and prognosis after any form of treatment for aneurysms are affected by the following variables: secondary bleeding before occlusion of the aneurysm (5-10%), treatment-related complications (4-8%), occurrence of vasospasm-related infarction (27-31%), malabsorptive hydrocephalus (10-45%), and medical complications (10-15%). The long-term course is determined by the extent of neurological losses, as well as neuropsychological deficits and psychosocial environment.
Intensive-care medicine
Patients with acute intracerebral or subarachnoid bleeding due to intracranial aneurysms, arteriovenous malformations, and other vascular malformations should receive intensive-care treatment or monitoring until their vital parameters have stabilized until there is no further acute risk of secondary bleeding or vasospasm. In addition to the specific therapy for these patients in collaboration among neurologists, neurosurgeons, neuroradiologists, and intensive-care specialists, excellent basic intensive care is decisive for the prognosis. The intensive care includes optimization of respiration and oxygenation, hemodynamics, and of the blood glucose level, fluid and electrolyte balance.
Respiratory therapy. The aim should be to achieve adequate oxygenation of arterial blood (Sao2 > 92%), which can be critically important for metabolism in the critically perfused brain tissue. If adequate oxygenation cannot be achieved by supplying oxygen via a nasal probe or face mask, or if the patient has limited protective reflexes due to the bleeding, or a pathological respiratory pattern, he or she should be intubated and given controlled ventilation.
Cardiac treatment. Particularly after subarachnoid bleeding, cardiac arrhythmia and changes on ECG that meet the criteria for acute myocardial infarction are not rare, even in patients who do not have coronary heart disease. Cardiac enzymes may also be raised in these patients. Close monitoring during the first days after the bleeding is therefore obligatory in these patients.
Blood-pressure adjustment. Optimizing cardiac output, with systemic blood-pressure values in the high normal range, is also important. The patient should receive adequate volume substitution, and additional administration of catecholamines may also be required. Blood-pressure spikes must be fastidiously avoided in patients who have suffered subarachnoid bleeding with an aneurysm that has not yet been treated. However, drastic drops in blood pressure must also be avoided in these patients.
Glucose metabolism. In patients with acute cerebral pathology, hyperglycemia is an independent risk factor for a poor outcome. The raised glucose values that are often found in these patients should not be regarded merely as a stress response by the body but should be actively treated.
Control of fluid and electrolyte metabolism. Both disturbances of fluid metabolism and severe disturbances of electrolyte homeostasis are frequently observed after intracerebral and subarachnoid hemorrhage. In patients with acute cerebral pathology, hypernatremia may occur in cases of diabetes insipidus, as well as hyponatremia in patients with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or cerebral salt-losing nephritis.
Prophylaxis and treatment for vasospasm after SAB. The calcium antagonist nimodipine (Nimotop®) significantly reduces the risk of secondary neurological injury triggered by vasospasms after SAB and it should therefore be administered prophylactically. Adequate data are only available for oral administration of nimodipine (60 mg p.o. every 4 h, daily dosage 360 mg in all patients after day of admission for approximately 20 days). In patients who are unconscious and those with unclear enteral absorption, nimodipine can be started i.v. at a dosage of 1 mg/h (5 mL/h) in the first 6 h and after blood-pressure controls can be initially raised to 1.5 mg/h and after a further 6 h to the maintenance dosage of 2 mg/h (10 mL/h). Ensuring adequate (130–150 mmHg systolic) and stable blood pressure takes priority over nimodipine administration. Other pharmacological approaches for prophylaxis against cerebral vasospasm after SAB, such as administration of magnesium sulfate, statins, and endothelin receptor antagonists are still controversial. Hypertensive hypervolemic hemodilution (triple-H therapy) can be carried out when vasospasms are present after SAB, although the value of this form of treatment has so far not been demonstrated in larger randomized studies. For triple-H therapy, blood pressure and blood volume are raised by administering crystalloid or colloid infusion solutions and catecholamines. Triple-H therapy is not recommended for prophylactic treatment against cerebral vasospasms.
1.3.1.6 Special types of aneurysm
As mentioned initially, there are also special types of aneurysm—i.e., vascular abnormalities with a specific pathogenesis that does not