49 Mycotic Intracranial Aneurysms
Abstract
Mycotic aneurysms represent 1 to 6% of all intracranial aneurysms. These aneurysms most commonly arise from intravascular spread of septic emboli that lodge into distal vessels weakening the muscularis of proximal vessels causing aneurysm formation. They are most commonly found in the distal middle and anterior cerebral artery and occasionally in the posterior cerebral artery. Symptomatic patients present with subarachnoid and/or intracerebral hemorrhage. Computed tomography (CT) and CT angiography are the initial imaging evaluation. Digital subtraction angiography is the gold standard for aneurysm visualization and characterization. Cardiac and bacteriological workup is also mandatory. Ruptured mycotic aneurysms should be treated as an absolute emergency due to their fragility to rerupture. All patients should receive antibiotic or antifungal treatment. When selecting the modality for treatment of mycotic aneurysms, factors such as patient′s age, clinical condition, aneurysm size and morphology, and the presence and size of intracerebral hemorrhage should be taken into consideration. Microsurgical clipping or resection is historically the treatment of choice; however, given the right conditions, certain endovascular techniques such as coiling can be acceptable alternatives. The outcome of mycotic aneurysms is variable and depends on initial clinical presentation, severity of systemic infection, preservation of the aneurysm′s parent vessel, and size of intracerebral hemorrhage. Appropriate clinical and radiological follow-up is mandatory in all intracranial aneurysms.
Introduction
Infectious intracranial aneurysms are also known as mycotic intracranial aneurysms (MIAs). They account for 1 to 6% of all intracranial aneurysms and are identified after or concomitantly with systemic bacterial infections. These aneurysms are sometimes associated with other systemic fungal and mycobacterial infections. They are most commonly found in the distal middle cerebral artery (MCA) and anterior cerebral artery (ACA) branches. The majority occur in distal branches of the MCA, the M3 and M4 branches, with 57 to 77% of MIAs found along the MCA. Approximately 10% of patients with subacute bacterial endocarditis tend to develop intracranial aneurysms. Management of MIAs can induce considerable unease due to the risks and difficulties that caring for a patient with this type of aneurysm imposes on a surgeon and the medical team. This patient population frequently has bacterial endocarditis or sepsis and therefore is often medically unstable. These aneurysms can be more perilous to treat than other aneurysm subsets due to the fragile nature of the affected parent artery and aneurysm wall.
Major controversies in decision making addressed in this chapter include:
Whether treatment is indicated.
Open versus endovascular treatment for ruptured and unruptured MIAs.
Management of MIAs that present with intracerebral hematoma.
When to consider advanced surgical or endovascular techniques, such as bypass or stenting.
Whether to Treat
The natural history of MIAs is not well described, but it is generally accepted that these aneurysms are associated with a high risk of rupture and morbidity. As with other intracranial aneurysms, the risk of rupture increases with size and previous subarachnoid hemorrhage (SAH) from the same or a new aneurysm in the same patient. Unruptured and ruptured MIAs are associated with mortality rates as high as 30 and 80%, respectively. Recent studies show combined rates of mortality in treated and untreated patients near 40%, pushing for treatment whenever possible without incurring serious risk of further neurological deficit. There are no clear clinical criteria for when to treat MIAs, although there are high-risk criteria that would suggest treatment is beneficial, including large aneurysm size, predisposing infection, fever on presentation, broad-based aneurysm neck, and history of rupture or intracerebral hemorrhage. Another consideration relates to the fact that these aneurysms often involve distal branches, which means they are inherently more likely to have a large size ratio (i.e., aneurysm size divided by parent vessel diameter) ( 1 , 2, 4 in algorithm ). Although no good history exists as to rupture rates and size criteria for MIAs, aneurysms less than 6 mm that cannot be easily accessed or obliterated and have not ruptured are frequently monitored by serial imaging with supportive medical management and antibiotic/antifungal therapy ( 5, 6 in algorithm ). However, the authors wish to make a clear point. We feel strongly that MIAs of any size or configuration are inherently risky to observe. Therefore, we do not advocate observation of any MIA if it can be safely treated.
Anatomical Considerations
Although the cavernous internal carotid artery (ICA) and proximal large vessels can be affected, the majority of affected vessels are more distal along distal branching points. MIAs tend to appear at the following locations, in order of frequency: distal MCA, proximal MCA, distal posterior cerebral artery (PCA), and distal ACA. The ACA segments that are most commonly affected are the A3 and A4 branches, which are located after the branching point of the callosomarginal and pericallosal arteries anterosuperior to the cingulate gyrus. The A4 segment is most commonly affected near distal branching points of the pericallosal artery. Similarly, the PCA segments most commonly affected are branch points off of the P4 distal to the ambient and quadrigeminal cisterns. The normal luminal diameters of these distal vessels are between 2 and 4 mm, with the proximal MCA segments being between 3 and 5 mm.
Pathophysiology/Classification
Most patients who have MIAs have sepsis or clinically significant bacterial endocarditis with valvular vegetations. These aneurysms most commonly arise from intravascular spread of septic emboli that then lodge into distal vessels. The most common causal organisms are bacteria, fungi, and parasites. Streptococcus and Staphylococcus species are the most common pathogens. Infection and development of proximal aneurysms are thought to arise from the contiguous spread of the offending pathogen from an abutting structure such as can be seen with cavernous sinus thrombophlebitis or meningitis. The underlying anatomical cause for the formation of MIAs relates to aneurysmal formation from weakening of the muscularis in proximal vessels. Animal studies have developed support for an understanding that bacteria enter the vasa vasorum and escape into the Virchow-Robin space, eventually eliciting an inflammatory reaction in the adventitial layer of distal vessels. Inward spread of the infection travels from there through the muscularis and inner elastic lamina, causing a weak vessel wall. Pulsatile pressure from arterial flow results in an often rapid formation of an aneurysm in distal branches.
There are no good classification systems for MIAs, but Kannoth et al developed a set of defining criteria for making the diagnosis. These criteria include predisposing infection, angiographic features demonstrating an aneurysm arising from distal vessels, less than 45 years of age, fever on presentation, and known bacterial endocarditis. These authors conclude that the presence of these criteria reinforces the likelihood of vascular abnormalities noted on imaging being MIAs rather than de novo, noninfectious intracranial aneurysms.
Workup
Clinical Evaluation
The most common clinical presentation of an MIA tends to be SAH with or without intracerebral hemorrhage. Large intracerebral hemorrhages tend to cause symptoms from local mass effect from pressure caused by the hematoma, seizures, infarction, and damage to local gray matter.
Imaging
Initial imaging tends to be computed tomography angiography (CTA) to evaluate for the possibility of hemorrhage as well as possible vascular malformations with possible or partial thrombosis. Digital subtraction angiography (DSA) is the gold standard diagnostic study, and a three-dimensional reconstruction of the aneurysm offers the most information for the best possible treatment options.
Differential Diagnosis
The differential diagnosis for lesions arising in this patient population tends to be based on the entire clinical scenario. The differential includes classic aneurysm, pseudoaneurysm (usually associated with a dissection and/or history of trauma), or MIA.
Treatment
Choice of Treatment and Influence of Intracerebral Hematoma
With advances in endovascular techniques and treatment modalities, most MIAs that require treatment can be treated via endovascular means. Although the general rule remains that any MIA that has ruptured should be treated, the difficulty and method of the treatment depends on the configuration and location of the aneurysm. Because of their fragile walls, the more proximal aneurysms sometimes require vessel sacrifice (endovascular or surgical) or bypass surgery. The more distal lesions can sometimes be treated with primary clipping or distal vessel sacrifice based on whether eloquent cortex is supplied.
Mycotic aneurysms presenting with symptomatic intracerebral hematoma should be treated urgently. One option is urgent craniotomy and clot evacuation with exploration of distal vessels and treatment of the aneurysm with either clip reconstruction or proximal occlusion. In a situation where a patient has a symptomatic hemorrhage from an MIA but the neurological condition is such that the patient could tolerate an attempt at endovascular treatment prior to craniotomy, it is not unreasonable to attempt endovascular treatment prior to the craniotomy. This provides control of the ruptured aneurysm prior to the exploration, which decreases the risk of bleeding intraoperatively.
In cases where bypass surgery or vessel sacrifice is being considered, having endovascular access simultaneously can sometimes be beneficial during the exploration in case of intraoperative rupture. According to several case reports, partial clot evacuation tends to be done prior to finding the aneurysmal dome and treating the aneurysm directly ( 1 in algorithm ). For ruptured mycotic aneurysms without large hematomas, treatment should be as early as possible. Although no natural history exists for rerupture rates for mycotic aneurysms, it is believed that rebleeding is still highest in the first 24 hours through 2 weeks, and early treatment is usually employed.
Conservative Management
Antibiotic/antifungal treatment of infectious etiologies for mycotic aneurysms is the classically proposed management technique for unruptured, less than 6 mm mycotic aneurysms ( 6 in algorithm ). However, as discussed earlier, the natural history of this pathology can be aggressive. Therefore, we find this to be the least attractive option for the initial management of these patients.
A bacteria or causative organism is found in less than 50% of the cases; and in these cases, it is recommended that patients undergo 4 weeks of intravenous broad-spectrum antibiotic/antifungal coverage. When a causal organism cannot be identified, counsel from infectious disease specialists is crucial. When the medication is changed or stopped, serial monitoring studies should be obtained to look for aneurysm progression or regression. If the aneurysm is stable or has decreased in size, continuing antibiotic/antifungal therapy for primary treatment is reasonable. However, increasing aneurysm size, despite appropriate medical therapy, should prompt aggressive treatment.
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