Infectious Intracranial Aneurysms
The earliest published case of an infectious aneurysm dates back to 1869, when Church described a 13-year-old boy with left hemiparesis who was found to have a ruptured right middle cerebral artery aneurysm and mitral valve endocarditis.1 The term mycotic aneurysm was introduced by Sir William Osler in 1885 to describe an aortic aneurysm in the setting of bacterial endocarditis.2 This term was subsequently used to describe all intra- and extracranial aneurysms of an infectious etiology. Because of the inaccuracy of this term in describing a condition most commonly due to bacterial involvement, several alternative terms have been suggested, such as infected, infectious, infective, inflammatory, septic, bacterial, and microbial. More recently, the term infectious intracranial aneurysm (IIA) has gained popularity. For this chapter, we reviewed the literature and found a total of 303 patients with 390 aneurysms from 1966 to 2008 that were associated with infection3–34 ( Table 11.1 ). These cases will help to illustrate the pathogenesis, presentation, microbiology, aneurysmal characteristics, natural history, and treatment strategies for IIA.
Epidemiology
The autopsy review of Fearnsides in 1916 estimated that 30% of all intracranial aneurysms were infectious in origin.35 More recent reviews have put the estimate at 2 to 6%.36–38 This decrease in the incidence is likely due to the introduction of antibiotic therapy. The difficulty in estimating the true incidence of IIA stems from the somewhat protean natural history of the disease. Bacterial IIAs have been observed to form and regress spontaneously with antibiotic therapy, whereas IIAs associated with fungal and tuberculous infections have been observed to be more persistent than bacterial infections.20,35,39–42 The increasing number of patients immunocompromised as a consequence of acquired immunodeficiency syndrome (AIDS), steroid therapy, chemotherapeutic regimens, or organ transplant presents a potential source for an increase in the number of IIAs in susceptible populations.
Although intracranial aneurysms are less common in children than in adults, those diagnosed in children are more likely to be infectious. Approximately 10% of aneurysms in children are estimated to be infectious in origin.43–47 Endocarditis, especially left-sided valve disease, is frequently associated with IIA. In the present analysis, 76% of patients with IIA had a diagnosis of infective endocarditis ( Table 11.2 ). Extravascular infections, such as meningitis, orbital cellulitis, and postcraniotomy infections, have been reported to lead to IIA.
Pathogenesis
The pathogenesis of IIA can be conceptualized into three different processes: intravascular, extravascular, and cryptogenic. The intravascular mechanism is the most common, involves septic emboli, and is commonly secondary to bacterial endocarditis. IIAs due to septic emboli are often located at vessel branch points in the distal vasculature. Showers of septic emboli can lead to the formation of multiple IIAs, seen in 17% of the reviewed cases ( Table 11.3 ). This result was consistent with the previously reported rate of 20%.48
Intravascular
In 1887, Eppinger49 described the infectious and inflammatory processes leading to weakening of the arterial wall and subsequent aneurysm formation. He observed that the inflammation involved the adventitia initially and then spread inward to the internal elastic membrane. This notion was confirmed in a mongrel dog model involving silicone rubber emboli.50,51 Although vasa vasorum play a role in aortic aneurysm formation after infection in a dog model,52 vasa vasorum are rarely present in intracranial vessels.53 Molinari and colleagues have suggested that in the absence of vasa vasorum, bacteria can escape from the lumen of the vessel through the occluded origins of the thin-walled penetrating vessels into the Virchow-Robin space and from there to the adventitia of the occluded vessel.
In the experimental model by Molinari et al,51 aneurysm formation occurred at the proximal end of the occluded segment, overlapping the embolus and the adjacent segment with a patent lumen, indicating the importance of arterial pulse pressure in the dilation of the diseased, weakened arterial wall. Chronic aneurysms were also induced by subtherapeutic doses of antibiotics. These aneurysms were found to be firmly adherent to both the leptomeninges and pachymeninges and had intact, indurated, fibrotic walls. Inadequate antibiotic treatment permitted microorganisms to disseminate through penetrating vessels into the infarcted intraparenchymal area, causing brain abscess.
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