A distinction had in the past been made between the neuropathologic effects of endocarditis caused by different organisms. What had been divided into acute bacterial endocarditis (ABE) and subacute bacterial endocarditis (SBE) are now instead characterized by the virulence of the causative organism. For example, endocarditis from the implantation in the brain of streptococci of low virulence (alpha and gamma streptococci) or similar organisms on heart valves previously damaged by rheumatic fever seldom gives rise to a brain abscess. In contrast, organisms such as S. aureus and gram-negative bacteria have a propensity to cause abscesses. The cerebral lesions in all forms of endocarditis are a result of embolic occlusion of vessels by fragments of vegetations and bacteria, which cause infarction of brain tissue and a restricted inflammatory response around the involved blood vessels and the overlying meninges (cerebritis). It is the subsequent evolution of the process that is dependent on the inherent tendency of the organism to be invasive. Therefore, the former distinction between acute and subacute bacterial endocarditis has become less useful. The cerebral symptoms of a stroke may be the first clinical manifestations of the disease. Over time, sometimes within days but usually longer, the inflamed artery may form an aneurysm (mycotic aneurysm) that later gives rise to parenchymal or subarachnoid hemorrhage (see Chap. 33). Bacterial meningitis rarely develops with abscess and most often the CSF is sterile but there are exceptions.
Rapidly evolving cerebral signs in patients with acute endocarditis are usually caused by septic embolic infarction or hemorrhage and not by an abscess. Anticoagulation has not been shown to reduce the incidence of embolization from endocarditis; the risk of inducing hemorrhage is uncertain but the rate of hemorrhage may have been overestimated in the past. In patients with endocarditis on a prosthetic heart valve, anticoagulation may be continued, but this treatment is suspended if there is a hemorrhagic brain infarction. Existing anticoagulation need not be reversed unless a cerebral hemorrhage evolves.
It has been estimated that 5 percent of cases of congenital heart disease are complicated by brain abscess (Cohen; Newton). Viewed from another perspective, in children, more than 60 percent of cerebral abscesses are associated with congenital heart disease. The abscess is usually solitary; this fact, coupled with the potentially correctable underlying cardiac abnormality, makes the recognition of brain abscess in congenital heart disease a matter of considerable practical importance. For some unknown reason, brain abscess associated with congenital heart disease is rarely seen before the third year of life. The tetralogy of Fallot is the most common anomaly implicated, but the abscesses may occur with any right-to-left intracardiac or pulmonary shunt that allows venous blood returning to the heart to enter the systemic circulation without first passing through the lungs. Pulmonary emboli, by increasing the back pressure in the right heart, may open (make patent) an occult foramen ovale. A pulmonary arteriovenous malformation has a similar effect. Nearly half of the reported cases of pulmonary arteriovenous fistulas have hereditary hemorrhage (Osler-Weber-Rendu) telangiectasia. When the filtering effect of the lungs is thus circumvented, pyogenic bacteria or infected emboli from a variety of sources may gain access to the brain, where, aided by the effects of venous stasis and perhaps of infarction, an abscess is established.