Infective endocarditis

As transient bacteraemias caused by dental and related procedures are known to play a major role in the pathogenesis of infective endocarditis, all dental practitioners should possess a sound knowledge of the disease process and the rationale of preventive therapy.

Although infective endocarditis can rarely develop on a normal heart valve, an abnormal valve is usually involved in the pathogenesis of the disease. The main causes of cardiac valvular disease which predispose to infective endocarditis are shown in Table 12.1.

Pathogenesis

The development of infective endocarditis entails the sequential interaction of several events as shown in Figure 12.1. A breach of the integrity of the endocardium, or an abnormality of the endocardial surface per se, is the initial pathological event which makes the valvular surface eventually succumb to infection. Such a breach may occur due to the acute inflammatory valvulitis of rheumatic fever (consequential to Streptococcus pyogenes infection). In congenital heart diseases such as aortic valve disease and ventricular septal defect (Table 12.1) alterations of the blood flow patterns (haemodynamic turbulence) can result in a tendency for the deposition of fibrin and platelets at foci where high velocity jets of blood hit the valvular surface (Figure 12.1). These microscopic platelet aggregations may detach and emobolize harmlessly or stabilize and consolidate through fibrin deposition. The result is the formation of a thrombus at the site which is thus a potential trap for circulating microbes. Such sterile thrombus formation is sometimes referred to as non-bacterial thrombotic endocarditis. This tendency towards platelet aggregation is not only limited to areas of damaged or denuded endocardium; platelets also have the potential to adhere to other ’foreign’ surfaces such as prosthetic valves. It is important to realize that non-bacterial thrombotic endocarditis is usually asymptomatic, provided impaction of emboli in vital areas does not occur.

The next crucial event in the pathogenesis of the disease occurs when microorganisms circulating in the blood attach to or become trapped in the thrombotic endocardium or the prosthetic device. The resultant platelet–fibrin–bacterial mass, now called the bacterial vegetation, constitutes the primary pathology of infective endocarditis (Figure 12.2). Although the detailed mechanics of the microbial ecosystem of the vegetation is not clear, it is probable that once the organisms are attached to the lesion they multiply and colonize this niche in an exuberant manner. As a result, further aggregation of platelets and fibrin deposition would ensue, thus protecting the organisms from the body defences. The organisms now reside in a sanctuary inaccessible to phagocytes by virtue of the fibrin-platelet barrier. Further, the bacteria may be sheltered from antibiotics and host antibodies, as the vegetation is essentially avascular in nature. As a result, it is necessary to use an intensive course of prolonged, high-dose antibiotic therapy to eradicate such an infective focus.

If endocarditis is successfully treated, the healed valve is permanently scarred and thickened and such residual abnormalities make the patient highly vulnerable to episodes of reinfection.

A wide array of different bacterial species, fungi and chlamydiae can cause infective endocarditis. The most common causative organisms of endocarditis are shown in Table 12.2. More than 80% of infective endocarditis is caused by streptococci and staphylococci. The eminent position held by the Strep. viridans group of organisms in the league table (Table 12.2) indicates the major role played by the oral commensals in causing this life-threatening disease. Strep. viridans was responsible for about 90% of endocarditis cases some 50 years ago when most patients were young and rheumatic heart disease (related to Strep. pyogenes infection) was common. Although the patients seen today are older and the proportion of cases due to Strep. viridans (mainly Strep. sanguis) has fallen, this group of organisms is still the most frequent cause of endocarditis. It is noteworthy that nearly all patients with Strep. viridans endocarditis have a previous heart lesion and about a quarter give a history of a recent dental procedure as a precipitating factor.

Factors which cause bacteraemia

As noted above, infective endocarditis is initiated when circulating microbes attach and proliferate within the fibrin thrombi attached to the damaged endocardium. As early as 1935 clinicians were aware that the oral cavity acts as a point of entry for organisms causing bacteraemia and that dental manipulations may set in motion the disease process. Since then many studies have shown that bacteraemia can occur following dental procedures such as extractions, surgical or non-surgical endodontics, gingivectomy, root-planing and scaling, and flossing. The frequency of bacteraemia has also been shown to be related to the preoperative oral sepsis of the patient and the degree of trauma and tissue injury.

With optimum blood culture technique a detectable bacteraemia can be shown to occur during tooth extraction in almost every case, tooth scaling in over a third of cases and endodontics with instrumentation beyond the apex in less than one third of cases. Other procedures, such as raising a mucoperiosteal flap, incision of abscesses and suture removal may cause bacteraemia but to a relatively minor degree.

The real risk of development of infective endocarditis in a ’risk’ patient following dental procedures is difficult to ascertain. Whereas some suggest that less than 10% of infective endocarditis is attributable to bacteraemia of dental origin, others maintain this proportion to be as high as 90%. Furthermore, a proportion of infections are thought to be associated with random transient bacteraemias which commonly follow mastication, and even tooth brushing, in patients with chronic periodontitis.

Infective endocarditis prophylaxis

Since dental-related endocarditis may well be the most common potentially fatal complication of dental treatment, all practitioners must have a good working knowledge of the problem. There is good evidence that dentists know about endocarditis and its prevention. However, some of the prophylactic regimens which have been used in the past have been purely empirical and in recent years a more scientific approach has been used. Table 12.3 shows the key principles of prophylaxis.