The diagnosis of IE is rejected when:- There is a definitive alternative diagnosis.
- The clinical manifestations of IE resolve after four or less days of antimicrobial
therapy. - There is no pathological evidence of IE after four or fewer days of antimicrobial
therapy.
In general, these criteria are quite useful with certain exceptions. The modified Duke
criteria of 2000 include the category of possible IE. This represents findings that are consistent
with IE but neither fulfill the definite criteria nor fit the rejected criteria (188). The category of
possible IE contributes little to the diagnostic process. In addition, the Duke criteria are more
slanted to the diagnosis subacute disease because of the preponderance of immunological
phenomena in this variety of valvular infection.
Table 10 presents the differential diagnosis of IE.
MIMICS OF ENDOCARDITIS
Many disease processes, both infectious and noninfectious, mimic IE especially the subacute
variety (189). Echocardiography may readily exclude many of these entities. This discussion
will focus on those diseases that mimic IE by damaging cardiac valves, producing valvular
vegetations and producing many of the signs and symptoms of IE (immunological
phenomena, embolic events, and musculoskeletal complaints). Through a variety of
mechanisms, these mimics induce endothelial damage that results in the development of the
sterile platelet/fibrin/thrombus. Most of these disease processes are autoimmune in nature.
They result in quite friable vegetations that have a high rate of embolization. Blood cultures are
sterile in these situations except when the NBTE becomes secondarily infected. IE, which
complicates rheumatoid arthritis and systemic lupus erythematosus (SLE), occurs more
frequently in the setting of renal failure and in those patients who are receiving prednisone or
cyclophosphamide. Many autoimmune disorders such as scleroderma systemic vasculitis lead
to valvular damage. However these diseases usually about associated with thromboembolic
phenomena in and so should not pose a real diagnostic challenge (190,191).
The most effective mimic of all is atrial myxoma. Upto 50% of left atrial myxomas
embolize, most frequently to the central nervous system. Significant fever is documented in
50% of cases. Often the only way to distinguish myxoma from valvular infection is by
microscopic examination of tissue that has been recovered from a peripheral artery embolus or
at the time of cardiac surgery (192). Tables 11 and 12 present the most diagnostically
challenging mimics of endocarditis along with their clinical and laboratory features.
Table 10 Differential Diagnoses
Noninfectious entities
Marantic endocarditis
Antiphospholipid syndrome
Atrial myxoma
Cardiac neoplasms
Polymyalgia rheumatica
Reactive arthritis and Reiter’s syndrome
Systemic lupus erythematosus
Thrombotic nonbacterial endocarc
Temporal arteritis and other forms vasculitis
Cholesterol emboli syndrome
Infectious entities
Lyme disease
Viral hepatitis
Disseminated gonococcal infection/gonococcal arthritis
The presence of a continuous bacteremia differentiates IE from its infectious and noninfectious mimics.
Infective Endocarditis and Its Mimics in Critical Care 237