the conduction system of the heart. Multiple myocardial abscesses are seen primarily in
S. aureusIE (20% of fatal cases). These may erode into the pericardial sack resulting in fatal
cardiac tamponade (128). They may also erode into the intraventricular septum leading to
perforation and a left to right shunt. Pericarditis may be the result of erosion of a
myocardial or ring abscess into the pericardial space or by deposition of organisms during
the BSI. Rarely, it is secondary to a septic coronary artery embolus or rupture of a mycotic
aneurysm.
Septic arterial embolization is the second most common complication of IE (35%–50% of
cases). Unlike those of subacute disease, they produce metastatic infection. These are more
frequently seen younger patients, in left -sided disease and in PVE.Candidaspp.,S. aureus,H.
influenzae,Aspergillus spp., and group B streptococci. For example, the right-sided septic
emboli ofS. aureusIVDA IE, produce many small pulmonary abscesses and infarcts. These
vegetations may embolize up to 12 months after microbiological care of the valvular infection.
Left-sided emboli commonly travel to the spleen, brain, kidneys, coronary arteries, and
meninges. Cerebral emboli and have been traditionally estimated to occur in 30% of cases of
acute and subacute IE. It appears that when MRI and cerebrospinal fluid analysis were used to
study of the rate of cerebrovascular complications in patients with left-sided IE, the incidence
of brain damage was much higher than previously appreciated, approximately 65%. Cases
were approximately split evenly between symptomatic and asymptomatic (129). The middle
cerebral artery is the most frequently involved. Coronary artery emboli are detected at autopsy
in 40% to 60% of cases. They are usually clinically unimportant and infrequently produce any
significant changes in the patient’s electrocardiogram.
Splenic abscesses and infarcts that result from septic emboli may be the source of
persistent bacteremia despite successful treatment of the valvular infection itself (130).
Abscesses and infarcts of the spleen may have very similar presentations. These include left
upper quadrant abdominal pain, back and pleuritic pain, and fever. Despite advanced imaging
techniques (MRI, CT scan, and ultrasonography), splenic aspiration may be the only way to
distinguish the two.
Table 8 presents, by organ system, the clinical manifestations of NVIE. It is important to
note that the distinction between the two types of IE has become blurred because of the use of
antibiotics to treat unrecognized IE. Such misdirection of antibiotic therapy suppresses the
growth of bacteria with the thrombus and so diminishes many of the clinical abnormalities of
IE, the state of “muted endocarditis.” Under such circumstances, the diagnosis of IE is often
delayed or missed completely.
Prosthetic Valve Endocarditis
It is clinically useful to describe cases of be the into early, intermediate, and late since the
profile of infecting organisms reflects primarily the site and timing of their acquisition
(131,132). Early PVE extends through three months past the time of implantation; intermediate
3 to 12 months and late after 12 months. CoNS dominates in the early and intermediate stages.
The health care environment (operating world, recovery room, intravascular lines) is the
source of the organisms of early PVE that produces infection with diphtheroids,S. aureus
CoNS, and fungi. The pathogens that are involved in late PVE resemble closely those found in
NVIE (Table 2).
The clinical features of PVE generally are quite similar to those of NVIE. There are
notable exceptions. If PVE begins within a few weeks of valve placement, its presence may be
obscured by the more common surgical infections such as pneumonia or wound infections.
Early PVE, due toS. aureus, may present as septic shock if an overwhelming paravalvular
abscess develops. This deep-seated extension of the valvular infection can lead to calculate
incompetence, conduction disturbances, and septic emboli (133). Ten percent of mechanical
PVE are complicated by thrombosis of the valve outlet. Forty percent of cases are complicated
by arterial emboli. There is a high rate of cerebral emboli within the first three days ofS. aureus
early PVE (134). Because PVE is superimposed on previously damaged hearts, congestive heart
failure appears earlier and is more severe than that of NVIE.
Late PVE most frequently follows a subacute or chronic course. There is a high rate of
peripheral stigmata of valvular infection such as the skin and changes as well as the presence
Infective Endocarditis and Its Mimics in Critical Care 229