Page 161 - Small Animal Internal Medicine, 6th Edition

CHAPTER 6 Acquired Valvular and Endocardial Disease 133

surface. Nonseptic (so-called “bland”) emboli can break off with endocarditis have evidence of past or concurrent infec-
from such vegetations and cause infarctions elsewhere. Sub- tion, a clear history of predisposing factors often is absent.
VetBooks.ir sequent bacteremia can cause a secondary infective endocar- Possible relationship between severe periodontal disease and
risk of endocarditis is unclear; small breeds of dog, which
ditis too.
Valve damage generally causes progressively worsening
CMVD, have a low prevalence of endocarditis. Neutropenic
valve regurgitation with secondary volume overload. Signs often are affected with severe periodontal disease and
of CHF can develop acutely or gradually, depending on the and otherwise immunocompromised animals may be at
extent and progression of valve damage, and whether both greater risk for endocarditis.
mitral and aortic valves or other predisposing factors are The combination of fever, lameness, and a cardiac murmur
involved. LV diastolic and LA pressures can rise relatively (especially if new, altered in quality, or diastolic in timing)
quickly, leading to rapid onset of pulmonary edema. Aortic should strongly raise suspicion of infective endocarditis.
endocarditis, especially, is likely to cause acute CHF and Nevertheless, the clinical signs of endocarditis are variable
fulminant pulmonary edema. Left heart dilation can be and relate to the underlying infection, immune-mediated
minimal when disease progression is rapid or multiple valves effects, TE events, and progressive valvular or myocardial
are involved. In the few cases where vegetative lesions also dysfunction. The presenting signs can result from left-
cause valve stenosis, cardiac workload and risk of CHF are sided CHF or arrhythmias; however, cardiac signs often are
further increased. overshadowed by signs of systemic infarction, infection,
Cardiac function can be compromised by myocardial immune-mediated disease (including polyarthritis), or a
injury resulting from coronary arterial embolization causing combination of these. Nonspecific signs of lameness or stiff-
myocardial infarction and abscess formation, or from direct ness (possibly shifting from one limb to another), lethargy,
extension of the infection into the myocardium. Reduced trembling, recurrent fever, weight loss, inappetence, vomit-
contractility and atrial or ventricular tachyarrhythmias often ing, diarrhea, and weakness may be the predominant com-
result. Aortic valve endocarditis lesions may extend into the plaints. A majority of cases with bacterial endocarditis are
AV node and cause partial or complete AV block. Arrhyth- febrile or have waxing/waning temperature spikes, although
mias can cause weakness, syncope, and sudden death or some are normothermic (especially those with Bartonella
contribute to the development of CHF. endocarditis). Palpable joint effusion may be present. A
Fragments of vegetative lesions often break loose. Embo- cardiac murmur is heard in most dogs with endocarditis,
lization of other body sites can cause infarction or metastatic although an audible murmur can be absent if the endocarditis
infection, which results in diverse clinical signs. Larger and lesions have caused only minimal or no valve regurgitation.
more mobile vegetations (based on echocardiographic Murmur characteristics depend on the valve involved. Ven-
appearance) are associated with a higher incidence of tricular tachyarrhythmias are common, but supraventricular
embolic events in people and, presumably, also in animals. tachyarrhythmias or AV block (especially with aortic valve
Emboli can be septic or bland (noninfective). Septic arthritis, infection) also occur. Infective endocarditis often mimics
diskospondylitis, urinary tract infections, and renal and immune-mediated disease. Dogs with endocarditis are com-
splenic infarctions are common in affected animals. Local monly evaluated for a “fever of unknown origin.” Some of
abscess formation resulting from septic thromboemboli con- the consequences of infectious endocarditis are outlined in
tributes to recurrent bacteremia and fever. Hypertrophic Box 6.3.
osteopathy has also been associated with bacterial endocar- Signs of CHF in an unexpected clinical setting or in an
ditis. Circulating immune complexes and cell-mediated animal with a murmur of recent onset may herald infective
responses contribute to the disease syndrome. Sterile poly- valve damage, especially if other suggestive signs are present.
arthritis, glomerulonephritis, vasculitis, and other forms of However, a “new” murmur can be a manifestation of nonin-
immune-mediated organ damage are common. fective acquired disease (e.g., CMVD, cardiomyopathy), a
previously undiagnosed congenital disease, or physiologic
Clinical Features alterations (e.g., fever, anemia). Conversely, endocarditis
The prevalence of bacterial endocarditis is low in dogs (esti- may develop in an animal known to have a murmur caused
mates range widely from 0.05% to over 6%) and even lower by another cardiac disease. Although a change in murmur
in cats. Most reports suggest larger (>15 kg) dogs are at quality or intensity over a short time frame may indicate
greater risk, although middle-aged medium-breed dogs active valve damage, physiologic causes of murmur variation
sometimes are affected. German Shepherd Dogs and possi- are common. The onset of a diastolic murmur at the left heart
bly Boxers, Golden Retrievers, and Labrador Retrievers base is suspicious for aortic valve endocarditis, especially if
might be overrepresented. Male dogs are affected more com- fever or other signs are present.
monly than females.
Either the aortic or the mitral valve is involved in virtually Diagnosis
all cases; the prevalence of mitral endocarditis may be slightly It can be difficult to establish a definitive antemortem diag-
greater than that of aortic endocarditis. Both valves are nosis. Presumptive diagnosis of infective endocarditis is
affected in some cases. Subaortic stenosis is a known risk made based on two or more positive blood cultures (or posi-
factor for aortic valve endocarditis. Although some animals tive Bartonella testing; see Chapter 94), in addition to either