Page 299 - Feline Cardiology

Chapter 20: Arterial Thromboembolism 307

nicity in some cats cannot be ruled out (Smith and 18% with dilated cardiomyopathy (Ferasin 2003; Sisson
Tobias 2004). Therefore, feline cardiogenic ATE is a mul- et al. 1991). The prevalence tends to be higher in nec-
tifactorial process, with the most important factor being ropsy based reports (up to 48% of HCM cats).
blood flow stasis associated with dilated left atrium; In the general feline population, the reported preva-
other contributing factors such as endothelial damage lence has ranged from 1 in 142 (Buchanan et al. 1966)
or hypercoagulability may be involved to a lesser extent. to 1 in 175 cats evaluated (Smith et al. 2003).
Gross Pathology
SIGNALMENT
In general, arterial thrombi are composed primary of
platelets and fibrin because the rapid intravascular blood Male cats have been reported to be overrepresented, but
flow tends to exclude erythrocytes. Consequently, they one study suggests they are at increased risk for HCM
are most often pale beige or gray in appearance. However, or hypertrophic obstructive cardiomyopathy (HOCM)
red blood cells are often enmeshed in saddle thrombi and rather than specifically for ATE (Smith et al. 2003). The
they can therefore have a reddish appearance. This is in age of affected cats ranged from 1 to 20 years with a
contrast to postmortem clots, which tend to be red, soft, mean of 7.7 years and a median of 10.5 years (Laste and
and gelatinous (or the appearance of a “chicken fat clot” Harpster 1995).
secondary to settling of erythrocytes leaving a yellow,
gelatinous layer on the surface of the clot) (Mosier 2007). HISTORY AND CHIEF COMPLAINT
The lack of an adequate blood supply to the hindlimbs
results in coagulative necrosis, in which tissue architec- Most cats presenting for ATE have underlying heart
ture is maintained because lysosomal enzymes are dena- disease; however, clinical manifestations often are absent
tured and do not cause proteolysis of tissues. Grossly prior to the ATE event (Smith et al. 2003). Thus, the
affected muscle appears paler than surrounding well vas- thromboembolic event is often the first overt sign of Arterial Thromboembolism
cularized tissue and it will be dry on the cut surface. heart disease in a subset of cats. The site of cardiogenic
Because muscle cells are labile and undergo mitosis, they embolization varies, but the distal aorta (“saddle
will replicate following the insult and will help reform embolus”) is the most common site, representing 71%
the tissue. of the cases in one large study (Smith et al. 2003).
It is important to consider other possible sites of embo- Historically, it was believed that the right brachial artery
lism and underlying inciting factors. A 17-year, retrospec- was more likely to be obstructed than the left brachial
tive study at the University of Pennsylvania veterinary artery (Bond 2005). However, a larger objective study
school, which analyzed records from cats evaluated showed the frequency of involvement was similar
through the necropsy service from 1986 to 2003, found between the right and left forelegs (Smith et al. 2003).
that out of 3400 feline necropsies, 131 cats had throm- Less commonly, various abdominal organs can be embo-
boembolic disease as a major factor contributing to their lized. The location of the occlusion is dependent on the
illness or death (3.9%). Seventy of these cats had saddle size of the embolus as well as the vascular anatomy.
emboli associated with heart disease. Thirty-eight cats Affected cats can present a variety of initial signs
had thromboemboli in other arteries and/or veins associ- depending on the site of embolization, the duration of
ated with the following: cardiac disease (n = 2), neoplasia occlusion, and the degree of functional collateral circu-
(n = 9), multisystemic inflammation/sepsis (n = 12), lation. Distal arterial embolization affecting the limb(s)
chronic tubulointerstitial nephritis (n = 4), undeter- usually results in peracute signs of paresis (Figures 20.2,
mined (n = 6), hyperthyroidism (n = 3), pericardial/ 20.3), vocalization, and pain. Many animals present with
diaphragmatic hernia or trauma (n = 2) (Van Winkle concurrent congestive heart failure (CHF) with typical
2010). clinical signs (dyspnea, tachypnea, etc.). Radiographic
evidence of CHF has been reported to range from 40–
Prevalence 66% in cats affected with ATE (Smith and Tobias 2004).
When cardiogenic emboli develop in cats they result in A murmur, gallop heart sound, or arrhythmia may lend
significant morbidity and mortality. Most clinical studies additional support to a diagnosis of cardiogenic throm-
have reported incidences of arterial thromboembolism boembolism, although many cats (39%) have normal
ranging from 12 to 28% of cats with heart disease. auscultation findings (Laste and Harpster 1995).
Specifically, reported percentages of cats that develop Therefore, one cannot rule out underlying heart disease
ATE with the various cardiomyopathy ranges from 56% based on a normal auscultation. Additionally, ausculta-
with restrictive cardiomyopathy (Stalis et al. 1995), 12– tion of abnormal sounds may be obscured by respira-
17% with HCM (Rush et al. 2002; Atkins et al. 1992), tory noise or vocalization secondary to pain.