Page 251 - Small Animal Internal Medicine, 6th Edition

CHAPTER 12 Thromboembolic Disease 223

BOX 12.1 and nephrotic syndrome in some animals. Thrombocytosis
alone, without an increase in platelet aggregability, is not
VetBooks.ir Diseases Potentially Associated With Thromboembolism thought to increase the risk for thrombosis. Defective fibri-
nolysis can promote pathologic thrombosis by preventing
Endothelial Disruption
Sepsis efficient breakdown of physiologic clots. This can result from
either reduced levels of fibrinolytic substances (e.g., t-PA,
Systemic inflammatory disease plasminogen, urokinase) or increased production of PAIs;
Heartworm disease the latter is a major mechanism of TE disease in humans
Neoplasia with hypertension. Finally, any severe systemic disease that
Massive trauma progresses to the systemic inflammatory response syn-
Shock
Intravenous catheterization drome (SIRS; e.g., pancreatitis, sepsis, neoplasia, heatstroke,
Injection of irritating substance immune-mediated disease) can lead to gross thrombosis, as
Atherosclerosis well as disseminated intravascular coagulopathy (DIC). DIC
Arteriosclerosis involves massive activation of thrombin and plasmin, with
Hyperhomocysteinemia generalized consumption of coagulation factors and plate-
lets. DIC produces extensive thrombosis and hemorrhage in
Abnormal Blood Flow the microcirculation, resulting in widespread tissue ischemia
Vascular obstruction (e.g., mass lesion, adult heartworms, and multiorgan failure (see p. 1400).
catheter or other device) The most common, although not the only, cause of TE
Heart disease (especially cardiomyopathy in cats) disease in cats is myocardial disease (see Chapter 8). Cats
Cardiovascular neoplasia with cardiomyopathy are at risk for intracardiac thrombus
Endocarditis
Shock formation and subsequent arterial embolization. Mecha-
Hypovolemia/dehydration nisms involved include poor intracardiac blood flow and
Prolonged recumbency blood stasis, especially within an enlarged left atrium (LA).
Hyperviscosity (e.g., polycythemia, leukemia, Cats with HCM have increased platelet expression of
hyperglobulinemia) P-selectin and platelet-endothelial cell adhesion molecules,
Hypoviscosity (anemia) as well as increased plasma concentrations of fibrinogen,
Anatomic abnormality (e.g., aneurysm, AV fistula) thrombin-antithrombin-complex, and D-dimers, suggesting
a possible role for systemic hypercoagulability as well. Addi-
Increased Coagulability tionally, abnormal turbulence from mitral regurgitation or
Glomerular disease/protein-losing nephropathy dynamic outflow tract obstruction could be a factor. Some
Hyperadrenocorticism cats with TE disease have decreased plasma arginine and
Immune-mediated hemolytic anemia (±thrombocytopenia)
Pancreatitis vitamin B 6 and B 12 concentrations; hyperhomocysteinemia
Protein-losing enteropathy might be a factor in some cases. Hyperhomocysteinemia and
Sepsis/infection low plasma vitamin B concentrations are risk factors for
Neoplasia thromboembolism in people. It is not known if hypercoagu-
Disseminated intravascular coagulation lability induced by a genetic abnormality exists in some cats,
Heart disease as it does in people.
Three common systemic diseases associated with TE
disease in dogs are protein-losing nephropathy, immune-
mediated hemolytic anemia (IMHA), and hyperadreno-
walls. Poor flow also can promote local tissue hypoxia and corticism. Protein-losing nephropathy (resulting from
endothelial injury. Abnormal turbulence has also been asso- glomerulonephritis, renal amyloid deposition, or hyperten-
ciated with thrombus formation because it can mechanically sive injury) can lead to marked AT deficiency. Because of
injure the endothelial surface. its small size, AT is lost through damaged glomeruli more
Hypercoagulability can develop secondary to various sys- easily than most procoagulant proteins, which predisposes
temic diseases in dogs and cats. Multiple mechanisms are to thrombosis. Protein-losing enteropathies also cause AT
thought to be involved. AT deficiency is a common cause deficiency, but concurrent loss of larger proteins tends to
of hypercoagulability. Excessive loss, increased consump- maintain a balance between procoagulant and anticoagulant
tion, or possibly inadequate hepatic synthesis all can lead factors. Other factors also could contribute to TE disease in
to AT deficiency. Decreased protein C activity and other animals with protein-losing nephropathies, such as increased
mechanisms (including hyperfibrinogenemia and increases platelet aggregation secondary to hypoalbuminemia.
in factors II, V, VII, VIII, IX, X, or XII) also can contrib- Thrombosis associated with IMHA also is thought to be
ute to hypercoagulability. Increased platelet aggregability, multifactorial, with the systemic inflammatory (immune-
another mechanism of hypercoagulability, has been associ- mediated) response playing a large role. Thrombocytopenia,
ated with neoplasia, some heart diseases (including hyper- hyperbilirubinemia, and hypoalbuminemia have been iden-
trophic cardiomyopathy [HCM] in cats), diabetes mellitus, tified as risk factors for TE disease. The role of high-dose