Page 1429 - Small Animal Internal Medicine, 6th Edition

CHAPTER 87 Disorders of Hemostasis 1401

rapidly, and repeatedly during treatment. This syndrome is function, and inactivation of clotting factors); and (2) why
relatively common in dogs and cats. one of the therapeutic approaches that appears to be benefi-
VetBooks.ir Pathogenesis cial in halting the bleeding in dogs and cats with DIC is to
administer heparin or other anticoagulants paradoxically
Several general mechanisms can lead to the activation of
coagulation, which in turn decreases activation of the fibri-
intravascular coagulation and therefore to the development (i.e., if sufficient AT is available, heparin halts intravascular
of DIC, including the following: nolytic system, thus releasing its inhibitory effect on the
clotting factors and platelet function).
• Endothelial damage In addition to the events just described, impaired tissue
• Platelet activation perfusion results in the development of secondary enhancers
• Release of tissue procoagulants of DIC, including hypoxia; lactic acidosis; hepatic, renal,
and pulmonary dysfunction; and the release of myocardial
Endothelial damage commonly results from electrocu- depressant factor. The function of the mononuclear-
tion or heat stroke, although it may also play a role in sepsis- phagocytic system also is impaired so that FDPs and other
associated DIC. Platelets can be activated by a variety of by-products, as well as bacteria absorbed from the intestine,
stimuli, but mainly they are activated by viral infections (e.g., cannot be cleared from the circulation. These factors also
FIP in cats) or sepsis. Tissue procoagulants (likely TF) are must be dealt with therapeutically (see p. 1403).
released in several common clinical conditions, including The prevalence of primary disorders associated with DIC
trauma, hemolysis, pancreatitis, bacterial infections, acute in 50 dogs and 21 cats evaluated by the author is depicted in
hepatitis, and possibly some neoplasms (e.g., HSA). TF is Table 87.5. Neoplasia (primarily HSA), liver disease, and
ubiquitous and is expressed in almost every cell membrane, immune-mediated blood diseases were the most common
except for inactive or resting endothelial cells; therefore disorders associated with DIC in dogs, whereas liver disease
exposure of any cell membrane to circulating blood activates (primarily hepatic lipidosis), neoplasia (mainly lymphoma),
the extrinsic system. and FIP were the disorders most frequently associated with
The best way to understand the pathophysiologic process DIC in cats.
of DIC is to consider the entire vascular system as a single, In my experience, symptomatic DIC in dogs (i.e., that
giant blood vessel and the pathogenesis of the disorder as an associated with bleeding) is most commonly associated with
exaggeration of the normal hemostatic mechanisms. Once HSA, followed by sepsis, pancreatitis, hemolytic anemia,
the coagulation cascade has been activated in this giant gastric dilation-volvulus, and liver disease. Symptomatic
vessel (i.e., it is widespread within the microvasculature in DIC is extremely rare in cats but hemostatic evidence of DIC
the body), several events take place. Although they are is common, accounting for approximately two thirds of the
described sequentially, most of them actually occur simulta- abnormal hemostatic profiles in this species. As noted, DIC
neously, and the intensity of each varies with time, thus is common in cats with liver disease, hypertrophic cardio-
making for an extremely dynamic process. myopathy, sepsis, malignant neoplasms, or FIP. We have also
First, the primary and secondary hemostatic plugs are observed symptomatic DIC in two cats receiving methima-
formed (see p. 1387). Because this is happening in thousands zole. The pathogenesis of DIC in dogs with HSA appears to
or tens of thousands of small vessels simultaneously, mul- be complex and multifactorial; the major mechanism trig-
tiple thrombi form in the microcirculation. If this process gering intravascular coagulation in dogs with this neoplasm
is left unchecked, ischemia (resulting in MOF) eventually was thought to be the abnormal irregular endothelium in the
develops. During this excessive intravascular coagulation, neoplasm (i.e., exposure to subendothelial collagen and the
platelets are consumed and destroyed in large quantities, activation of coagulation). However, some canine HSAs
leading to thrombocytopenia. Second, the fibrinolytic appear to synthesize a cancer procoagulant because dogs
system is activated systemically, resulting in clot lysis and with small HSAs can have severe DIC, whereas some dogs
the inactivation (or lysis) of clotting factors and impaired with widely disseminated HSA have normal hemostasis.
platelet function. Third, AT, proteins C and S, and other
natural anticoagulant systems are consumed in an attempt Clinical Features
to halt intravascular coagulation, leading to exhaustion of Dogs with DIC can have several clinical presentations; the
these systems. Fourth, the formation of fibrin strands within two common forms are chronic silent (subclinical) and acute
the microcirculation leads to the development of hemolytic (fulminant) DIC. In the chronic silent form, the patient does
anemia and further compounds the thrombocytopenia as not have evidence of spontaneous bleeding, but clinicopath-
the RBCs are sheared by these fibrin strands (i.e., fragmented ologic evaluation of the hemostatic system reveals abnor-
RBCs or schistocytes). malities compatible with this syndrome (see later). This form
When all these events are considered, it is easy to under- of DIC appears to be common in dogs with malignancy and
stand the following: (1) why an animal with multiple organ other chronic disorders. The acute form may represent a true
thrombosis caused by excessive intravascular coagulation acute phenomenon (e.g., after heat stroke, electrocution, or
and the depletion of natural anticoagulants is bleeding spon- acute pancreatitis) or, more commonly, it represents acute
taneously (as a result of thrombocytopenia, impaired platelet decompensation of a chronic silent process (e.g., HSA).