Coagulation abnormalities are commonly encountered in critical illness. Traditionally, clinically relevant coagulation disorders
have consisted mostly of bleeding associated with advanced stages of disseminated intravascular coagulation or toxin ingestion.
However, advances in critical care have highlighted hypercoagulability as a clinically relevant state that must be recognized
and treated to optimize the chances of a positive outcome.
Systemic inflammation is a potent trigger of coagulation, mainly through cytokine-mediated tissue factor expression on the
surface of both activated inflammatory cells and the damaged vascular endothelium. Endogenous anticoagulant systems such as
protein C, antithrombin, and tissue factor pathway inhibitor are simultaneously activated to control coagulation but are ultimately
overwhelmed when severe systemic inflammation predominates, leading to fibrin deposition in the microvasculature and reduced
oxygen delivery to capillary beds. This clinically silent phenomenon may be identifiable by a mildly reduced platelet count
on the CBC.
Diseases associated with severe inflammation include sepsis, pancreatitis, burn injury, polytrauma, and immune mediated hemolytic
anemia In addition prolonged immobility, mechanical ventilation, and recent major surgery or episodes of cardiovascular
instability also stimulate inflammation and can therefore be associated with a hypercoagulable tendency. In general, hypercoagulability
should be suspected in any critically ill animal with mild thrombocytopenia. Due to the small time period making up the normal
range for coagulation testing, a shortened PT and aPTT is not considered helpful for the diagnosis of hypercoagulability.
Fibrin(ogen) degradation products detect the breakdown of both fibrin and fibrinogen, and are therefore not very sensitive
indicators that coagulation has occurred. The D-dimer test, however, specifically detects the breakdown of crosslinked fibrin,
and is superior to FDPs in suggesting that coagulation has been activated. In general, a hypercoagulable state is considered
less likely if D-dimers are negative. A positive test, however, may or may not support excessive coagulation. Finally, thromboelastography
is gaining popularity for the detection of hypercoagulability in veterinary medicine. Changes in thromboelastogram consistent
with a hypercoagulable state include shortened R time, increased angle, and increased MA.
Evidence for thromboembolism in animals with naturally occurring disease is present in veterinary literature, mostly in the
form of isolated case reports and retrospective studies. In a necropsy study of 29 dogs with pulmonary thromboembolism (PTE),
neoplasia, systemic bacterial infection and immune mediated hemolytic anemia were the most common diagnoses associated with
PTE. Thromboembolism was suspected in 11 of 17 dogs showing respiratory signs, because of the concurrent presence of a disease
known to be associated with a hypercoagulable state. In this study, thrombosis was noted in organs other than the lung in
31% of cases. In another study, 54% of dogs with splenic vein thrombosis had neoplasia, while 43% were receiving exogenous
corticosteroids. Other diseases associated with splenic thrombus formation included immune mediated disease, SIRS, pancreatitis,
non-proteinuric renal failure, and protein losing nephropathy. Portal vein thrombosis is another common site of thrombus formation.
A retrospective study of 6 cats found that all cats with PVT also had hepatic disease. Concurrent diseases associated with
PVT included congenital portosystemic shunt formation, hepatic neoplasia, and acute pancreatitis. In one study of PVT in dogs,
concurrent conditions included pancreatic necrosis, peritonitis, neoplasia, and exogenous corticosteroid administration. Ultimately,
the awareness of thromboembolism as a complication of disease processes has evolved, and as a result clinicians are faced
with the decision of whether or not to initiate anticoagulant therapy.