Hemostatic disorders usually manifest as excessive hemorrhage in animals, however certain hemostatic disorders, such as disseminated intravascular coagulation (DIC), are characterized by thrombosis more than hemorrhage, particularly in horses and cats. Historical details and signalment are important when evaluating an animal with a suspected hemostatic disorder. Recurrent clinical signs, particularly in a young animal, are highly suggestive of an inherited defect whereas a sudden onset in an older animal is more likely to be secondary to an acquired defect, associated with underlying disease or drug administration. Certain breeds are known to have inherited defects in hemostasis and this should be considered in a young animal with clinical signs suggestive of a hemostatic disorder.
Disorders in primary and secondary hemostasis and accelerated fibrinolysis can result in excessive hemorrhage. In animals that present with excessive hemorrhage, the site and nature of the hemorrhage can be helpful in determining which hemostatic pathway is defective.
- Primary hemostasis: Typical signs are hemorrhage from mucosal surfaces (epistaxis, hematuria, melena), petechiae (pinpoint hemorrhages), purpura (larger than petechiae) and ecchymoses (bruise or larger areas of hemorrhage).
Note: Petechiae are rarely seen in vWD. Also, the definition of purpura varies depending on who you read. Some medical dictionaries use it as a generic term to encompass petechiae and ecchymoses. Other sources use it to define hemorrhages that are a size between petechiae (< 3mm) and ecchymoses (>1 cm), e.g. Wikipedia.
- Secondary hemostasis: Typical signs are ecchymoses, hematomas and bleeding into body cavities, including joints.
The severity of the defect also affects the type of hemorrhage that occurs. Severe defects in primary hemostasis can result in intra-cavity hemorrhage and hematomas, just like secondary hemostatic disorders.
Thrombosis can be more clinically important than hemorrhage because it causes hypoxic injury to vital organs (liver, kidney) and can result in organ dysfunction, failure and even death. Unfortunately, thrombosis is very difficult to diagnosis based on current laboratory or imaging modalities. Indeed, thrombosis may only manifest as developing or worsening organ function, e.g. azotemia with renal thrombosis, dyspnea with pulmonary thromboembolism.
Thrombosis results from the following three abnormalities (called Virchow’s triad):
- Endothelial injury
- Alterations in blood flow: This could be due to turbulence or stasis, however stasis is thought to be more important for initiating thrombosis, e.g. stasis of blood within an enlarged right atrium is thought to result in atrial thrombosis with subsequent aortic thromboembolism in cats with cardiomyopathy.
- Hypercoagulability: This is defined as an abnormally activated hemostatic system that predisposes a patient to thrombosis. This can result from:
- Hyperfunctional platelets
- Activation of coagulation, with generation of excessive thrombin
- Deficiency of inhibitors
Hypercoagulability is a characteristic feature of DIC and occurs in conditions known to initiate DIC in animals, including severe inflammation, sepsis cancer, and IMHA (dogs), and gastrointestinal disorders associated with endotoxemia (e.g. strangulating obstructions, colitis in horses).