BASICS
- Results in hemostatic dysfunction and subsequent bleeding tendencies
- They may be classified as:
- Disorders that impair fibrin clot formation, known as coagulation defects
- Disorders that impair platelet plug formation due to platelet function deficiencies (e.g. idiopathic thrombocytopenia, thrombasthenia, antiplatelet drug administration) or endothelial damage (e.g. vasculitis)
- Disorders in which primary hemostasis and coagulation factor pathways are inadequate due to a consumptive coagulopathy (e.g. DIC)
- Vitamin K is essential for hepatic synthesis of several coagulation factors (II, VII, IX, and X) and protein C
- Vitamin K deficiency results in a gradual decrease of circulating coagulation factors, causing progressive coagulation impairment and unexpected bleeding
- The rate of decrease in coagulation factor concentrations depends on their half-lives. Factor VII has the shortest half-life (<6–7 h) and its concentration decreases rapidly, affecting the extrinsic coagulation pathway and prolonging PT. As the condition progresses, concentrations of other coagulation factors decrease, affecting also the intrinsic pathway and prolonging aPTT
- In cases of hepatic failure, a coagulation defect occurs as a result of a decrease in coagulation factor synthesis, especially fibrinogen and the vitamin K-dependent factors
- An acquired coagulation factor VIII (hemophilia A) deficiency was recently reported in a mare with hematomas, hemoabdomen, and blood loss anemia. The development of anti-factor VIII antibodies was considered idiopathic. The mare responded to transfusions of fresh whole blood and plasma and immunosuppressive treatment
- Hemic/lymphatic/immune—coagulation deficiencies are associated with prolonged bleeding after wounds/trauma or spontaneous hemorrhages
- Other systems may be affected, depending on the sites of hemorrhage. The most frequently affected systems are the musculoskeletal, respiratory, and GI systems
- Vitamin K deficiency in horses is very rare. However, toxicosis caused by ingestion of moldy sweet clover (Melilotus officinalis) hay has been reported
- Anticoagulant toxicosis is rare now because warfarin administration is currently not recommended in horses, and heparin administration is restricted to patients receiving critical care
- Abnormal coagulation is common in horses (up to 50%) with hepatic disease
- Historical findings depend on etiology
- Clinical signs of acquired coagulation defects are similar to those of the hemorrhagic form of DIC, but must be differentiated in order to institute appropriate therapy
- Excessive hemorrhage after minor trauma or surgery
- Unexplained epistaxis or other mucosal bleeding
- Previous exposure to moldy sweet clover hay or rodenticides
- Previous anticoagulant administration
- Characterized by spontaneous bleeding from body orifices or into body cavities and hematoma formation
- The most common signs associated with spontaneous hemorrhage include SC or IM hematomas, hemarthrosis, epistaxis, hematuria, melena, and ecchymoses in mucous membranes
- Prolonged bleeding from wounds or after minor surgical procedures possible
- Usually, there are no petechial hemorrhages in mucous membranes. This may be used to distinguish this condition from a primary hemostatic deficiency (e.g. platelet disorder) and DIC. In cases of DIC, other clinical signs associated with the underlying disease are also observed
- The most common causes of vitamin K deficiency are:
- Ingestion of moldy sweet clover (Melilotus spp.); fresh, in hay or in silage
- Ingestion of plants containing coumarine glycosides—ferns, some pines, and the Mediterranean plant Ferula communis
- Accidental ingestion of rodenticides containing first- or second-generation anticoagulants
- Chronic intestinal malabsorption problems that decrease vitamin K absorption
- Hepatic failure
- Anticoagulants used in equine medicine that may cause a coagulation deficiency disorder are:
- Warfarin, which has previously been advocated as an oral anticoagulant for use in horses (no longer recommended)
- Heparin (unfractionated and LMWH), which is recommended for treatment of endotoxemia
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS