− | As described above, the onset of clinical signs in anticoagulant rodenticide toxicosis is delayed for up to five days while vitamin K dependent factors become depleted, due to the gradual degradation of functional factors already in the circulation. When signs occur, they are related to defective haemostasis and unchecked haemorrhage. Visible signs can include external haematomas, bruising, excessive bleeding from venupuncture sites, epistaxis, haematemesis, haemtotochezia, melaena or haematuria<sup></sup> Symptoms may be non-specific | + | As described above, the onset of clinical signs in anticoagulant rodenticide toxicosis is delayed for up to five days while vitamin K dependent factors become depleted, due to the gradual degradation of functional factors already in the circulation. When signs occur, they are related to defective haemostasis and unchecked haemorrhage although depression and anorexia may be seen before bleeding begins. Visible signs can include external haematomas, bruising, epistaxis, hyphaema, haematemesis, haemtotochezia, melaena, haematuria or excessive bleeding from sites of venupuncture or injury<sup>1-8</sup>. Lameness may also occur if there are haemorrhages into joints. Non-specific symptoms are also possible, related to internal bleeding. Such examples are weakness, ataxia, dyspnoea, abdominal swelling and pallor. |
− | Clinical signs generally reflect some manifestation of hemorrhage, including anemia, hematomas, melena, hemothorax, hyphema, epistaxis, hemoptysis, and hematuria. Signs dependent on hemorrhage, such as weakness, ataxia, colic, and polypnea, may be seen. Depression and anorexia occur in all species even before bleeding occurs.
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