Pearls

  • Disorders of PRIMARY hemostasis (platelets, von Willebrand factor, blood vessels) result in superficial hemorrhages involving skin and mucosal surfaces. Petechial, purpural, and sometimes ecchymotic hemorrhages are hallmarks of vascular or platelet disorders. With routine surgery, persistent oozing from skin incisions and small/non-ligated vessels can occur from the time of the initial skin incision. Normal daily functions can result in epistaxis, oral and ocular hemorrhages, melena, hematochezia, hematuria, etc. Trauma superimposed on disorders of primary hemostasis can result in larger hematoma formation mimicking disorders of secondary hemostasis.
  • Disorders of SECONDARY hemostasis (coagulation factor deficiency, inhibitors, or antagonists) are more likely to result in large spreading hematomas, hemarthrosis, and bleeding into body cavities. With routine surgery, delayed severe bleeding can occur (often a problem is not noted until a WHITE animal is found in the cage following the procedure).
  • The FIRST thing to do in the laboratory assessment of a bleeding patient (a good history and physical examination may already point you in the right direction) is a CBC. In veterinary medicine, thrombocytopenia is the single most common cause of bleeding and this is easily identified by doing a CBC and evaluating the peripheral blood smear. Fewer than 2-3 platelets per 100X oil field (< 50 x 109/L platelets) can result in spontaneous superficial bleeding.
  • Particularly in dogs, thrombocytopenia is often immune-mediated. Bone marrow examination is indicated if response to immunosuppressive therapy is poor or if other underlying disease is suspected. If peripheral destruction of platelets is occurring, megakaryocytic hyperplasia should be seen on bone marrow examination, provided sufficient time has passed for this response.
  • If thrombocytopenia is chronic and waxing and waning, iron deficiency anemia may be a significant finding on the hemogram.
  • If platelet numbers are normal, but a disorder of primary hemostasis is still suspected (vWD, NSAID-effect, etc.), a BMBT can be done. If prolonged, then consider a platelet function defect or vWD (extrinsic to the platelet). vWF can then be measured or other tests of platelet function (e.g. platelet aggregation, etc.) performed. If the BMBT is normal, reassess the history and clinical findings. Local disease can sometimes mimic a disorder of primary hemostasis (e.g. nasal tumor resulting in epistaxis).
  • If history and findings suggest a disorder of secondary hemostasis (coagulopathy), then coagulation screening tests should be done. The activated clotting time (ACT) can be done in house and is basically a crude PTT, which measures the intrinsic and common coagulation pathways. The ACT is unaffected by even extremely low platelet numbers. Where PTT will detect a factor deficiency at <30% of activity, the ACT detects deficiency only at <10% of activity.
  • Prolongation of the intrinsic pathway (PTT) means there is a deficiency, inhibitor, or antagonist of one or more of the contact factors (prekallikrein, HMWK, FXII), FXI, FIX, or FVIII, provided the prothrombin time (PT) is normal (indicating that FVII and the common pathway are not affected). Spontaneous bleeding due to a contact factor deficiency is RARE, so a bleeding animal with abnormal PTT and normal PT, most likely has a problem with FVIII, IX or XI. Individual factor assays are then required if a congenital factor deficiency is suspected based on preliminary testing, history, age, sex etc.
  • Prolongation of the PT with a normal PTT means there is a problem with factor VII. The most common cause is very early vitamin K antagonism with rodenticide poisoning or coumarin toxicity. Of the 4 factors affected by these toxicities, FVII has the shortest half-life and is therefore affected first. Congenital FVII deficiency is rare.
  • Generally, by the time animals with rodenticide or coumarin toxicity are presented, FII, FVII, FIX, and FX are all affected, causing the intrinsic, extrinsic and common pathways to be inhibited; PTT and PT will both be prolonged at this stage.
  • The other main cause of prolongation of both pathways is DIC&F.
  • If DIC&F is suspected, look at the CBC for other indicators such as, thrombocytopenia (consumption), anemia, schizocytes and keratocytes (fibrin strand injury to RBCs). Fibrin/fibrinogen degradation products (FDPs) can be measured to help support the diagnosis. If available and validated for use in the species of interest, a D-dimer test would also be useful.
  • A serious underlying disease is preliminary to the development of DIC&F. Examples are heatstroke, neoplasia, severe inflammatory disease, sepsis, immune-mediated hemolytic anemia, etc. Look for a cause if you diagnosis DIC&F; it is not a primary condition.
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Veterinary Clinical Pathology: An Introduction Copyright © by Marion Jackson; Beverly Kidney; and Nicole Fernandez is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, except where otherwise noted.

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