Interpretation summary

The tables below provide a general summary of interpretation of platelet count results (degree of thrombocytopenia can provide information on mechanism, and thus cause, of thrombocytopenia) and screening coagulation panel results. Note, only common diseases are listed (not all possibilities are covered. See also the algorithm for an approach to diagnostic testing for an animal with a suspected bleeding disorder.

Degree of thrombocytopenia

**How degree of thrombocytopenia can guide identification of mechanism (and cause)**
Mechanism	Degree*
Decreased production: Expect megakaryocytic hypoplasia or aplasia, no increase in reticulated platelets (if done), platelet size may be variable (may be large if production is abnormal). Immune-mediated: Dog > cat Infectious agents: Bacteria (e.g. Ehrlichia canis), viruses (e.g. feline leukemia virus, canine distemper virus, parvovirus) Drugs: Direct cytotoxicity or immune-mediated Neoplasia: Crowding out of normal cells (myelophthisis), competition for nutrients, altered microenvironment, immune-mediated, defective production (e.g. acute leukemia, myelodysplastic syndrome, multiple myeloma), consumption (histiocytic sarcoma) Bone marrow necrosis: Secondary to drugs, hypoxic injury, neoplasia, toxins	Mild to severe (usually moderate to severe)
Increased clearance (destruction): Expect megakaryocytic hyperplasia, may or may not see increased numbers of reticulated platelets, may or may not see large platelets (or have a high MPV) Immune-mediated Primary (ITP): Isolated thrombocytopenia (common; dog>cat) Neonatal thrombocytopenic purpura Secondary (common): Infectious agents (e.g. Anaplasma, Ehrlichia, Rocky mountain spotted fever, Borrelia, Babesia, Leishmania, canine distemper virus), neoplasia (e.g. lymphoma in dogs), drugs (e.g. sulphonamides in dogs, methimazole and propylthiouracil in cats), post-transfusion purpura, clearance by over-reactive histiocytes (which can be secondary to various infectious or neoplastic diseases), immune-mediated disorders (e.g. SLE) Non immune-mediated: Consumption by neoplastic (e.g. histiocytic sarcoma).	Moderate to severe (usually severe) with primary ITP, mild to moderate with secondary or non-immune mediated disorders
Increased use (consumption): Expect megakaryocytic hyperplasia, may or may not see increased numbers of reticulated platelets, may or may not see large platelets (or have a high MPV) Activation with subsequent aggregation: This can occur in animals with or without clinical or laboratory evidence of DIC, e.g. secondary to drugs (protamine sulphate), snake venoms, inflammation (heat stroke, pancreatitis, vasculitis), infectious agents (bacterial sepsis, feline infectious peritonitis virus, Babesia), neoplasia (e.g. hemangiosarcoma) Secondary to excessive activation of hemostasis: Disseminated intravascular coagulation	Mild to moderate (infrequently severe)
Sequestration/redistribution: Since frequently transient, may not see a bone marrow response (i.e. no megakaryocytic hyperplasia) Splenomegaly of any cause (e.g. vascular engorgement, altered blood flow due to infiltrates, sedative or anesthetic agents, hypothermia) Pulmonary circulation: Secondary to sepsis, endotoxemia	Mild to moderate, usually transient (unlikely to see clinically) unless persistent splenomegaly
Loss: Since this mechanism is usually seen with acute severe hemorrhage, a bone marrow response may not be evident. With time, the bone marrow should respond to the thrombocytopenia. Massive severe hemorrhage, e.g. trauma, anticoagulant rodenticide toxicity, may result in thrombocytopenia. Other mechanisms may be operative, such as trauma-associated DIC or consumption. *Hemorrhage is usually a consequence than a cause of severe thrombocytopenia.*	Mild to moderate
* In all species other than the horse: Mild: 100-200 x 10³/μl, moderate: 30-100 x 10³/μl, severe: <30 x 10³/μl; Horse: Mild: 70-100 x 10³/μl, Moderate: 30-70 x 10³/μl, severe: <30 x 10³/μl

Table reproduced and modified with permission from the BSAVA Manual of Canine and Feline Clinical Pathology, 3rd edition.

Screening coagulation panels

**Interpretation of screening coagulation profiles (secondary hemostasis)**
PT	APTT	TCT	Location of defect	Associated disorders	Notes
Normal	Normal	Normal	Likely not a disorder of secondary hemostasis	vWD, thrombopathia, Scott syndrome, fibrinolytic defects, hypercoagulable syndromes (e.g. non-overt DIC)	Some secondary hemostatic defects, e.g. mild hemophilia A, may be missed if non-optimized screening tests are used. Normal screening coagulation results do not rule out a hemostatic disorder
↑	Normal	Normal	Extrinsic pathway (factor VII)	Inherited factor VII deficiency, early vitamin K deficiency or antagonism, DIC, warfarin treatment, liver disease (cholestatic, liver failure)	A prolonged PT in isolation supports factor VII deficiency (tissue factor is part of the reagent in the PT assay)
Normal	↑	Normal	Intrinsic pathway (deficient factors XII, XI, IX, VIII)	Inherited deficiencies, DIC, liver disease, unfractionated heparin therapy, artifact of collection	The APTT is more sensitive to collection artifact than the PT. Times can be prolonged or shortened with poor venipuncture technique
Normal	Normal	↑	Hypofibrinogenemia or dysfibrinogemia	Isolated fibrinogen production defect, inhibitors of fibrin polymerization (high FDP, paraproteins), inherited fibrinogen disorder	This is an unusual result, although the TCT is more sensitive to isolated hypofibrinogenemia than the APTT or PT (with the assays used at Cornell University). Usually, causes of hypofibrinogenemia (DIC, liver failure) will result in additional factor deficiencies and prolong the PT and/or APTT
↑	↑	N	Common pathway (Factors X, V, II) or defects in intrinsic and extrinsic pathway	Overt DIC (FDPs not high enough and fibrinogen not low enough to prolong the TCT), vitamin K deficiency or antagonism, liver disease (cholestatic, failure), inherited defect in common pathway factors (excluding fibrinogen), warfarin and unfractionated heparin therapy., over-dilution of blood (too little blood for the citrate, standard collection of blood in an anemic patient), incorrect sample handling (see collection guidelines, factors are unstable)	Expect the platelet count and AT activity to be low in overt DIC and normal in vitamin K deficiency or antagonism (there are always exceptions) in dogs. Animals with overt DIC should have an initiating disease (e.g. inflammation, neoplasia, bacterial sepsis). D-dimer may be high with overt DIC and non-DIC causes of prolonged PT and APTT (increased intravascular and extravascular fibrinolysis).
↑	↑	↑	Common pathway (Factors X, V, II, I) or defects in intrinsic and extrinsic pathway	Severe hypofibrinogenemia alone (<50 mg/dL dog, <75 mg/dL other species – see causes above), overt DIC, synthetic liver failure, unfractionated heparin therapy, possibly over-dilution of blood, inappropriate storage of sample	Fractionated or low molecular weight heparin will not prolong clotting times (inhibits FXa primarily, not thrombin).