The Bleeding Patient: Diagnosis and Treatment Approach
World Small Animal Veterinary Association Congress Proceedings, 2017
Duana McBride, BVSc, DACVECC, MVMedSc, MRCVS
Queen Mother Hospital for Animals, Royal Veterinary College, North Mymms, UK


The haemostatic system can be broken down into 3 main components: 1) Primary haemostasis; 2) Secondary haemostasis; and 3) Fibrinolysis. All 3 systems are occurring as a continuum, and there are continued advances in the understanding of haemostasis, which is described by the 'cell-based model of coagulation.' However, in this lecture, to better understand the bases of diagnostics and treatment of the bleeding patient, we will be discussing haemostasis in the traditional sense.

Primary Haemostasis

Primary haemostasis involves the interaction between platelets and the subendothelial matrix to form a temporary primary haemostatic (platelet) plug. When injury occurs to vessels (endothelium), platelets adhere to the subendothelial matrix (collagen) via von Willebrand factor (vWF). Once platelets are adhered to the subendothelial matrix, they are activated by several different mechanisms, including collagen, adenosine diphosphate (ADP), thromboxane A2 (TXA2), thrombin, and platelet activating factor to name a few. Platelets change shape to an activated form, having an ability to aggregate together forming a platelet plug. The platelet plug forms a framework for secondary haemostasis to occur. Therefore the 3 important components to primary haemostasis are: normally functioning platelets, vWF, and the endothelium.

Secondary Haemostasis

Secondary haemostasis involves several enzymatic reactions which we commonly refer to as the intrinsic, extrinsic and common pathways, eventually forming fibrin which stabilises the clot.

Important things to remember about the secondary cascade:

  • All factors involved in the secondary cascade are produced by the liver
  • Factors II, VII, IX, and X are vitamin K dependent
  • Factor VII has the shortest half-life of 4–6 hours


Coagulation is a continuum of processes, and therefore requires fibrinolysis to occur. Plasminogen is converted to plasmin, which is responsible for the breakdown of the fibrin clot. Once the fibrin clot breaks down, fibrin degradation products (FDP), including D dimers, are produced. Fibrin degradation products are eventually removed by the liver.

Approach to the Bleeding Patient

Primary Haemostatic Disorder

Diagnostic tests

  • Clinical signs
    • Petechial haemorrhages and ecchymosis, bleeding of mucosal surfaces
  • Platelet count (CBC)
    • Normal >200,000/µL. Less than 40,000/µL can lead to clinical signs.
  • Platelet count (blood smear)
    • One platelet represents 15,000–20,000/µL
    • Look for clumps on the feathered edge which could falsely lower your platelet count
  • Buccal mucosal bleeding time (BMBT)
    • Normal: 1.7–4.2 minutes (dog); 1.4–2.4 minutes (cat)
    • Procedure: Ensure normal platelet count, as thrombocytopenia will result in prolonged BMBT
    • Prolonged BMBT indicates thrombocytopathia or vasculopathy
  • vWF:Ag

Differential diagnosis

  • Thrombocytopenia
    • Myeloproliferative disease (FeLV; immune mediated; drug induced [e.g., oestrogen, cytotoxics]; bone marrow aplasia)
    • Primary immune-mediated thrombocytopenia
    • Secondary immune-mediated thrombocytopenia (infections, neoplasia, drugs)
    • Consumptive disorders (DIC, sepsis, haemorrhage)
    • Sequestration (splenic torsion)
    • Angiostrongylus
  • Thrombocytopathia
    • Drugs (NSAIDs, aspirin, synthetic colloids, β-lactam antibiotics)
    • Uraemia
    • Hepatic disease
    • Ehrlichia
    • Hereditary
    • Angiostrongylus
  • vWD
  • Vascular - vasculitis
  • Angiostrongylus


  • Thrombocytopenia
    • Fresh whole blood, platelet-rich plasma, platelet concentrates, cryopreserved platelets
  • Thrombocytopathia
    • Fresh whole blood, platelet-rich plasma, platelet concentrates, cryopreserved platelets
    • Desmopressin - lasts 30–60 minutes
  • vWF
    • Fresh frozen plasma
    • Cryoprecipitate
    • Desmopressin - lasts 30–60 minutes

Secondary Haemostatic Disorders

Diagnostic tests

  • Clinical signs: Cavitary haemorrhage, haematoma, GIT, muscle, joint haemorrhage
  • Prothrombin time (PT)
    • Extrinsic and common pathways
    • Require 70% of factor VIIa to decrease to be prolonged
    • Prolonged PT, normal APTT - most likely vitamin K deficiency as tests for FVlla which is the vitamin K-dependent factor with the shortest half-life
  • Activated partial thromboplastin time (APTT)
    • Intrinsic and common pathways
    • Require 70% of one of the factors to decrease to be prolonged
    • Prolonged APTT, normal PT - Not vitamin K deficiency
  • Activated clotting time (ACT)
    • Intrinsic and common pathways
    • Use diethyl earth tube. Place 2 ml of blood in a pre-warmed tube. Invert every 10 seconds and observe clot to form while keeping the tube warm in a water bath.
    • Normal: 60–110 seconds (dog), 50–75 seconds (cat)
    • Requires 90% of factors to decrease to be prolonged
  • Factor measurements
    • Takes up to 2 weeks for results

Differential diagnosis

  • Vitamin K deficiency (e.g., rodenticides)
  • Hepatopathy
  • DIC
  • Angiostrongylus
  • Drugs (e.g., heparin, warfarin)
  • Inherited factor deficiencies
    • VIII - Haemophilia A (German shepherds, cross breeds, cats)
    • IX - Haemophilia B (various breed dogs, cats)
    • Others - I, II, VII, X, XI, XII


  • Fresh frozen plasma
    • 10–20 mL/kg
    • Standardly over 4 hours, but can give quicker (over 30 minutes) if very critical patient
  • Stored plasma
    • 10–20 mL/kg
    • No factor V or VIII, but vit K-dependent factors present
  • Fresh whole blood
    • If anaemic as well as coagulopathic
  • Stored whole blood
    • If anaemic as well as coagulopathic due to vit K-dependent factor deficiency


Diagnostic tests:

  • Fibrin degradation products (FOP)
    • Increase in DIC and hepatic disease
    • Not very sensitive or specific
  • D-dimers
    • Increase in recent (<5 hours) disease
    • More sensitive and specific than FDP
    • Increase in DIC, thromboembolism, neoplasia, hepatic, renal failure, cardiac failure, recent haemorrhage
    • Tissue plasminogen activated thromboelastography (needs to be inhouse)

Differential diagnosis

  • DIC
  • Congenital in some Greyhounds (post-operative bruising may occur)


References are available upon request.


Speaker Information
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Duana McBride, BVSc, DACVECC, MVMedSc, MRCVS
Royal Veterinary College
North Mymms, UK