NAVLE Hemic and lymphic

Canine Coagulopathy Study Guide

📅 March 28, 2026 ⏱ 25 min read 👁 5 views
Coagulopathies represent a significant category of bleeding disorders in dogs, encompassing both congenital (inherited) and acquired conditions that impair normal hemostasis.

Overview and Clinical Importance

Coagulopathies represent a significant category of bleeding disorders in dogs, encompassing both congenital (inherited) and acquired conditions that impair normal hemostasis. Understanding these disorders is essential for the NAVLE, as they present commonly in clinical practice and require prompt recognition and appropriate management.

The clinical presentation varies depending on whether the defect involves primary or secondary hemostasis. Primary hemostatic defects (platelet disorders, von Willebrand disease) typically cause petechiae, ecchymoses, and mucosal bleeding. Secondary hemostatic defects (coagulation factor deficiencies) characteristically cause deep tissue hemorrhage, hemarthrosis, and delayed bleeding after trauma or surgery.

Feature Primary Hemostasis Secondary Hemostasis
Components Platelets, von Willebrand factor, blood vessel wall Coagulation factors (I-XIII), calcium, phospholipid surfaces
End Product Platelet plug (unstable) Cross-linked fibrin mesh (stable clot)
Typical Bleeding Petechiae, ecchymoses, mucosal hemorrhage Deep tissue bleeding, hemarthrosis, hematomas
Screening Tests Platelet count, BMBT, vWF:Ag PT, aPTT, ACT, fibrinogen

Hemostasis Physiology Review

Normal hemostasis involves a coordinated sequence of events that control bleeding while preventing inappropriate thrombosis. This process is traditionally divided into primary hemostasis (formation of the platelet plug) and secondary hemostasis (coagulation cascade activation and fibrin formation).

Primary vs Secondary Hemostasis

High-YieldOn the NAVLE, petechiae and ecchymoses suggest a PRIMARY hemostatic defect (platelets or vWD), while deep tissue bleeding and hemarthrosis suggest a SECONDARY hemostatic defect (coagulation factor deficiency).

The Coagulation Cascade

The coagulation cascade is traditionally divided into the intrinsic pathway (factors XII, XI, IX, VIII), the extrinsic pathway (tissue factor, factor VII), and the common pathway (factors X, V, II, I). Both pathways converge at factor X activation, leading to thrombin generation and fibrin formation.

Coagulation Tests and Their Interpretation

Board Tip - Memory Aid: "PT = PaTh out" (extrinsic); "aPTT = inTrinsic PaTh". Factor VII has the shortest half-life (4-6 hours), so PT is the first test to become prolonged in vitamin K deficiency or rodenticide toxicosis.

Test Pathway Evaluated Factors Assessed Clinical Use
PT Extrinsic and Common VII, X, V, II, I Rodenticide toxicosis, liver disease
aPTT Intrinsic and Common XII, XI, IX, VIII, X, V, II, I Hemophilia A/B, heparin, DIC
BMBT Primary hemostasis Platelet function, vWF vWD screening; normal less than 4 min

Congenital Coagulopathies

Von Willebrand Disease (vWD)

Von Willebrand disease is the most common inherited bleeding disorder in dogs, affecting over 50 breeds. It results from a deficiency or dysfunction of von Willebrand factor (vWF), essential for platelet adhesion to damaged endothelium and as a carrier protein for Factor VIII.

Types of vWD

Clinical Signs

  • Mucosal bleeding: epistaxis, gingival bleeding, hematuria, melena
  • Prolonged bleeding from minor wounds, surgery, or venipuncture
  • May be subclinical until triggered by trauma or surgery
  • Hemorrhage during estrus or parturition

Diagnosis

  • vWF:Ag assay: Gold standard; less than 50% indicates at risk; less than 25% severely affected
  • BMBT: Prolonged (greater than 4 minutes in dogs)
  • PT and aPTT: Normal (key differentiator from hemophilia)
  • Platelet count: Normal

Treatment

High-YieldDoberman Pinschers have the highest prevalence of vWD (over 70% carriers). Always consider vWD testing before elective surgery in Dobermans. DDAVP only works for Type 1 vWD.

Hemophilia A (Factor VIII Deficiency)

Hemophilia A is the most common severe inherited coagulation disorder in dogs. It is an X-linked recessive disorder caused by deficiency of Factor VIII.

Genetics and Breeds

  • X-linked recessive: Males typically affected; females are carriers
  • Carrier females have 40-60% Factor VIII activity and are usually asymptomatic
  • All daughters of hemophilic males are obligate carriers
  • Breeds: German Shepherd (most common), Labrador, Golden Retriever, Rottweiler

Clinical Signs

  • Prolonged bleeding from umbilical cord, tail docking, dewclaw removal in puppies
  • Hemarthrosis (bleeding into joints) causing shifting leg lameness
  • Spontaneous hematomas, hemorrhagic body cavity effusions
  • Deep intramuscular bleeding after minor trauma or injections

Diagnosis

  • aPTT: Prolonged (key finding)
  • PT: Normal
  • Platelet count: Normal
  • Factor VIII:C activity: Severely reduced (less than 6% = severe; 6-20% = moderate)

Treatment

  • Cryoprecipitate: Preferred treatment; rich in Factor VIII
  • Fresh frozen plasma: 10 mL/kg IV q8-12h for active bleeding
  • Avoid: IM injections, NSAIDs, surgery when possible
NAVLE TipHemophilia A = prolonged aPTT with NORMAL PT and platelet count. Deep tissue bleeding and hemarthrosis are classic. Remember: X-linked means affected males, carrier females. All daughters of hemophilic males are obligate carriers.

Hemophilia B (Factor IX Deficiency)

Hemophilia B (Christmas disease) is clinically indistinguishable from Hemophilia A but caused by Factor IX deficiency. Also X-linked recessive.

  • Key difference: Treatment requires fresh frozen plasma (FFP)
  • Cryoprecipitate is NOT useful because Factor IX is not concentrated in cryoprecipitate
Type Defect Severity Breeds Affected
Type 1 Quantitative deficiency; all vWF multimers present but reduced Mild to moderate; most common type Doberman (over 70% carriers), German Shepherd, Golden Retriever
Type 2 Qualitative defect; large vWF multimers absent Moderate to severe German Shorthaired Pointer, German Wirehaired Pointer
Type 3 Complete absence of vWF Most severe; life-threatening Scottish Terrier, Chesapeake Bay Retriever, Shetland Sheepdog

Acquired Coagulopathies

Anticoagulant Rodenticide Toxicosis

Anticoagulant rodenticide (AR) toxicosis is one of the most common acquired coagulopathies in dogs. These compounds inhibit vitamin K epoxide reductase, depleting vitamin K-dependent clotting factors (II, VII, IX, X).

Types of Rodenticides

Pathophysiology

  • ARs inhibit vitamin K epoxide reductase enzyme
  • Depletes active vitamin K needed for gamma-carboxylation of factors II, VII, IX, X
  • Factor VII has shortest half-life (4-6 hours) - PT prolonged first

Clinical Signs

  • Onset 3-7 days post-ingestion after clotting factors depleted
  • Lethargy, weakness, anorexia, pale mucous membranes
  • Hemorrhage: epistaxis, hemoptysis, hemothorax, hemoabdomen, melena
  • Dyspnea (pulmonary hemorrhage or hemothorax)

Diagnosis

  • PT: Prolonged FIRST (Factor VII has shortest half-life)
  • aPTT: Prolonged (after PT becomes prolonged)
  • Platelet count: Normal (key differentiator from DIC)
  • Response to vitamin K1: PT normalizes within 24-48 hours - diagnostic
  • PIVKA test: Detects inactive clotting factors

Treatment

High-YieldPT becomes prolonged BEFORE aPTT because Factor VII has the shortest half-life. Use VITAMIN K1 (phytonadione), NOT K3 (menadione - can cause hemolytic anemia). Give PO with fatty food for absorption. Check PT 48-72 hours after stopping vitamin K1 to ensure adequate clotting.

Memory Aid - "1972" for Vitamin K-Dependent Factors: Factors II, VII, IX, X (1-9-7-2 rearranged) require vitamin K for gamma-carboxylation.

Disseminated Intravascular Coagulation (DIC)

DIC is an acquired, complex hemostatic disorder characterized by systemic activation of coagulation leading to microvascular thrombosis and subsequent consumption of clotting factors and platelets. DIC is always secondary to an underlying disease.

Underlying Causes

  • Sepsis/severe infection - most common trigger
  • Neoplasia: Hemangiosarcoma (most common), mammary carcinoma, lymphoma
  • IMHA - common complication
  • Other: Pancreatitis, GDV, heat stroke, snake envenomation, massive trauma

Pathophysiology

  • Triggering event causes systemic coagulation activation
  • Widespread microvascular thrombosis
  • Consumption of platelets and clotting factors
  • Secondary fibrinolysis with elevated FDPs/D-dimers
  • Results in paradoxical bleeding AND thrombosis

Clinical Spectrum

Diagnosis

No single test is diagnostic. DIC is diagnosed by a combination of findings:

  • Thrombocytopenia
  • Prolonged PT and aPTT
  • Elevated D-dimers or FDPs
  • Decreased fibrinogen
  • Decreased antithrombin
  • Schistocytes on blood smear (microangiopathic hemolysis)

Treatment

  • Treat underlying cause - MOST IMPORTANT
  • Fresh frozen plasma: 10-15 mL/kg IV; replaces clotting factors and antithrombin
  • Heparin: Controversial; may be used in thrombotic DIC
  • Supportive care: IV fluids, oxygen, blood transfusions as needed
  • Prognosis: Guarded; approximately 40% survival
High-YieldDIC is ALWAYS secondary to underlying disease. Classic lab findings: thrombocytopenia + prolonged PT/aPTT + elevated D-dimers + decreased fibrinogen. The key to management is treating the underlying cause. Normal platelets with prolonged PT/aPTT suggests rodenticide toxicosis instead of DIC.

Immune-Mediated Thrombocytopenia (ITP)

ITP results from antibody-mediated platelet destruction. It can be primary (idiopathic) or secondary to underlying disease.

Signalment and Predisposition

  • Middle-aged dogs (mean 5-6 years)
  • Female predisposition (approximately 70%)
  • Breeds: Cocker Spaniel, Poodles, Old English Sheepdog

Secondary Causes

  • Tick-borne diseases (Ehrlichia, Anaplasma, Babesia)
  • Neoplasia (lymphoma, hemangiosarcoma)
  • Drugs (sulfonamides, cephalosporins)
  • Recent vaccination
  • Evans syndrome: Concurrent ITP + IMHA (30% of ITP cases)

Clinical Signs

  • Petechiae, ecchymoses (especially on ventral abdomen, pinnae, gums)
  • Mucosal hemorrhage: epistaxis, hematuria, melena
  • Often otherwise clinically well unless severe bleeding

Diagnosis

  • Platelet count: Severely decreased (often less than 30,000/mcL, frequently less than 10,000/mcL)
  • PT and aPTT: Normal
  • Blood smear: Rare to absent platelets; may see megathrombocytes
  • Rule out secondary causes: tick-borne disease panel, imaging for neoplasia

Treatment

Prognosis

  • Survival rate: 70-90%
  • Relapse rate: 9-39%; may occur months to years later
  • Poor prognostic indicators: Melena, elevated BUN, concurrent IMHA (Evans syndrome)
NAVLE TipITP = severely low platelets (often less than 10,000/mcL) with NORMAL PT/aPTT. SLOW steroid taper over 4-6 months is essential to prevent relapse. Platelet transfusions are generally NOT helpful as transfused platelets are rapidly destroyed by antibodies. Rule out tick-borne diseases and check for concurrent IMHA (Evans syndrome).
Treatment Dose Notes
Cryoprecipitate 1 unit per 10 kg IV Preferred; rich in vWF and Factor VIII
Fresh frozen plasma 10-15 mL/kg IV Alternative if cryoprecipitate unavailable
DDAVP (Desmopressin) 1 mcg/kg SC/IV, 30 min pre-op Type 1 vWD only; causes vWF release from endothelium

Differential Diagnosis Summary

Laboratory Pattern Recognition

Generation Examples Treatment Duration
First-generation Warfarin, pindone, chlorphacinone 1-2 weeks vitamin K1
Second-generation Brodifacoum, bromadiolone, difethialone 4-6 weeks vitamin K1
Treatment Dose Notes
Vitamin K1 (Phytonadione) 2.5-5 mg/kg PO q12-24h Give with fatty food for absorption; 2-6 weeks
Fresh frozen plasma 10-15 mL/kg IV For active bleeding; provides clotting factors
Packed RBCs 10-20 mL/kg IV For severe anemia; PCV less than 20%
Feature Thrombotic DIC (Early/Chronic) Hemorrhagic DIC (Late/Fulminant)
Platelets Normal to decreased Severely decreased
PT/aPTT Normal or shortened Prolonged
Fibrinogen Normal or increased Decreased
D-dimer/FDPs Increased Markedly increased
Clinical Signs Organ dysfunction, thromboembolism Petechiae, hemorrhage, shock
Treatment Dose Notes
Prednisone 2 mg/kg PO q12h First-line; slow taper over 4-6 months
Vincristine 0.02 mg/kg IV once Stimulates platelet release from megakaryocytes
Azathioprine 2 mg/kg PO q24-48h Second-line; takes 2-3 weeks for effect
Mycophenolate 10 mg/kg PO q12h Alternative second-line agent
Human IVIg 0.5-1 g/kg IV once For severe, life-threatening cases
Condition PT aPTT Platelets Key Features
vWD Normal Normal Normal Prolonged BMBT; low vWF:Ag
Hemophilia A/B Normal Prolonged Normal X-linked; males affected; hemarthrosis
AR Rodenticide Prolonged Prolonged Normal PT prolonged first; responds to vitamin K1
DIC Prolonged Prolonged Low High D-dimers; underlying disease
ITP Normal Normal Very low Petechiae; immunosuppression works

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