Clotting Overview
- Endothelial Cells are Damaged
- Platelets Respond to Exposed Collagen and Stick
- Platelets Release Recruiting Factors
- More Platelets are Attracted
- Soluble Fibrinogen Turns to Insoluble Fibrin
- Fibrin Seals the Clot
- Clot Dissolves
- Liver Produces Clotting Factors
Coagulation Cascade
- Secondary Hemostasis
- Intrinsic Pathway
- Partial Thromboplastin Time (PTT)
- Heparin
- Extrinsic Pathway
- Prothrombin Time (PT)
- Warfarin
- Common Pathway
- Thrombin
- Convert Fibrinogen to Fibrin
- Stabilizes the Platelet Plug
Thrombotic Thrombocytopenic Purpura (TTP)
- Inhibition or deficiency of ADAMTS 13
- vWF Multimers are Not Degraded
- Microthrombi (and Emboli)
- FAT RN Pentad
- Fever
- Anemia
- Thrombocytopenia
- Renal Dysfunction
- Neurologic Abnormalities (Altered Mental status)
- Plasmapheresis
- Corticosteroids
- Splenectomy
Hemolytic Uremic Syndrome (HUS)
- Children
- Preceded by Acute Diarrheal Illness
- Endothelial Damage
- Microangiopathic Hemolytic Anemia (MAHA)
- Thrombocytopenia
- Renal Failure
- Helmet cells
- LDH
- Dialysis
- Supportive
Disseminated Intravascular Coagulation (DIC)
- Bleeding State
- Activation of Clotting Factors
- Deficiency of Clotting Factors
- Sepsis
- Trauma
- Obstetric Complications
- Acute Pancreatitis
- Malignancy
- Nephrotic Syndrome
- Transfusion
Disseminated Intravascular Coagulation (DIC) Assessment
- Improper Initiation of Clotting Cascade
- Systemic Bleeding
- Petechiae, Purpura, Ecchymosis
- Change in LOC
- Increased PT and PTT
- Cyanosis
- Increased Fibrin Degradation Products (FDP)
- Decreased Platelets and Fibrinogen
Disseminated Intravascular Coagulation (DIC) Interventions
- Risk for Shock
- Renal Failure
- Treat Underlying Cause
- Manage Bleeding
- Maintain Fluid and Hemodynamic Balance
- Transfusion
- Oxygenation
- Heparin Drip
Primary Immune Thrombocytopenia
- Preceding Infection or Vaccination
- Antiplatelet Antibodies
- Often Asymptomatic
- Bleeding
- Petechiae
- Thrombocytopenia
- Increased Megakaryocytes
- Corticosteroids
- Intravenous Immunoglobulin (IVIG)
- Rituximab
- Splenectomy
Hemophilia
- Genetic Mutation
- Prolonged Bleeding
- Pain
- Hemarthrosis
- Clotting Factor Replacement Therapy
- DDAVP (Desmopressin Acetate)
- Antifibrinolytic Therapy
- Analgesics
- Genetic Counseling
- Prevent Injury
Von Willebrand Disease
- Mixed platelet and coagulation disorder
- Autosomal Dominant Condition Leading to Reduced vWF
- Defect in platelet plug formation
- Increased Bleeding Time
- PTT increased
- Factor VIII decreased
- Normal platelet count
- DDAVP (synthetic vasopressin)
Factor V Leiden Thrombophilia
- Most Common Genetic Clotting Disorder in Caucasians
- Genetic Point Mutation
- Glutamine Replaces Arginine
- Mutant Factor V
- Resistant to Degradation by Activated Protein C
- Hypercoagulability
- Recurrent DVT (Increased Risk of Thromboembolism)
- Avoid Oral Contraceptives
- Caution During Pregnancy
Protein C or S Deficiency
- Autosomal Dominant
- Inability to Inactivate Factor Va and VIIIa
- Hypercoagulable State
- Recurrent DVTs or DVTs at Young Age
- Begin Heparin
- Slowly Bridge to Warfarin
- Hemorrhagic Skin Necrosis
Heparin Induced Thrombocytopenia (HIT)
- 5-10 Days After Heparin Exposure
- Heparin-Platelet Factor 4 Complex
- Autoantibodies Form Against Complex
- Heparin-Platelet Factor 4-Antibody Complex Binds Platelets
- Platelet Aggregation
- Procoagulant Release
- Thrombocytopenia
- Serotonin Release Assay (SRA)
- Stop Heparin, Start Direct Thrombin Inhibitor