Approach to bleeding disorders and acute anemia
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This document provides an overview of approaches to evaluating and treating bleeding disorders and acute anemia. It discusses evaluating the clinical history and laboratory tests to distinguish between local and systemic bleeding issues and primary versus secondary hemostatic defects. Common causes of bleeding like hemophilia, von Willebrand disease, liver disease, and medications are reviewed. Emergency treatment options and dosing calculations for replacing coagulation factors in hemophilia are also covered.
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Approach to bleeding disorders and acute anemia
- 1. Approach to Bleeding Disorders and Acute Anemia Bundarika Suwanawiboon, M.D. May 10, 2006
- 4. FVIIa/TF FXa/FVa FIXa/FVIIIa FVIIa/TF FVIIa FVII FVIIa FIX FIXa FX FXa Prothrombin T FV FVa T FVIII FVIIIa T FXI FXIa T FBG Fibrin (soluble) FXIIIa FXIII T Fibrin (Insoluble)
- 19. Pseudothrombocytopenia Must be Excluded
- 20. Immune Thrombocytopenic Purpura
- 22. Thrombotic Thrombocytopenic Purpura (TTP)
- 23. Bleeding Time
- 29. Intrinsic Pathway Extrinsic Pathway Common Pathway XII XIIa XI HK/PK IXa/ IX VIIIa XIa XII XIIa XI XIa HMWK IXa IX VIIIa/PL Tenase Ca ++ X Xa II IIa Va/PL Ca ++ Fibrinogen Fibrin X-linkedFibrin XIIIa Prothrombinase VIIa/TF VII VIIa TF Ca ++ X Xa II IIa Va/PL Ca ++ Fibrinogen Fibrin
- 30. Prothrombin Time (PT) PT : test extrinsic and common pathway
- 31. Activated Partial Thromboplastin Time (aPTT) aPTT : test intrinsic and common pathway
- 32. Mixing Study + 0% 100% 50% <30% Correctable Normal coagulation time Uncorrectable prolonged coagulation time Deficiency Inhibitor
- 33. Isolated prolonged PT Mixing study Correctable Uncorrectable Deficiency Inhibitor Hereditary: FVII FVII Acquired: early liver impairment vitamin K antagonist vitamin K deficiency
- 34. Isolated prolonged aPTT Bleeding No bleeding Mixing study Mixing study Correctable Uncorrectable Correctable Uncorrectable Deficiency Inhibitor Deficiency Inhibitor Factor VIII / vWD Factor VIII Factor XII Factor XII Factor IX Factor IX HMWK HMWK Factor XI Factor XI Prekallekrein Prekallekrein Lupus anticoagulant
- 35. Prolonged aPTTand PT Correctable Uncorrectable Deficiency Inhibitor Hereditary:single factor FII, V, or X Hypofibrinogenemia Afibrinogenemia Dysfibrinogenemia Acquired:multiple factors Acquired: early liver impairment Heparin vitamin K antagonist Lupus anticoagulant vitamin K deficiency DIC
- 42. NEJM 2002;346(13):995 Pathophysiology of ITP
- 55. vWF panel: Interpretation Test/Type 1 2A 2B 2M 2N 3 BT N or ↑ ↑ ↑ N or ↑ ↑ ↑ N ↑↑↑↑ vWF:Ag ↓ ↓ ↓ ↓ or N ↓ or N ↓↓↓↓ vWFR:Co ↓ ↓↓↓ ↓↓ ↓ ↓ or N ↓↓↓↓ LD-RIPA - - ↑ - - - FVIII N or ↓ N or ↓ N or ↓ N ↓↓↓ ↓↓↓ Multimer N but ↓ abnormal abnormal N but ↓ N but ↓ absent
- 61. Laboratory Evaluation PT aPTT TCT Fibrinogen D-dimer Hemophilias NL ↑↑ NL NL NL Liver disease ↑↑ ↑ NL or ↑ NL or ↓ NL or ↑ DIC (acute) ↑ ↑ NL or ↑ NL or ↓ ↑↑ Vit K Def. ↑ ↑ NL NL NL Heparin NL ↑↑ ↑↑ NL NL Warfarin ↑↑ NL or ↑ NL NL NL Acquired ↑* ↑* NL NL NL Inhibitors (*depends on type of inhibitors)
- 62. Hemophilias
- 66. Classification Severity % Factor Clinical Bleeding Mild 5-25 Associated with moderate degree of injuries Moderate 1-5 Associated with mild degree of injuries Severe < 1 Spontaneous bleeding
- 75. Thrombosis Organ dysfunction DVT Thrombolysis Increased FDP Platelet dysfunction Coagulation activation Prolonged PT Prolonged aPTT Hemorrhage Trigger agents Hypofibrinogenemia Platelet activation Thrombocytopenia Pathophysiology
- 76. Group Associated Diseases Trigger Agents 1 - Septicemia Endotoxin - Gram negative bacili 2 - Obstetric complications Thromboplastin - Malignancy - Burn/crush injuries - Snake bite - Hemorrhagic pancreatitis 3 - Anaphylaxis Ag-Ab complex 4 - Infection from rickettsial, virus Endothelial injuries - Giant hematoma 5 - Malaria Unknown - Hemolytic transfusion reaction
- 77. Advanced CA prostate with bone marrow involvement and DIC
- 79. Microangiopathic Hemolytic Anemia Schistocytes
- 84. Mixing Study + = Patient Normal O% 100% 50%
- 85. XII XIIa XI XIa HMWK IXa IX VIIIa/PL Ca ++ X Xa VIIa/TF VII VIIa TF Tenase II IIa Va/PL Ca ++ Fibrinogen Fibrin X-linkedFibrin XIIIa Prothrombinase Intrinsic Pathway Extrinsic Pathway Common Pathway
- 86. NL PT, ↑ aPTT ↑ PT, NL aPTT ↑ PT, ↑ aPTT NL PT, NL aPTT 50:50 mixing study Factor def.: FXI,IX, VIII Inhibitor Specific: XI, IX, VIII NS:antiphos-pholipid FVII def., Vit. K def, liver dz, DIC Normal Prolonged Inhibitor Specific: VII (rare) NS:antiphos-pholipid Factor def.: V, X, II, I Inhibitor Specific: X, V, II, I NS:antiphos-pholipid -Dysfibrinogenemia -FXIII deficiency - α 2-Antiplasmin def -Mild isolated factor def. -Elevated FDP -Monoclonal gammopathy -Qualitative or quantitative platelet disorders -Vascular Disorders
- 96. Acute Myeloid Leukemia Auer Rod
Editor's Notes
- After TF binds to FVIIa, the complex enhances more conversion of FVII VIIa (CHECK ACCURACY) and also form extrinsic tenase which activates FX to activated form and FIX to IXa. FX activation is more efficient. FXa then converts small amounts of II—> IIa. This low conc. Of thrombin is suff. To amplify coagulation by activating FV and VIII (key cofactors in coagulation), plts and plt-bound FXI. 2) Coagulation is propagted when FIXa binds to VIIIa on the surface of activated plts to form intrinsic tenase, the complex that efficiently activates FX. FXa then binds to FVa on the activated plts surface in the presence of Ca++ to form prothrombinase, which converts prothrombin to thrombin. Thrombin also activate plt-bound FXI which will promotes more FXa generation. FXa also promotes more activation of FVII VIIa , all of which help promote propagation of coagulation. 3) The final step is fibrin formation is when thrombin converts FBG fibrin. Thrombin also activates FXIII, which cross-links and stabilizes the fibrin network. n the presence of Ca++, PL
- Bleeding time is not predictive for post-op bleeding, should not be used solely to make a diagnosis of clinical bleeding risk, may begin to prolong when plt. < 100K but usua. Is not out of the upper normal range until plt. are < 50K Superimposed qualitative plt. Abn. Will cause a greater prolongation of the bleeding time than a decrease in plt. Count alone.
- Emergency splenectomy prior to emergency craniotomy for intracranial hemorrhage. Treatment is generally not required at Plt >30-50 K. Life-threatening hemorrhage rarely occurs at Plt.> 10,000
- Scan plt. Agg tracing
- if > 2 hrs. there may be decay of labile clotting factors : FV and FVIII may cause erroneous results
- Will discuss in more details in the second part of this lecture when talking about clinical approach of bleeding disorders
- Antibodies were directed against platelet GP complexes e.g. GPIIb/IIIa, Ib/Ix, Ia/IIa, V, and IV
- rapidly increase in platelet number after splenectomy removal of RE cells decreased antibody production
- Ticlopidine
- ASA irreversibly inhibit both COX1 (found in plts), COX2 block TXA2 no plt. Aggregation for the life of plts (7-10 d) NSAIDs reversible effect. Effect on TXA2 depends on half-life of the drug
- Liver synthesize almost all the hemostatic protein except vWF and tPA. FFP 4-6 units if FVII level < 10% (INR > 2.5) q 4-6 hrs. Low dose vit K 0.5-1 mg IV
- Prednisolone 1-2 mg/kg/d, Dexamethasone 5 mg iv q 6 hr