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APPROACH TO BLEEDING 
TENDENCY 
Hamad Emad H. Dhuhayr
CONTENT 
• Overview 
• approach to bleeding tendency 
1. Taking history 
2. Physical examination 
3. Laboratory 
• references
VASCULAR CONTRACTION 
1. Local myogenic spasm 
2. Local autacoid factors from traumatized tissue and 
blood platelets 
3. Nervous reflexes
Red blood cell 
Platelet
Red blood cell 
Platelet
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor
Red blood cell 
Platelet 
Von Willebrand factor 
Fibrin polymer
Red blood cell 
Platelet 
Von Willebrand factor 
Fibrin polymer
Red blood cell 
Platelet 
Von Willebrand factor 
Fibrin polymer
EVALUATION OF THE PATIENT 
•HISTORY 
•PHYSICAL EXAMINATION 
•LABORATORY EVALUATION
History taking 
Identify if the bleeding problem is due to 
Local vs. Systemic defect 
Location: single vs. Multiple sites 
Severity: spontaneous? Appropriate to trauma? 
Hereditary vs. Acquired disorder 
Onset 
Family history 
Underlying disease 
Medication 
Primary vs. Secondary hemostatic disoder
Primary Hemostatic 
defect 
Secondary Hemostatic 
defect
PHYSICAL EXAMINATION 
• Current hemorrhage 
• Nature and extent 
• Intercurrent illnesses 
• Liver disease 
• Petechiae/ecchymoses
LABORATORY ASSESSMENT 
• GUIDED BY HISTORY 
• SCREENING TESTS 
• PT 
• APTT 
• PLATELET COUNT 
• FIBRINOGEN 
• THROMBIN TIME
ASSESSMENT OF PRIMARY HEMOSTASIS 
PLATELET 
COMPLETE BLOOD COUNT (CBC) 
BLEEDING TIME/ PFA-100 
PLATELET AGGREGATION STUDY 
BLOOD VESSEL 
BLEEDING TIME 
VON WILLEBRAND FACTOR (VWF) 
BLEEDING TIME 
VWF ANTIGEN, VWF: RCO, VWF MULTIMER, FVIII
COMPLETE BLOOD COUNT (CBC) 
PLATELET NUMBER 
NORMAL PLATELET COUNT: 150,000 –400,000/UL 
> 100,000/UL BLEEDING UNLIKELY 
< 20,000/UL ↑ RISK FOR SPONTANEOUS 
BLEEDING 
MUST EXCLUDE PSEUDOTHROMBOCYTOPENIA 
ASSESS FOR PLATELET MORPHOLOGY
Etiology of Thrombocytopenia 
Decreased Production 
• Hypoproliferation 
• Aplastic Anemia, Amegakaryocytic 
• Ineffective Thrombopoiesis 
thrombocytopenia, infection, toxins, 
drugs 
Infiltrative marrow disease, TAR 
Increased Destruction • Megaloblastic anemia 
• Immune 
• Non-immune 
• Alloimmune, Autoimmune: ITP, SLE 
• DIC, TTP, HUS 
Others 
• Splenic sequestration 
• Dilutional 
• Hypersplenism 
• Massive blood transfusion
BLEEDING TIME
BLEEDING TIME: INTERPRETATION 
Normal value* : 1-9 min 
Prolonged bleeding time: 
Thrombocytopenia/ anemia (hct < 20%) 
Hereditary platelet dysfunction 
Von willebrand disease 
Severe hypofibrinogenemia 
Blood vessels disorders 
Uremia 
Myeloproliferative disorders 
Medication: aspirin, nsaids,other antiplatelet 
drugs
PLATELET AGGREGATION STUDY
ASSESSMENT OF SECONDARY HEMOSTASIS 
SCREENING TESTS: 
PT 
APTT 
MIXING STUDY 
ADDITIONAL TESTS 
FIBRINOGEN 
THROMBIN TIME 
REPTILASE TIME 
COAGULATION 
FACTOR ASSAYS 
D-DIMER 
FIBRIN DEGRADATION 
PRODUCT 
EUGLOBULIN LYSIS 
TIME
PROTHROMBIN TIME (PT) 
PT : test extrinsic and common 
pathway
ACTIVATED PARTIAL 
THROMBOPLASTIN TIME (APTT) 
aPTT : test intrinsic and common 
pathway
MIXING STUDY 
+ 
0% 100% 
50% 
<35% 
Correctable 
Normal 
coagulation 
time 
Uncorrectable 
prolonged 
coagulation 
time 
Deficienc 
y 
Inhibit 
or 
Prolonged PT or aPTT occurs 
when coagulation factor < 35- 
40%
INTERPRETATION OF ABNORMAL 
COAGULOGRAM 
ISOLATED PROLONGED PT 
ISOLATED PROLONAGED APTT 
PROLONGED PT AND APTT
Isolated prolonged PT 
Mixing study 
Correctable Uncorrectable 
Deficiency Inhibitor 
Hereditary: FVII FVII (rare) 
Lupus anticoagulant 
Acquired: 
Early liver impairment 
Vitamin K antagonist 
Vitamin K deficiency
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 
Heparin Lupus 
anticoagulant
Acquired FVIII inhibitor
Prolonged aPTT and PT 
Mixing study 
Correctable Uncorrectable 
- FII,FV or FX deficiency - FII, V, or X inhibitor 
- FV and VIII deficiency - Lupus anticoagulant 
- Liver disease - LAC + Factor inhibitor 
- Vitamin K antagonist 
- Vitamin K deficiency 
- DIC
SUMMARY 
• HISTORY & PHYSICAL EXAMINATION 
• LABORATORY TESTS 
• SCREENING TESTS 
• SPECIFIC DIAGNOSTIC TESTS 
• DIAGNOSIS-SPECIFIC THERAPY 
• FACTOR REPLACEMENT 
• DRUGS
REFFERENCES 
• KUMAR 
• CECIL 
• WEBSITE
Bleeding tendency

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Bleeding tendency

  • 1. APPROACH TO BLEEDING TENDENCY Hamad Emad H. Dhuhayr
  • 2. CONTENT • Overview • approach to bleeding tendency 1. Taking history 2. Physical examination 3. Laboratory • references
  • 3. VASCULAR CONTRACTION 1. Local myogenic spasm 2. Local autacoid factors from traumatized tissue and blood platelets 3. Nervous reflexes
  • 4. Red blood cell Platelet
  • 5. Red blood cell Platelet
  • 6. Red blood cell Platelet Von Willebrand factor
  • 7. Red blood cell Platelet Von Willebrand factor
  • 8. Red blood cell Platelet Von Willebrand factor
  • 9. Red blood cell Platelet Von Willebrand factor
  • 10. Red blood cell Platelet Von Willebrand factor
  • 11. Red blood cell Platelet Von Willebrand factor
  • 12. Red blood cell Platelet Von Willebrand factor
  • 13. Red blood cell Platelet Von Willebrand factor
  • 14. Red blood cell Platelet Von Willebrand factor
  • 15. Red blood cell Platelet Von Willebrand factor Fibrin polymer
  • 16. Red blood cell Platelet Von Willebrand factor Fibrin polymer
  • 17. Red blood cell Platelet Von Willebrand factor Fibrin polymer
  • 18.
  • 19. EVALUATION OF THE PATIENT •HISTORY •PHYSICAL EXAMINATION •LABORATORY EVALUATION
  • 20. History taking Identify if the bleeding problem is due to Local vs. Systemic defect Location: single vs. Multiple sites Severity: spontaneous? Appropriate to trauma? Hereditary vs. Acquired disorder Onset Family history Underlying disease Medication Primary vs. Secondary hemostatic disoder
  • 21.
  • 22. Primary Hemostatic defect Secondary Hemostatic defect
  • 23. PHYSICAL EXAMINATION • Current hemorrhage • Nature and extent • Intercurrent illnesses • Liver disease • Petechiae/ecchymoses
  • 24. LABORATORY ASSESSMENT • GUIDED BY HISTORY • SCREENING TESTS • PT • APTT • PLATELET COUNT • FIBRINOGEN • THROMBIN TIME
  • 25. ASSESSMENT OF PRIMARY HEMOSTASIS PLATELET COMPLETE BLOOD COUNT (CBC) BLEEDING TIME/ PFA-100 PLATELET AGGREGATION STUDY BLOOD VESSEL BLEEDING TIME VON WILLEBRAND FACTOR (VWF) BLEEDING TIME VWF ANTIGEN, VWF: RCO, VWF MULTIMER, FVIII
  • 26. COMPLETE BLOOD COUNT (CBC) PLATELET NUMBER NORMAL PLATELET COUNT: 150,000 –400,000/UL > 100,000/UL BLEEDING UNLIKELY < 20,000/UL ↑ RISK FOR SPONTANEOUS BLEEDING MUST EXCLUDE PSEUDOTHROMBOCYTOPENIA ASSESS FOR PLATELET MORPHOLOGY
  • 27. Etiology of Thrombocytopenia Decreased Production • Hypoproliferation • Aplastic Anemia, Amegakaryocytic • Ineffective Thrombopoiesis thrombocytopenia, infection, toxins, drugs Infiltrative marrow disease, TAR Increased Destruction • Megaloblastic anemia • Immune • Non-immune • Alloimmune, Autoimmune: ITP, SLE • DIC, TTP, HUS Others • Splenic sequestration • Dilutional • Hypersplenism • Massive blood transfusion
  • 29. BLEEDING TIME: INTERPRETATION Normal value* : 1-9 min Prolonged bleeding time: Thrombocytopenia/ anemia (hct < 20%) Hereditary platelet dysfunction Von willebrand disease Severe hypofibrinogenemia Blood vessels disorders Uremia Myeloproliferative disorders Medication: aspirin, nsaids,other antiplatelet drugs
  • 31. ASSESSMENT OF SECONDARY HEMOSTASIS SCREENING TESTS: PT APTT MIXING STUDY ADDITIONAL TESTS FIBRINOGEN THROMBIN TIME REPTILASE TIME COAGULATION FACTOR ASSAYS D-DIMER FIBRIN DEGRADATION PRODUCT EUGLOBULIN LYSIS TIME
  • 32. PROTHROMBIN TIME (PT) PT : test extrinsic and common pathway
  • 33. ACTIVATED PARTIAL THROMBOPLASTIN TIME (APTT) aPTT : test intrinsic and common pathway
  • 34. MIXING STUDY + 0% 100% 50% <35% Correctable Normal coagulation time Uncorrectable prolonged coagulation time Deficienc y Inhibit or Prolonged PT or aPTT occurs when coagulation factor < 35- 40%
  • 35. INTERPRETATION OF ABNORMAL COAGULOGRAM ISOLATED PROLONGED PT ISOLATED PROLONAGED APTT PROLONGED PT AND APTT
  • 36. Isolated prolonged PT Mixing study Correctable Uncorrectable Deficiency Inhibitor Hereditary: FVII FVII (rare) Lupus anticoagulant Acquired: Early liver impairment Vitamin K antagonist Vitamin K deficiency
  • 37. 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 Heparin Lupus anticoagulant
  • 39. Prolonged aPTT and PT Mixing study Correctable Uncorrectable - FII,FV or FX deficiency - FII, V, or X inhibitor - FV and VIII deficiency - Lupus anticoagulant - Liver disease - LAC + Factor inhibitor - Vitamin K antagonist - Vitamin K deficiency - DIC
  • 40. SUMMARY • HISTORY & PHYSICAL EXAMINATION • LABORATORY TESTS • SCREENING TESTS • SPECIFIC DIAGNOSTIC TESTS • DIAGNOSIS-SPECIFIC THERAPY • FACTOR REPLACEMENT • DRUGS
  • 41. REFFERENCES • KUMAR • CECIL • WEBSITE