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Bleeding Disorders For Surgeons

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Presentation on theme: "Bleeding Disorders For Surgeons"— Presentation transcript:


2 Bleeding Disorders For Surgeons
J. Bormanis

3 Bleeding disorders What are the possibilities
What questions have good yield What are screening tests What Lab tests are worrisome and what is the risk

4 Clinical Approach When did it start ? Dental history
Spontanous bruising Bleeding at surgery Bleeding into joints Menstrual bleeding Epistaxis One site only? Where ? When ?

5 High yield questions Family history Pattern of bleeding - where
Difficult to stop or Re-bleeds Drug history Alcohol intake Co Morbid disease

6 Physical Examination in Bleeding Disorders
Check sites of bleeding Is it local or generalized ? what are the manifestations, petichiae, ecchymoses, hematoma ? Are there vessel wall abnormalities, telangectasia, “palpable purpura, perifollicular hemorrhages” ? Are there signs of a connective disease process Are There signs of a systemic disease The type of bleeding should give a good clue as to which part of hemostasis is affected as well as the severity

7 Laboratory testing History and physical Type of tests guided by clinical features Screening tests Further tests Definitive tests

8 Normal Hemostasis

9 Screening Tests INR Extrinsic pathway
PTT (activated partial thromboplastin time) intrinsic pathway Thrombin time final pathway Platelet count Bleeding time – PFA (not useful)

10 Laboratory tests further testing
INR PTT TT thrombin time Factor assays Tests of fibrinolysis platelet count Bleeding time platelet function tests Special tests

11 Inerpretation of tests
If isolated abnormality likely a single defect eg PTT - possible hemophilia, vWd If unexplained do mixing test for inhibitor IF more than one abnormality then more complex eg. INR and PTT - vitamin K- Coumadin eg. PTT,TT heparin eg INR , PTT, TT, Platelets DIC or liver disease

12 Clinical Cases

13 Case 1 It is Friday at 4:40pm Lab calls
Your patient is being preped for urgent surgery. INR 6.5 What to do ?

14 Why INR’s go out of control

15 Vitamin K Warfarin affects factors II,VII,IX and X
These are the vitamin K dependent factors Can reverse warfarin effect Takes time Available forms ?

16 Efficacy of route of administration

17 Reversing INR wityh vitamin K
Depends on clinical scenario Complete reversal Partial reversal (too high INR) IV or oral forms prefered For complete reversal 5-10 mg IV q12h for 2 doses will reverse completely in hours. 1-2 mg will decrease INR to therapeutic Level within hrs


19 Current practice Sent as 2 vials in a 50 cc mini bag to infuse at 3c/min

20 Case 2 You are on call for ENT and are asked to see an 18 year old girl with refractory nosebleed. The nose is packed and bleeding does not stop. You notice a few bruises Blood sent off to lab. The lab calls at 6:00 Pm with a “critical” platelet count of 10 What is likely diagnosis What to do ?

21 ITP Immune thromboctopenic purpura
What is needed for diagnosis Bone marrow examination Anti platelet antibodies When isolated and very low ITP is most likely diagnosis Could be a part of another disease but not likely (SLE , inf mono) Does it require hospitalization ?

22 ITP continued If mucosal bleeding platelets are less than 6
Needs action Steroids IVIG Anti D What about splenectomy New treatments Rituximab TPO agonists

23 Case3 A 48 year old woman appears in emerg with jaundice of 3 weeks duration Exam – jaundice - some RUQ pain an palpation Blood tests CBC Hgb 125, WBC Plat 345 INR 2.6 ptt 42 What is likely diagnosis What to Do ?

24 Vitamin K deficiency Obstructive jaundice
Malabsorption of Vit K dependent factors Older people at risk Post surgery at risk Treatment Oral or IV Vitamin K

25 Case 4 A 54 year old male comes to emerg feeling unwell. Exam
Mild jaundice, some telangectasis on skin Mod ascites. CBC - Hgb 110 WBC plat 68 INR 1.6 Ptt 41 TT 25 What is likely diagnosis ?

26 Hepatic dysfunction - Cirrhosis
Liver makes and degrades Coagulation is affected by decreased production and impaired degradation of activated factors Chronic DIC Splenomegaly Trearment only if bleeding Liver transplant

27 Case 5 18 year old male scheduled for tonsillectomy
History of easy bleeding Exam normal no bruises CBC normal INR 1.1 PTT 45 What is likely diagnosis ? How to diagnose ?

28 Hemophilia X linked bleeding disorders characterized by spontaneous development of large hematomes in deep tissues. May lead to joint bleeding, or into other closed structures Joint cavity bleeding leads to deformed joints bleeding may be spontaneous or asssociated with mild or moderate injury

29 Hemophilia types Hemophilia A Hemophilia B
absent or decreased factor VIII Hemophilia B lack of factor IX similar in symptoms to Hemophilia A Hemophilia A is 10 times more common than hemophilia B

30 Genetics of Factor VIII
Single chain polypeptide Produced mainly in Liver remember linked to VWf Gene deletion - no factor VIII Point mutation - abnormal factor VIII Base deletion - Abnormal Factor VIII Coded on X chromosome -therefore only males affected (transmitted by female carriers)

31 Hemophilia types Subclassified by level of factors
Levels correspond to clinical symptoms Mild % factor activity Moderate 1-5% activity Severe <1% activity

32 Hemophilia - Clinical Picture
Mild- do not develop spontaneous bleeding, but do bleed after injury or surgery Many patients have sever disease Joint Bleeding results in severe disability hemarthroses chronic arthritis muscle bleeds Social, economic,psychological problems

33 Case 6 17 year old girl with mennorhagia History of easy bruising
Possible history of easy bruising CBC normal INR 1.1 PTT 32 (2 sec prolonged) What is diagnosis How to diagnose ? Treatment ?

34 Von Willebrand’s Disease
Most frequent inherited bleeding disorder 1% - 1/100 of western population less severe than hemophilia Disease results from a decrease or absence of Von Willebrand factor for platelet adhesion Affects primary hemostasis

35 Von Willebrand’s Disease and Factor VIII
VW factor produced in megakaryocytes and endothelial cells Coded on chromosome 12 Autosomal dominant inheritance Large molecule, and multimeric Monomers undergoglycolisation and multimerization before secretion Different multimer size = disease

36 Von Willebrand’s Disease and Factor
VW is carrier for factor VIII Factor VIII-VWf complex Factor VIII protein carried in circulation as complex with VWf Reacts with platelet via GP Ib Therefore can be problems with platelets and factor VIII

37 Clinical features of Von Willebrand’s Disease
Generally mild bleeding - often unrecognized until surgery or injury epistaxis, menorrhagia, easy bruising, dental and post operative bleeding Can be severe in certain types Requires accurate diagnosis Requires specific treatment

38 VW -types Type I Type II Type III
most frequent, quantitave defect (decreased VWf ) Type II qualitative defect (abnormal VWf ) Type III severe, rare, (absence of VWf )

39 How to diagnose Von Willebrands disease
Clinical history Factor VIII level Bleeding time Measure VWf and perform aggregation tests Do gel electrophoresis for multimers

40 Anti platelet agents ASA Not likely to create problems
Safer to give if there for cardiovascular reasons Clopidogrel If elective stop before. Minimum 3 days More than 5 days likely unnecessary

41 Massive bleeding

42 What are the critical issues ?

43 Questions

44 Massive Transfusion Protocol
The Ottawa Hospital Ottawa, Ontario

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