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COAGULATIONREVIEW
J. Bormanis/ cg edits
Clinical Approach
When did it start ? Dental history Spontanous bruising Bleeding at surgery Bleeding into joints Menstrual bleeding Epistaxis One site only? Where ? When ?
High yield questions
Family history Pattern of bleeding - where Difficult to stop or Re-bleeds Drug history Alcohol intake Co Morbid disease
Approach to testing
History and physical Type of tests guided by
clinical features Screening tests Further tests Definitive tests
Normal Hemostasis
Blood Coagulation & Tests
Thrombin time
Screening Tests
Platelet count INR Extrinsic pathway PTT (activated partial thromboplastin
time) intrinsic pathway Thrombin time final pathway fibrinogen
Laboratory tests further testing
Factor assays Tests of fibrinolysis platelet function tests Special tests
Who is likely to bleed
Cirrhosis Renal dysfunction Age Drugs Right heart failure
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 (Cirrhosis) New anticoagulants
Dabigatran: TT, PTT Rivaroxaban: antiXa, PT/INR
PossibilitiesINR PTT TT PLAT Dx
2.4 43 16 396
1.3 65 >60 287
1.1 52 17 387
1.2 90 18 321
1.6 46 54 56
1.2 65 >60 24
1.4 41 >60 396
CLINICAL CASES
Case 1
It is Friday at 4:40pm Lab calls You are patient is being preped for urgent
surgery. INR 6.5
What to do ?
Why INR’s go out of control
Vitamin K
Warfarin affects factors II,VII,IX and X These are the vitamin K dependent
factors Can reverse warfarin effect (Vitamin K,
prothrombin complex concentrates)
Efficacy of route of administration
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 36-48 hours.
1-2 mg will decrease INR to therapeutic Level within 12-24 hrs
Current practice
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 ?
ITP Immune thromboctopenic purpura
What is needed for diagnosis? 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 ?
ITP continued
If mucosal bleeding platelets are less than 10
Needs action Steroids IVIG Anti D
splenectomy Newer treatments
Rituximab TPO agonists
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 7.6 Plat 345 INR 2.6 ptt 42 What is likely diagnosis What to Do ?
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
Case 4
A 54 year old male comes to office feeling unwell.
Exam Mild jaundice, some telangectasis on skin Mod ascites. CBC - Hgb 110 WBC 2.5 plat 68 INR 1.6 Ptt 41 TT 25
What is likely diagnosis ?
Hepatic dysfunction - Cirrhosis
Liver makes and degrades Coagulation is affected by decreased
production and impaired degradation of activated factors
Chronic DIC Splenomegaly
Treatment only if bleeding Liver transplant
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 ?
Hemophilia
X linked bleeding disorders characterized by spontaneous development of large hematomas 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 associated with mild or moderate injury
Hemophilia types
Hemophilia A 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
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)
Hemophilia types
Subclassified by level of factors Levels correspond to clinical symptoms
Mild 5-30% factor activity Moderate 1-5% activity Severe <1% activity
Hemophilia - Clinical Picture
Mild- do not develop spontaneous bleeding, but do bleed after injury or surgery
Many patients have severe disease Joint Bleeding results in severe disability
hemarthroses chronic arthritis muscle bleeds
Social, economic,psychological problems
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 ?
Von Willebrand’s Disease
Most frequent inherited bleeding disorder 1% of western population less severe than hemophilia Disease results from a decrease or
absence of Von Willebrand factor for platelet adhesion
Affects primary hemostasis
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
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
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
VW -types
Type I most frequent, quantitave defect (decreased
VWf ) Type II
qualitative defect (abnormal VWf ) Type III
severe, rare, (absence of VWf )
How to diagnose Von Willebrands disease
Clinical history Factor VIII level Antigen and activity tests (Ristocetin
cofactor activity) Do gel electrophoresis for multimers
Anti platelet agents
ASA Not likelely to create problems Safer to give if there for cardivascular
reasons
Clopidogrel If elective stop before. Minimum 3 days More than 5 days unnecessary
Venous Thrombosis
common DVT, PE Splanchnic/portal vein thrombosis
Signs and Symptoms: Pain, swelling, erythema in an extremity SOB, CP, tachycardia, hypoxia
Diagnosis Clinical prediction models: Wells’ score D-dimer testing Imaging: US, CTPA, VQ Underlying risk factors
Thrombophilia: inherited, acquired
Venous Thrombosis
Treatment Low molecular weight heparin warfarin* IV unfractionated heparin warfarin
HIT (T): to consider if drop in platelet count in patient on a heparin agent
*continue LMWH for first 6 months after diagnosis of cancer associated VTE
New oral anticoagulant agents Rivaroxaban (Xarelto) Apixaban (Eliquis)
QUESTIONS