A Case of Warfarin induced SDH

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  • The four Vitamin K dependent clotting factors are synthesized in the liver.
  • Warfarin acts as an anticoagulant by blocking the ability of Vitamin K to carboxylate the Vitamin K dependent clotting factors, thereby reducing their coagulant activity.
  • The signs of warfarin overdosage are listed on this slide. Hemorrhagic complications from warfarin therapy are more likely to occur with excessive degrees of anticoagulation, but even with an INR in the therapeutic range, bleeding can occur. Because of the likelihood of finding an underlying lesion in an individual who has gastrointestinal bleeding or significant genito-urinary bleeding in the face of therapeutic levels of anticoagulation, one is advised to consider and evaluate for underlying abnormalities predisposing to the bleeding. The return on such evaluations in the face of an excessive degree of anticoagulation diminishes, and one must use judgement whether or not to pursue an evaluation.
  • A Case of Warfarin induced SDH

    1. 1. TRAUMA DUE TO TREATMENT Prof.S.Ramaswamy’s unit,M1 Dr.Sangeetha.C.Joseph
    2. 2. Case <ul><li>Najumuneesha , 50 years , F </li></ul><ul><li>Presenting complaints: </li></ul><ul><ul><li>Headache- 3 days </li></ul></ul><ul><ul><li>Vomiting- 3 days </li></ul></ul><ul><ul><li>Breathlessness- exacerbated since 3 days </li></ul></ul><ul><ul><li>Decreased urine output- exacerbated since 3 days </li></ul></ul>
    3. 3. History of presenting complaints <ul><ul><li>Known case of RHD for past 4 years on treatment </li></ul></ul><ul><ul><li>Complaints of headache – </li></ul></ul><ul><ul><ul><li>severe, occipital headache, continuously present </li></ul></ul></ul><ul><ul><ul><li>Not relieved with any medication </li></ul></ul></ul><ul><ul><ul><li>No history trauma/ seizures . </li></ul></ul></ul><ul><ul><ul><li>History of altered sensorium – on & off </li></ul></ul></ul><ul><ul><li>Vomiting- </li></ul></ul><ul><ul><ul><li>Nausea, non projectile,non bilious. </li></ul></ul></ul>
    4. 4. History of presenting complaints (contd.) <ul><li>It was associated with exacerbation of breathlessness </li></ul><ul><ul><li>History of orthopnea and PND present. </li></ul></ul><ul><li>History of decreased urine output and facial puffiness was present </li></ul>
    5. 5. <ul><li>Past history: </li></ul><ul><ul><li>Known case of RHD for 4 years on treatment . No history of Hypertension, Diabetes mellitus, Tuberculosis, Asthma. No history of trauma in the past. No surgery in past. Not willing for valve surgery. </li></ul></ul><ul><li>Family history- </li></ul><ul><ul><li>Nil relevant </li></ul></ul><ul><li>Treatment history- </li></ul><ul><ul><li>T. Digoxin,Penicillin, Lasix, Slactone, Warfarin-3mg OD </li></ul></ul><ul><li>Personal History- </li></ul><ul><ul><li>Decreased urine output </li></ul></ul><ul><li>Menstrual history- </li></ul><ul><ul><li>Has attained menopause </li></ul></ul>
    6. 6. On Examination <ul><li>Patient conscious, obeying few commands </li></ul><ul><li>GCS- 11/15 </li></ul><ul><li>Afebrile, facial puffiness </li></ul><ul><li>Pallor+, bilateral pedal oedema </li></ul><ul><li>No icterus/ cyanosis/ clubbing </li></ul><ul><li>Vital signs- PR- 92/ min, irregularly irregular, BP- 130/90, RR- 20/ min, Temp- 99.4˚F ,JVP elevated </li></ul>
    7. 7. <ul><li>CVS: </li></ul><ul><ul><li>apex in 5th left intercostal space in 1 cm lateral to mid clavicular line </li></ul></ul><ul><ul><li>P2 palpable </li></ul></ul><ul><ul><li>S1 variable intensity, P2 Loud </li></ul></ul><ul><ul><li>MDM +, OS + </li></ul></ul><ul><li>CHEST </li></ul><ul><ul><li>NVBS heard, B/L basal crepts+ </li></ul></ul><ul><li>PER ABDOMEN </li></ul><ul><ul><li>Soft, No HSM </li></ul></ul>
    8. 8. CNS <ul><li>GCS- 11/15 </li></ul><ul><li>PUPILS- B/L equally reacting to light </li></ul><ul><li>Tone normal in all 4 limbs </li></ul><ul><li>Deep tendon reflexes B/L normal and B/L plantar flexor. </li></ul><ul><li>No s/o meningeal irritation </li></ul><ul><li>Fundus normal </li></ul>
    9. 9. INVESTIGATIONS <ul><li>Hb-9gm/dl </li></ul><ul><li>TC-7400 </li></ul><ul><li>DC-P54 L44 </li></ul><ul><li>PCV-25% </li></ul><ul><li>ESR-6/14 </li></ul><ul><li>PLC-1.8 </li></ul><ul><li>RBS-112 </li></ul><ul><li>BLOOD UREA-18 </li></ul><ul><li>S.CRATININE-0.9 </li></ul><ul><li>RUE-WNL </li></ul>
    10. 10. 1.7 2.1 3.64 4.65 INR 21 21.2 22.4 21.3 aPTT Control-21 12.1 18.2 38.4 40.7 PT Control-11 DAY 8 DAY 6 DAY 3 DAY 1 INV
    11. 11. <ul><li>ECG—Atrial fibrillation/RVR </li></ul><ul><li>ECHO-MS severe,PHT severe </li></ul><ul><li>LA dilated,no LA clot </li></ul><ul><li>advised to stop warfarin </li></ul>
    12. 13. <ul><li>All cardiac drugs continued except Warfarin </li></ul><ul><li>Vit K given </li></ul><ul><li>By day 6 pt became fully conscious and was relieved of headache and vomiting </li></ul><ul><li>Repeat CT brain –resolved SDH </li></ul>
    13. 14. <ul><li>FINAL DIAGNOSIS </li></ul><ul><li>RHD/MS SEVERE/PHT/CCF/ATRIAL FIBRILLATION/WARFARIN INDUCED ACUTE SDH </li></ul>
    14. 15. <ul><li>WARFARIN </li></ul>
    15. 16. HEMOSTASIS <ul><li>VASCULAR SPASM </li></ul><ul><li>PLATELET PLUG </li></ul><ul><li>BLOOD COAGULATION </li></ul><ul><li>GROWTH OF FIBROUS TISSUE IN CLOT </li></ul>
    16. 17. WHEN DOES BLOOD COAGULATE? <ul><li>Procoagulants > Anticoagulants </li></ul><ul><li>Injury to blood vessel </li></ul><ul><li>Blood stasis </li></ul>
    17. 18. INITIATION OF BLOOD COAGULATION Extrinsic Pathway Tissue trauma Leakage of Tissue Factor X Xa Prothrombin activator Ca +2 , factor VII Ca +2 Prothrombin Thrombin (factor II) Ca +2 Intrinsic Pathway Blood trauma/ contact with collagen Activation of factor XII, IX, VIII X Xa Ca +2 Prothrombin activator Prothrombin Thrombin (factor II) Activation of certain factors (VII, II, X and protein C and S) is essential for coagulation. This activation requires vit K (reduced form)
    18. 19. Vitamin K-Dependent Clotting Factors Vitamin K Synthesis of Functional Coagulation Factors VII IX X II
    19. 20. Warfarin Mechanism of Action Warfarin Synthesis of Non Functional Coagulation Factors Antagonism of Vitamin K Vitamin K VII IX X II
    20. 21. WARFARIN: MECHANISM OF ACTION Inactive factors II, VII, IX, and X Proteins S and C Proteins S and C Active factors II, VII, IX, and X Vitamin K epoxide Vitamin K reduced WARFARIN <ul><li>Prevents the reduction of vitamin K, which is essential for activation of certain factors </li></ul><ul><li>Has no effect on previously formed thrombus </li></ul>
    21. 22. PLASMA HALF-LIVES OF VITAMIN K-DEPENDENT PROTEINS Peak anticoagulant effect may be delayed by 72 to 96 hours 36h Factor X 24h Factor IX 6h Factor VII 72h Factor II
    22. 23. Warfarin - Pathophysiology <ul><li>Anticoagulant effect mediated by inhibition of vitamin K dependent  -carboxylation of factors II, VII, IX, X </li></ul><ul><ul><li>Proteins become biologically inactive </li></ul></ul><ul><li>Effect of warfarin delayed until clotting factors are cleared from the circulation ~ 36-72hrs </li></ul><ul><li>Equilibrium reached in about 1 week </li></ul>
    23. 24. INDICATIONS <ul><li>Prophylaxis and treatment of venous thromboembolism (deep vein thrombosis and pulmonary embolism) </li></ul><ul><li>Prophylaxis and treatment of Atrial fibrillation </li></ul><ul><li>Valvular stenosis </li></ul><ul><li>Heart valve replacement </li></ul><ul><li>Myocardial infarction </li></ul>
    24. 25. WHY TO MONITOR WARFARIN THERAPY? <ul><li>Narrow therapeutic range </li></ul><ul><li>Can increase risk of bleeding </li></ul>
    25. 26. MONITORING OF WARFARIN THERAPY <ul><li>Prothrombin time </li></ul><ul><li>PT ratio </li></ul><ul><li>INR (International Normalized Ratio) </li></ul>
    26. 27. PROTHROMBIN TIME (PT) <ul><li>Time required for blood to coagulate is called PT </li></ul><ul><li>Performed by adding a mixture of calcium and thromboplastin to citrated plasma </li></ul><ul><li>As a control, a normal blood sample is tested continuously </li></ul><ul><li>PT ratio (PTR) = Patient’s PT </li></ul><ul><li> Control PT </li></ul>
    27. 28. PROBLEMS WITH PT/PTR <ul><li>Thromboplastins are extracts from brain, lung or placenta of animals </li></ul><ul><li>Thromboplastins from various manufacturers differ in their sensitivity to prolong PT </li></ul><ul><li>May result in erratic control of anticoagulant therapy </li></ul>
    28. 29. INTERNATIONAL NORMALISED RATIO (INR) INR = [PT pt ] ISI [PT Ref ] PT pt – prothrombin time of patient PT Ref – prothrombin time of normal pooled sample ISI – International Sensitivity Index
    29. 30. OPTIMIZING WARFARIN THERAPY <ul><li>Dosage to be individualized according to patient’s INR response. </li></ul><ul><li>Use of large loading dose may lead to hemorrhage and other complications. </li></ul><ul><li>Initial dose: 2-5 mg once daily </li></ul><ul><li>Maintenance dose: 2-10 mg once daily </li></ul><ul><li>Immediate anticoagulation required: Start heparin along with loading dose of warfarin 10 mg. Heparin is usually discontinued after 4-5 days. Before discontinuing, ensure INR is in therapeutic range for 2 consecutive days </li></ul>
    30. 31. How frequently we should monitor? <ul><li>Monitor daily until INR is in therapeutic range </li></ul><ul><li>then 3 times weekly for 1-2 weeks, </li></ul><ul><li>then less often (every 4 to 6 weeks) </li></ul>
    31. 32. Commencement & discontinuation of AC guidelines british committee for hematology <ul><li>Recommendation </li></ul><ul><li>For outpatients who do not require rapid anticoagulation a slow loading regimen is safe and achieves therapeutic anticoagulation in the majority of patients within3 to 4 weeks. This appears to avoid overanticoagulation andbleeding associated with rapid loading. </li></ul><ul><li>For patients requiring rapid initiation of oral anticoagulation, regimens that start with 5mg doses or a single 10mg dose followed by 5mg doses may be preferable to regimens that start with repeated 10mg doses in certain patientgroups, e.g. the elderly (>60 years old), those with liver disease or cardiac failureand those at high risk of bleeding. </li></ul>
    32. 33. Guide lines for dosing RECOMMENDATIONS american college of cardiology <ul><li>LEVEL 1 </li></ul><ul><ul><li>W dose adjusted based on target INR </li></ul></ul><ul><ul><li>Better to avoid a loading dose of 10 mg </li></ul></ul><ul><li>LEVEL 2 </li></ul><ul><ul><li>All should have baseline INR value </li></ul></ul><ul><ul><li>Daily PT / INR chart till INR value becomes stable </li></ul></ul><ul><li>LEVEL 3 </li></ul><ul><ul><li>Patients with significant drug interactions / risk factors start on low dose warfarin </li></ul></ul><ul><ul><li>If significant drug interaction daily PT / INR until INR stable </li></ul></ul>
    33. 35. OPTIMAL THERAPEUTIC RANGE 2.0-3.0 2.5-3.5 (high risk patients) Myocardial infarction,recurrent DVT and PTE 2.0-3.0 2.5-3.5 Heart valve replacement Bioprosthetic valve Mechanical valve 2.0-3.0 Mitral valve stenosis 2.0-3.0 Atrial fibrillation 2.0-3.0 Treatment of venous thromboembolism 2.0-3.0 Prophylaxis of venous thromboembolism INR Indication
    34. 36. <ul><li>Indications </li></ul><ul><li>Atrial Fibrillation </li></ul><ul><ul><li>Valvular </li></ul></ul><ul><ul><li>Nonvalvular </li></ul></ul><ul><li>Cardioversion </li></ul><ul><li>Mural Thrombus </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Mechanical Prosthetic Valve Mitral </li></ul><ul><li>Mechanical Prosthetic Valve Aortic </li></ul><ul><li>Bioprosthetic Valve </li></ul>2.5 2.5 2.5 2.5 / 3.0 2.5 2.5 3.0 – 3.5 2.5 – 3.0 2.5 Target INR . Warfarin Indications – Systemic
    35. 37. Usually indefinite Oral Anticoagulation for prevention of Thromboembolism <ul><li>Valvular </li></ul><ul><li>Rheumatic Heart Disease (MS) </li></ul><ul><li>Prosthetic Heart Valve </li></ul><ul><li>Prior Thromboembolism </li></ul><ul><li>Persistent Atrial Thrombus on TEE </li></ul>INR – 2 to 3 INR – 2.5 to 3.5 <ul><li>Nonvalvular </li></ul><ul><li>Age ≥ 60 years with DM or CAD (INR – 2-3) (Aspirin is added) </li></ul><ul><li>Age ≥ 75 years (INR – 2) </li></ul><ul><li>Heart Failure </li></ul><ul><li>LVEF < 30% </li></ul><ul><li>Thyrotoxicosis </li></ul><ul><li>Hypertension </li></ul>Oral Anticoagulants inAtrial Fibrillation
    36. 38. FACTORS INFLUENCING DOSE RESPONSE <ul><li>Inaccurate lab testing </li></ul><ul><li>Poor patient compliance </li></ul><ul><li>Concomitant medications </li></ul><ul><li>Levels of dietary vitamin K </li></ul><ul><li>Alcohol </li></ul><ul><li>Hepatic dysfunction </li></ul><ul><li>Fever </li></ul>
    37. 39. CONTARINDICATIONS AND PRECAUTIONS <ul><li>Hypersensitivity to warfarin </li></ul><ul><li>Condition with risk of hemorrhage </li></ul><ul><li>Hemorrhagic tendency </li></ul><ul><li>Inadequate laboratory techniques </li></ul><ul><li>Protein C & S deficiency </li></ul><ul><li>Vitamin K deficiency </li></ul><ul><li>Intramuscular injections </li></ul>
    38. 40. SIDE EFFECTS <ul><li>Hemorrhage </li></ul><ul><li>Skin necrosis </li></ul><ul><li>Purple toe syndrome </li></ul><ul><li>Microembolization </li></ul><ul><li>Teratogenecity </li></ul><ul><li>Agranulocytosis, leukopenia, diarrhoea, </li></ul><ul><li>nausea, anorexia. </li></ul>
    39. 41. <ul><li>Major A/E is bleeding </li></ul><ul><li>Risk of bleeding depends on </li></ul><ul><li>1.intensity of anticoagulation </li></ul><ul><li>2.concomitant clinical disorders </li></ul><ul><li>3.use of other medications </li></ul><ul><li>4.management quality </li></ul>
    40. 42. Bleeding risk high in elderly d/t <ul><li>Increased age and sensitivity at usual doses </li></ul><ul><li>Co-morbid conditions </li></ul><ul><li>Increased drug interactions </li></ul>
    41. 43. Etiology in elderly <ul><li>Older adults-increased risk for SDH d/t fragility of bridging cerebral veins----as cerebral atrophy develops----brain shrinks away from dura and bridging veins----predisposed to tearing due to increased stress. </li></ul><ul><li>Males increased risk for SDH-etiology not clear </li></ul>
    42. 44. May begin concomitantly with Heparin Therapy Heparin should be continued for a minimum of four days Time to peak antithrombotic effect of Warfarin therapy is delayed 96 hours (despite INR) When INR reaches desired therapeutic range, discontinue heparin ( after a minimum of four days ) Conversion from Heparin to Warfarin
    43. 45. SWITCHOVER FROM ONE BRAND OF WARFARIN TO ANOTHER/ ACENOCOUMAROL <ul><li>Check patient’s INR </li></ul><ul><li>Start with dose of 2 mg; increase dose slowly as required </li></ul>
    44. 46. Signs of Warfarin Overdosage <ul><li>Any unusual bleeding: </li></ul><ul><ul><li>Blood in stools or urine </li></ul></ul><ul><ul><li>Excessive menstrual bleeding </li></ul></ul><ul><ul><li>Bruising </li></ul></ul><ul><ul><li>Excessive nose bleeds/bleeding gums </li></ul></ul><ul><ul><li>Persistent oozing from superficial injuries </li></ul></ul><ul><ul><li>Bleeding from tumor, ulcer, or other lesion </li></ul></ul>
    45. 47. Causes of excessive anticoagulation <ul><li>High dose warfarin </li></ul><ul><li>Drug interactions </li></ul><ul><li>Genetic polymorphisms- variations in pts’ response to warfarin </li></ul><ul><li>Superimposed diseases (liver, malabsorption syndromes) </li></ul><ul><li>Vitamin K deficiency </li></ul><ul><ul><li>Poor dietary intake </li></ul></ul><ul><ul><li>TPN </li></ul></ul><ul><ul><li>Prolonged course of ABX </li></ul></ul>
    46. 48. THE OVERALL ANTICOAGULATION QUALITY IS SIGNIFICANTLY BETTER WITH WARFARIN AS COMPARED TO ACENOCOUMAROL 72% 67% 64% 66% 68% 70% 72% % Responders Warfarin Acenocoumarol Thrombosis And Haemostasis 1994; 71(2): 188-191
    47. 49. New Anticoagulation Drugs <ul><li>Direct Thrombin Inhibitors </li></ul><ul><ul><li>Ximelagatran, hirudin, bivalirudin, and argatroban </li></ul></ul><ul><li>Synthetic pentasaccharide </li></ul><ul><li>Acivated Protein C </li></ul><ul><li>Tissue Factor Pathway Inhibitor (TFPI) </li></ul>
    48. 50. Why do we need new anticoagulation drugs? <ul><li>Heparin-induced thrombocytopenia </li></ul><ul><li>Heparin prophylaxis is imperfect </li></ul><ul><li>Heparin-associated osteoporosis </li></ul><ul><li>Warfarin takes several days for its effect </li></ul><ul><li>Warfarin is not as effective in some situations e.g antiphospholipid syndrome </li></ul><ul><li>Warfarin interacts with many other drugs </li></ul><ul><li>Warfarin is dangerous if not monitored </li></ul>
    49. 51. Synthetic Pentasaccharide <ul><li>E.g Fondaparinux </li></ul><ul><li>Synthetic, single molecular entity </li></ul><ul><li>Targets Factor Xa </li></ul><ul><li>Does not cause thrombocytopenia </li></ul><ul><li>Shown promise in DVT prevention during orthopedic procedures. </li></ul><ul><li>Also being examined in ischaemic heart disease </li></ul>
    50. 52. Ximelagatran <ul><li>Promising oral direct thrombin inhibitor </li></ul><ul><li>Converted to the active form melagatran in vivo </li></ul><ul><li>No dosing problems </li></ul><ul><li>No monitoring needed. </li></ul><ul><li>Recent atrial fibrillation study showed it to possibly be superior to warfarin. </li></ul>
    51. 53. Dilemma for the physician in SDH <ul><li>Continuing anticoagulants-may increase volume of haemorrhage </li></ul><ul><li>Early reinstitution of drug-may cause recurrence of bleed </li></ul><ul><li>Reversal of drug-pt at risk for systemic embolization </li></ul>
    52. 54. Neurological complications of ac <ul><li>Cause bleeding in -----brain </li></ul><ul><li>------spinal cord </li></ul><ul><li>------peripheral nerve </li></ul><ul><li>BRAIN---SDH,ICH etc </li></ul><ul><li>SPINAL CORD-subdural hematoma </li></ul><ul><li>PERIPHERAL NERVE-most frequent is femoral nerve compression d/t bleeding into iliacus muscle </li></ul>
    53. 55. How safely and for how long can W be withheld in pts when admitted with major bleeds ? <ul><li>Depends on relative risk and benefit of treatment </li></ul><ul><li>Studies have shown that the risk of TE is low in prosthetic valve pts when W is withheld following a major bleed </li></ul><ul><li>No definite recommendations are there </li></ul><ul><li>Around 2 wks can be taken roughly for safety </li></ul>
    54. 56. <ul><li>No study has evaluated the optimal time for restarting in pts with SDH </li></ul><ul><li>If no evacuation done—rpt CT in 1-2 wks—serial CT in 4-6 wks---resolved----restart AC </li></ul>
    55. 57. <ul><li>Risk of ischemic stroke in pts with prosthetic heart valves after W discontinuation is 3% in 30 days </li></ul><ul><li>Recurrence of SDH after resuming treatment is very less </li></ul>
    56. 58. Withdrawal of oral anticoagulant treatment <ul><li>Whether treatment should be withdrawn </li></ul><ul><li>abruptly or gradually withdrawn (&quot;tailed off&quot;) </li></ul><ul><li>is still debatable. </li></ul><ul><li>Theoretically, the &quot; rebound hypercoagulability &quot; which results from sudden discontinuation might predispose to rebound thrombosis. </li></ul><ul><li>Some clinicians tail off long term treatment over several weeks but withdrawl for short term treatment can be done suddenly. </li></ul>
    57. 59. Discontinuation of ac british committee standards of hematology <ul><li>Concern of a ‘ rebound hypercoagulable state’ after stopping oral anticoagulant therapy has resulted in uncertainty as to whether treatment should be stopped abruptly or gradually. </li></ul><ul><li>Laboratory markers indicate a hypercoagulable state in some patients following withdrawal of oral anticoagulant therapy, regardless of the speed of withdrawal (Palareti and Coccheri 1996, Palareti , et al 1994). </li></ul><ul><li>In many patients this is probably the result of a pre-existing prothrombotic state that may have contributed to the thrombotic event necessitating anticoagulant treatment. </li></ul><ul><li>Recommendation </li></ul><ul><li>Oral anticoagulant therapy can be discontinued abruptly when the duration of therapy is completed. </li></ul>
    58. 60. Reversal Options <ul><li>Holding warfarin dose </li></ul><ul><li>Holding dose + Vit K </li></ul><ul><ul><li>Vit K </li></ul></ul><ul><ul><ul><li>Oral </li></ul></ul></ul><ul><ul><ul><li>Subcutaneous </li></ul></ul></ul><ul><ul><ul><li>Intraveneous </li></ul></ul></ul><ul><li>FFP </li></ul><ul><li>FactorVIIa-15-20mcg/kg </li></ul><ul><li>Prothrombin complex concentrate </li></ul>
    59. 61. <ul><li>In Asymptomatic pts ; </li></ul><ul><li>INR-3.5-4.5=stop W till INR returns to normal therapeutic range </li></ul><ul><li>INR->4.5=low doses of sublingual vit K </li></ul><ul><li>INR-4.5-9=vit K 1mg will be enough </li></ul><ul><li>INR>9=vit K 2-3mg can be used </li></ul>
    60. 62. <ul><li>In pts with serious bleeding, </li></ul><ul><li>Vit K 10mg can be given as slow IV infusion,addtl doses if needed </li></ul><ul><li>Add FFP to give vit K dependent coagulation factors </li></ul><ul><li>Life threatening bleeding FVIIa/prothrombin concentrates </li></ul>
    61. 63. Recommendations for reversal guide lines on oral ac by british society of hematology <ul><li>A Life threatening haemorrhage </li></ul><ul><li>Immediately give 5 mg vitamin K, by slow intravenous infusion and a concentrate of factor II, IX, X, with factorVIIconcentrate. </li></ul><ul><li>B Less severe haemorrhage such as haematuria and epistaxis </li></ul><ul><li>Withhold warfarin for one or more days and consider giving vitaminK, 0. 5-2 mg intravenously </li></ul><ul><li>C INR of > 4.5 without haemorrhage </li></ul><ul><li>Withdraw warfarin for one or two days then review </li></ul><ul><li>D Unexpected bleeding at therapeutic levels </li></ul><ul><li>Investigate possibility of underlying cause such as unsuspected renal or alimentary tract disease </li></ul>
    62. 64. <ul><li>OAC therapy – associated with inherent risk of bleeding </li></ul><ul><li>Proper anticoagulant initiation, dosages according to desired INR alleviates the risk of bleeding </li></ul><ul><li>Maintenance dosage and duration of therapy as per the underlying clinical condition and other risk factors </li></ul><ul><li>Physician’s role is vital in treatment, education, counseling and communication </li></ul>Message ……
    63. 65. <ul><li>THANK YOU </li></ul>

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