1. Welcome Applicants!! Welcome Applicants!! Morning Report Friday, October 28 th

3. DEEP VENOUS THROMBOSIS

4. What is a DVT?

5. Etiology Presence of a CVL*Presence of a CVL* Genetic risk factors (thrombophelia)Genetic risk factors (thrombophelia) Underlying medical conditionsUnderlying medical conditions MalignancyMalignancy SepsisSepsis Nephrotic syndromeNephrotic syndrome VasculitisVasculitis Congenital heart diseaseCongenital heart disease

6. Risk Factors AgingAging Immobilization longer than 3 daysImmobilization longer than 3 days PregnancyPregnancy Major surgery in the past 4 weeksMajor surgery in the past 4 weeks TraumaTrauma IV drug useIV drug use Use of OCPsUse of OCPs

7. Clinical Features Extremity pain/ tendernessExtremity pain/ tenderness SwellingSwelling Palpable cordPalpable cord Discoloration (erythema)Discoloration (erythema) Venous distentionVenous distention Prominence of superficial veinsProminence of superficial veins CyanosisCyanosis

9. Diagnosis Gold standard= venographyGold standard= venography Doppler USDoppler US Adequate for Dx of lower extremity DVTAdequate for Dx of lower extremity DVT Not very sensitive for upper extremity DVTNot very sensitive for upper extremity DVT

10. When to Consider Thrombophelia… Positive family historyPositive family history History of recurrent clotsHistory of recurrent clots Thrombi in unusual locationsThrombi in unusual locations Thrombosis at an early ageThrombosis at an early age

11. Activated Protein C Resistance Most common genetic disorder causing thrombopheliaMost common genetic disorder causing thrombophelia 3-8% Caucasians3-8% Caucasians 1% African Americans1% African Americans Caused by Factor V Leiden mutationCaused by Factor V Leiden mutation  Loss of the ability of the activated protein C to neutralize ongoing activation of the factor V molecule  Loss of the ability of the activated protein C to neutralize ongoing activation of the factor V molecule Heterozygotes: threefold increased risk of DVTHeterozygotes: threefold increased risk of DVT Homozygotes: 30-fold increased riskHomozygotes: 30-fold increased risk

12. Prothrombin 20210A Mutation Second most common genetic risk factorSecond most common genetic risk factor Mutation  increased concentration of prothrombin in plasma  3-5 fold increase of thrombosisMutation  increased concentration of prothrombin in plasma  3-5 fold increase of thrombosis

13. Hyperhomocysteinemia Mutations in the genes for cystathionine and methylenetetrahydrofolate reductase  elevated homocystine levelsMutations in the genes for cystathionine and methylenetetrahydrofolate reductase  elevated homocystine levels Rarely causes arterial or venous thrombotic disease in childhoodRarely causes arterial or venous thrombotic disease in childhood

14. Deficiency of ATIII, Protein C or S Homozygous AT deficiency is incompatible with lifeHomozygous AT deficiency is incompatible with life Homozygous PC or PS deficiency  purpura fulminans within hours of birthHomozygous PC or PS deficiency  purpura fulminans within hours of birth Heterozygotes: 50% increased risk of developing thromboembolism by middle ageHeterozygotes: 50% increased risk of developing thromboembolism by middle age

15. Lipoprotein (a) Elevated levels associated with cardiac disease in adultsElevated levels associated with cardiac disease in adults Also has anti-fibrinolytic properties which can  thrombotic diseaseAlso has anti-fibrinolytic properties which can  thrombotic disease Serum levels >30mg/dL increase the likelihood of thromboembolism by a factor of sevenSerum levels >30mg/dL increase the likelihood of thromboembolism by a factor of seven

16. Antiphospholipid Syndrome Due to circulating antibodies against a protein-lipid complexDue to circulating antibodies against a protein-lipid complex Can occur with or without rheumatologic diseaseCan occur with or without rheumatologic disease Can lead to pregnancy-related complicationsCan lead to pregnancy-related complications MiscarriageMiscarriage

17. Labs to Order

18. Treatment Acute life-threatening occlusionsAcute life-threatening occlusions Thrombolytic therapyThrombolytic therapy Acute non-life threatening occlusionsAcute non-life threatening occlusions Initally…Initally… Unfractionated heparin ORUnfractionated heparin OR Low-molecular weight heparinLow-molecular weight heparin Then…Then… Transition heparin to warfarin ORTransition heparin to warfarin OR Continue LMWHContinue LMWH

19. Treatment Duration 3-6 monthsDuration 3-6 months May consider future prophylactic anticoagulation in patients with genetic predisposition during high-risk situationsMay consider future prophylactic anticoagulation in patients with genetic predisposition during high-risk situations

20. Complications Pulmonary embolismPulmonary embolism Recurrent thrombosisRecurrent thrombosis Postphlebitic syndromePostphlebitic syndrome Chronic pain, swelling and discoloration of the affected extremityChronic pain, swelling and discoloration of the affected extremity

21. Thanks for your attention!! Noon Conference: Class Housestaff! *Dr. Desselle will be coming by each class meeting to explain inservice scores as well as go over journal club presentations with the third years!*