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Welcome applicants! In this segment, we discuss Deep Venous Thrombosis (DVT), its etiology including risk factors like central venous lines, genetic disorders, malignancies, and certain medical conditions. We also delve into clinical features, diagnosis through gold-standard venography and Doppler ultrasound, and when to consider thrombophilia. Key genetic factors such as Activated Protein C Resistance and Prothrombin mutations will be explored. Lastly, we’ll cover treatment options, potential complications, and the importance of preventive measures in high-risk patients.
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Welcome Applicants!! Morning Report Friday, October 28th
Etiology • Presence of a CVL* • Genetic risk factors (thrombophelia) • Underlying medical conditions • Malignancy • Sepsis • Nephrotic syndrome • Vasculitis • Congenital heart disease
Risk Factors • Aging • Immobilization longer than 3 days • Pregnancy • Major surgery in the past 4 weeks • Trauma • IV drug use • Use of OCPs
Clinical Features • Extremity pain/ tenderness • Swelling • Palpable cord • Discoloration (erythema) • Venous distention • Prominence of superficial veins • Cyanosis
Diagnosis • Gold standard= venography • Doppler US • Adequate for Dx of lower extremity DVT • Not very sensitive for upper extremity DVT
When to Consider Thrombophelia… • Positive family history • History of recurrent clots • Thrombi in unusual locations • Thrombosis at an early age
Activated Protein C Resistance • Most common genetic disorder causing thrombophelia • 3-8% Caucasians • 1% African Americans • Caused by Factor V Leiden mutation • Loss of the ability of the activated protein C to neutralize ongoing activation of the factor V molecule • Heterozygotes: threefold increased risk of DVT • Homozygotes: 30-fold increased risk
Prothrombin 20210A Mutation • Second most common genetic risk factor • Mutation increased concentration of prothrombin in plasma 3-5 fold increase of thrombosis
Hyperhomocysteinemia • Mutations in the genes for cystathionine and methylenetetrahydrofolatereductase elevated homocystine levels • Rarely causes arterial or venous thrombotic disease in childhood
Deficiency of ATIII, Protein C or S • Homozygous AT deficiency is incompatible with life • Homozygous PC or PS deficiency purpurafulminans within hours of birth • Heterozygotes: 50% increased risk of developing thromboembolism by middle age
Lipoprotein (a) • Elevated levels associated with cardiac disease in adults • Also has anti-fibrinolytic properties which can thrombotic disease • Serum levels >30mg/dL increase the likelihood of thromboembolism by a factor of seven
Antiphospholipid Syndrome • Due to circulating antibodies against a protein-lipid complex • Can occur with or without rheumatologic disease • Can lead to pregnancy-related complications • Miscarriage
Treatment • Acute life-threatening occlusions • Thrombolytic therapy • Acute non-life threatening occlusions • Initally… • Unfractionated heparin OR • Low-molecular weight heparin • Then… • Transition heparin to warfarin OR • Continue LMWH
Treatment • Duration 3-6 months • May consider future prophylactic anticoagulation in patients with genetic predisposition during high-risk situations
Complications • Pulmonary embolism • Recurrent thrombosis • Postphlebitic syndrome • Chronic pain, swelling and discoloration of the affected extremity
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!*