Venous thrombosis & pulmonary embolism Ahmed Mahmoud, MD
Risk factors for DVT Surgery ; post op especially for long cases, pelvic operations (THR), Trauma ; long bone fractures, pelvic fractures (posterior ring), spinal cord injury Malignancy ;(more when chemotherapy is used ) Central venous catheters or pacemakers CHF General risk factors are; age >75, immbolization, acute infections, pregnancy, estrogen therapy, hypercoagulable state
DVT starts in soleus muscle venous plexus below the knee.only 25 % will propagate proximally. Left leg more than the right May -Thurner sydrome ; Left iliac vein compressed by right iliac artrey. Ileofemoral vein thrombosis ; phlegemsia cerula dolens, phlegemsia alba dolnes
Diagnosis D dimer ; FDPs not helpful in post op or trauma Compression ultrasound; duplex ultrasound. Sensitive and specific (95%) above knee and below inguinal ligament Surveillance ultrasound is not standard of care CT venogram ; CTV uses venous phase of contrast to visualize veins. >90% sensitive and specific. Can evaluate iliac veins and IVC
Anticoagulation (cont d) HEPARIN: Lovenox: if hemodynamically stable, no renal function problem 1mg/kg BID OR 1.5mg/kg QDay Heparin ttt: if hypotension, renal failure 80units/kg bolus then 18 units/kg infusion Goal PTT 1.5 to 2.5 times the upper limit of normal Factor X assay COUMADIN: Start once acute anticoagulation achieved Start with 5mg PO qday OR 10mg PO q day If start with 10mg then achieve therapeutic INR 1.4 days sooner Complications and morbidity no different in 5mg or 10mg start Goal INR 2 to 3
Duration of Anticoagulation for DVT or PE* Event Duration Strength of Recommendation First Time event of Reversible cause (surgery/trauma) First episode of idiopathic VTE Recurrent idiopathic VTE or continuing risk factor (e.g., thrombophilia, cancer) Symptomatic isolated calf-vein thrombosis At least 3 mos At least 6 mos At least 12 mos *From American College of Chest Physicians A A B 6 to 12 weeks A
IVC Filter Indication: Absolute contraindication to anticoagulation (i.e. active bleeding) Recurrent PE during adequate anticoagulation Complication of anticoagulation (severe bleeding) Also: Pts with poor cardiopulmonary reserve Recurrent P.E. will be fatal Patient s who have had embolectomy Prophylaxis against P.E. in select patients (malignancy)
Treatment of P.E. Respiratory Support: Oxygen, intubation Hemodynamic Support: IVF, vasopressors Anticoagulation Thrombolysis IVC Filter
Anticoagulation Start during resuscitation phase itself If suspicion high, start emperic anticoagulation Evaluate patient for absolute contraindication (i.e.: active bleeding)
Thrombolysis Considered once P.E. diagnosed If chosen, hold anticoagulation during thrombolysis infusion, then resumed Associated with higher incidence of major hemorrhage Indications: persistent hypotension, severe hypoxemia, large perfusion defecs, right ventricular dysfunction, free floating right ventricular thrombus, paten foramen ovale Chemical /mechanical or combined (Catheter directed, Ekos, angiojet )
Complications of PE Acute Right heart failure (most common mechanism of death) Chronic pulmonary hypertension
Hypercoagulability Work Up No consensus on who to test Increased likelihood if: Age <50y/o without immediate identifiable risk factors (idiopathic or provoked) Family history Recurrent clots If clot is in an unusual site (portal, hepatic, mesenteric, cerebral) Unprovoked upper extremity clot (no catheter, no surgeries) Patient s with warfarin induced skin necrosis (they may have protein C deficiency
Hypercoagulability Work Up Protein C/S deficiency Factor V leiden deficiency AntiThrombin III deficiency (how does heparin work?) Prothrombin 20210 mutation Antiphospholipid antibody High Homocysteine
Most Common Cause of Congenital Hypercoagulablity Protein C resistance d/t Factor V leiden mutation
Congenital Hypercoagulable state Antithrombin III deficiency may be congenital (autosomal dominant) or acquired as in liver disease,nephrotic syndrome,protein enteropathy Deficiency is clinically seen as massive recurrent thrombosis in arterial or venous system or resistance to heparin therapy Treatment is by FFPS
Protein C ; inhibits factors V,VIII- Protein C deficiency is the second most common of all.clinically, recurrent thrombosis in early teenager. Coumadin causes Skin necrosis in patients with Protein C deficiency Protein S; is a cofactor for C
Factor V Leiden mutation The most common cause of congenital hypercoagulability Is a mutation in a part of Factor V which renders factor V resistant to Protein C Factor V is not inhibited(regulated) by protein C Recurrent thrombosis ( 5 times more common than normal population) LMWH is prophylaxis
Complications of anticoagulation Bleeding Most common heparin Coumadin 1% / year intra cranial bleed Coumadin induced skin necrosis with sub clinical protein C deficiency
Heparin Induced Thrombocytopenia(HIT) Incidence 2-6%. Immune mediated IgG/PF 3 May occur with heparin flush Thrombosis at arteries and veins Bleeding is less common It takes up to one month for antibodies to disappear Alternative treatments are Dextran,Danaporoid (old treatment) OR; Antithrombins Hirudin and refludan (renal clearance), argatroban(hepatic)