Pocket Medicine



Suspect in Pts with venous or arterial thrombosis at young age or unusual locationsrecurrent thromboses or pregnancy loss or  FHx

Diagnostic evaluation (not routinely required for initial VTE)

•  APC resistance screen; prothrombin PCR test; functional assays for proteins C and S, ATIII; homocysteine level; factor VIII levels; anticardiolipin and lupus anticoagulant Ab.  Also consider nephrotic syndrome, PNH (esp. if mesenteric thrombus).

•  Consider JAK2 mutation testing if suspect MPN or splanchnic thrombosis.

•  Proteins C & S and ATIII levels are affected by acute thrombosis and anticoagulation ∴ levels best assessed ≥2 wk after completing anticoagulation course

•  Age-appropriate malignancy screening ( in 7–10% in “idiopathic” DVT; Annals 2008;149:323)


•  Asx w/ inherited risk factor: consider prophylactic anticoag. if develops acquired risk factor

•  Thrombosis w/ inherited risk factor: see “Venous Thromboembolism”

Antiphospholipid syndrome (APS) ( J Thromb Haemost 2006;4:295; NEJM 2013;368:1033)

•  Definition: dx requires ≥1 clinical & ≥1 laboratory criteria

Clinical: thrombosis (any) or complication of pregnancy (≥3 spont. abortions before 10 wk or ≥1 fetal loss after 10 wk or premature birth before 34 wk)

Laboratory:  moderate–high titer anticardiolipin (ACL),  lupus anticoagulant (LA) or β2-glycoprotein-I (β2-GP-I) Ab on ≥2 occasions at least 12 wk apart

•  Clinical: DVT/PE/CVArecurrent fetal lossthrombocytopenia, hemolytic anemia, livedo reticularis; “catastrophic APS” = ≥3 organ systems in <1 wk w/  APLA & tissue microthrombi (Lupus2003;12:530) → 44% mortality (Arth Rheum 2006;54:2568)

•  Antiphospholipid antibodies (APLA) ✓ if: SLE, age <40 y & arterial thromb, recurrent venous thromb, spontaneous abortion

ACL: Ab against cardiolipin, a mitochondrial phospholipid; IgG more specific than IgM

LA: Ab that prolongs phospholipid-dependent coagulation reactions; ∴ ↑ PTT that does not correct with mixing study but does correct with excess phospholipids or platelets; PT not affected b/c the reaction contains much more phospholipid

β2-GP-I:  Ab against β2-glycoprotein-I, IgG or IgM

False  VDRL: nontreponemal test for syphilis in which cardiolipin is part of Ag complex

Clinical significance of different Abs in pathogenesis uncertain

Risk of thromboembolic phenomena may increase with titer of APLs

•  Etiologies: primary (idiopathic) or secondary due to autoimmune syndromes (eg, SLE), malignancyinfections, drug reactions

•  Treatment: UFH/LMWH → warfarin after thromboembolic event (lifelong for most Pts)

Intensity of anticoagulation controversial (Arthritis Rheum 2007;57:1487)

Initial venous thrombosis: INR 2–3 (NEJM 2003;349:1133;   J Thromb Haemost 2005;3:848)

Initial arterial thrombosis: typically INR 2–3 + ASA 81, although some treat to INR 3–4

Recurrent thrombosis on warfarin: INR 3–4 vs. LMWH (Arth Rheum 2007;57:1487)

Consider ASA prophylaxis for high-risk asx Pt (eg, SLE)