• Etiologies: trauma, shock, infection, malignancy, obstetrical complications
• Pathogenesis: massive activation of coagulation that overwhelms control mechanisms thrombosis in microvasculature • ischemia • microangiopathic hemolytic anemia acute consumption of coagulation factors and platelets • bleeding chronic DIC — able to replete factors and platelets - thrombosis
• Diagnosis: t PT. ? PTT. i fibrinogen (may be nl b c acute phase). © FDP D-dimer. i pits.0 schisto. t LDH.i hapto;chronic DIC® FDP D-dimer. variable pits.other labs nl
• Treatment: treat underlying process; support with FFP. cryoprecipitate (goal fibrinogen
>100 mg dl).and platelets: consider activated protein C in severe sepsis Vitamin K deficiency
• Etiologies: malnutrition, i absorption (antibiotic suppression of vitamin K-producing intestinal flora or malabsorption), liver disease (I stores), warfarin
|
Properties |
and Antidotes for Anticoagulants A Fibrinolytics | ||
|
Anticoag. |
tin |
Labs |
Rx for O D w serious bleeding* |
|
UFH |
60-90' RES |
T PTT |
Protamine IV 1 mg 100 U UFH (max 50 mg). For infusions, dose to reverse 2 * UFH given per h. |
|
Bivalirudin |
25. K |
' PTT |
Dial/sis |
|
Lepirudin |
80 . K |
1 PTT |
Dial/sis |
|
Argatroban |
45'. L |
1 PTT |
! Dialysis |
|
Enoxaparin |
8°, K |
(antl-Xa) |
! Protamine (reversal incomplete) |
|
Fondaparinux |
24°. K |
(anti-Xa) |
! Dialysis |
|
Warfarin |
36°. L |
t PT |
No Weeding: INR -5: vit. K 1-5 mg PO (superior to SC. -IV at 24°; 2.5 mg for INR 6-10; 5 mg for INR -10 (AreKm 2003:163:2469) Binding: vit. K 10 mg IV + FFP 2-4 units IV q 6-8" |
|
Fibrinolytic |
20-90' LK |
I fbgn ! FDP |
Cryoprecipitate. FFP. • aminocaproic acid |
•Initial step should be immediate d c of anocoag. Decision to dalyse should take into account bme for anocoag. to be mctabolacd (noting any renal or liver insufficiency) w o dialysis vs. potential sequelae of bleeding while waiting Rx for warfahn O D w o bleeding is also given. K kidney. L liver. RES reticuloendothelial system.
•Initial step should be immediate d c of anocoag. Decision to dalyse should take into account bme for anocoag. to be mctabolacd (noting any renal or liver insufficiency) w o dialysis vs. potential sequelae of bleeding while waiting Rx for warfahn O D w o bleeding is also given. K kidney. L liver. RES reticuloendothelial system.
HYPERCOAGULABLE STATES
Suspect in Pts with venous or arterial thrombosis at young age or unusual locations, recurrent thromboses or pregnancy loss, (& FHx
|
Inherited Hypercoagulable States | |||
|
Risk factor |
Prevalence |
VTE |
Comments |
|
(Caucasians) |
risk | ||
|
Factor V Leiden |
4% |
7x |
Activated protein C (APC) resist. |
|
Prothrombin mutation |
2% |
2.8* |
G20210A -»t prothrombin level |
|
Hyperhomocysteinemia |
5-10% |
2.5 x |
Inherited or acquired |
|
Protein C or S deficiency |
0.3% |
10x |
Warfarin-induced skin necrosis risk |
|
Antithrombin III deficiency |
0.04% |
25 x |
May be relatively heparin-resistant |
|
Vascular Beds Affected by Inherited and Acquired Hypercoagulable States | ||
|
Venous |
Venous and arterial | |
|
Inher. |
Factor V Leiden Prothrombin mutation I protein C.S. or AT III |
? factor V Leiden * smoking Hyperhomocysteinemia (inherited or acquired) Dysfibrinogenemia |
|
Acquired |
Stasis: immobilization, surgery. CHF Malignancy Hormonal: OCPs. HRT. tamoxifen, pregnancy Nephrotic syndrome |
Platelet defects: myeloproliferative disorders. HIT. PNH Hyperviscosity: polycythemia vera. Waldenstrom's macroglobulinemia. sickle cell, acute leukemia Vessel wall defects: vasculitis, trauma, foreign bodies Others: antiphospholipid syndrome. IBD |
Diagnostic evaluation
• APC resistance screen; prothrombin PCR test; functional assays for protein C and S.
ATIII; homocysteine level; anticardiolipin and lupus anticoagulant antibody assays
• Proteins C & S and ATIII levels are affected by acute thrombosis and anticoagulation;
levels best assessed &2 weeks after completing anticoagulation course
• Age-appropriate malignancy screening (© in 12% with "idiopathic" DVT;A»wh 1996:125:785)
Treatment
• Asx w inherited risk factor: consider prophylactic anticoag. if develops acquired risk factor
• Thrombosis w inherited risk factor: see "Venous Thromboembolism"
Antiphospholipid syndrome (APS) (nejm 2002:346:752)
• Definition: 1 clinical & -1 laboratory criteria
Oinical: thrombosis (any) or complication of pregnancy ( -3 sponL abortions before 10
wks or -1 fetal loss after 10 wks or premature birth before 34 wks) Laboratory: '*> moderate-high titer anticardiolipin (ACL) or lupus anticoagulant (LA) antibodies on =i2 occasions at least 6 wks apart
• Clinical manifestations: DVT PE CVA. recurrent fetal loss, thrombocytopenia.
hemolytic anemia, livedo reticularis: "catastrophic APS" widespread acute thrombotic microangiopathy with multiorgan visceral damage — high mortality
• Etiologies: primary (idiopathic) or secondary due to autoimmune syndromes (eg.
SLE), malignancy, infections, drug reactions
• Diagnosis: antiphospholipid antibodies are classified by method of detection
ACLAb against cardiolipin. a mitochondrial phospholipid; IgG more specific than IgM LA.Ab that prolongs phospholipid-dependent coagulation reactions: .'. t PTT that does not correct with mixing study but does correct with excess phospholipids or platelets: standard PT is not affected because the reaction contains much more phospholipid false * VDRL nontreponemal test for syphilis in which cardiolipin is part of Ag complex
• Treatment: lifelong warfarin after a thrombotic event; goal INR -3 (nejm 1995:332^93)
or 2-3 (nejm 2003:349 1133); consider ASA prophylaxis for high-risk asx Pt (eg. SLE)
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