Disseminated intravascular coagulation DIC nejm 1W341 S86

• 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

(NEJM 2001:3+4:1222)

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)

Was this article helpful?

0 0

Post a comment