Vte and pregnancy
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VTE and Pregnancy. Huma Khan MD MCH fellow August 3 rd , 2011. objectives. Epidemiology of VTE in pregnancy to be able to identify the causes of vte To understand and identify the different diagnostic tools Understand prenatal management To be aware of the different pharmacotherapies

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Vte and pregnancy

VTE and Pregnancy

Huma Khan MD

MCH fellow

August 3rd, 2011


Objectives

objectives

Epidemiology of VTE in pregnancy

to be able to identify the causes of vte

To understand and identify the different diagnostic tools

Understand prenatal management

To be aware of the different pharmacotherapies

Identify risk factors for post natal management


Case 1

Case 1

AK is a 24 yr old obese AA G2P0010, who comes for an initial prenatal visit. She is very sure of her lmp which places her at about 8wk 3d GA. She states this a planned pregnancy and that she has been taking pnv’s.

Pmhx: DVT in her left leg 4yrs ago,

Pshx: none

Meds: pnv


Case 11

Case 1

Fhx: DM, cHTN

Shx: married, employed, no smoking, no etoh, hx of thc in college with occasional addition of other substances which she denies using once she graduated

Obhx: SAB 2 yrs ago at 6 wks different partner


Epidemiology

epidemiology

VTE( DVT & PE) occurs in 5 -12 per 10,000 pregnancies

Postpartum 3 -7 per 10,000 deliveries

7-10 fold increase in antepartum

15- 35 fold in post partum

PE leading cause of death in developing countries

current deaths from PE: 1.1 -1.5 per 100,000 deliveries


Anatomy

anatomy


Virchow s triad

virchow’s triad


Pathophysiology

pathophysiology

Virchow's triad

Venous stasis:

1st trimester to 36wk

Progesterone induced venodilation

Right iliac artery over left iliac vein

Gravid uterus

Immobilization


Pathophysiology1

pathophysiology

Virchow's triad

Vascular damage:

Compression at delivery

Assisted or operative delivery

Hypercoagulability:

 procoagulant factors

 anticoagulant activity

 fibrinolytic activity

= more thrombin generation + less clot dissolution


Vte and pregnancy


Other risk factors

Other risk factors

black race

Heart disease

Sickle cell disease

Diabetes

Lupus

  • Smoking

  • Multiple pregnancy

  • Ama

  • Obesity ( BMI > 30)

  • C-section( especially emergent or after long labor)


Thrombophilic disorders

Thrombophilic disorders

disorder of hemostasis predisposing to thrombotic event

Inherited

Factor V Leiden

Prothrombin G20210A

Acquired

Antiphospholipid antibody syndrome

Lupus anticoagulant


Thrombophilic disorders1

Thrombophilic disorders

cause 50 % of VTE in pregnancy

Occur only in 0.1% of pregnancies

Universal screening not cost effective

Screening affected in pregnancy

protein S levels fall in 2nd trimester

Massive thrombus & nephrotic syndrome decrease antithrombin levels

Liver disease decrease protein C & S levels

Screening should be done after pregnancy and when no longer taking anticoagulants


Thrombophilic disorders2

Thrombophilic disorders

Complications

Early and late losses

IUGR

Placental abruption


Presentation of vte

Presentation of vte

Difficult to differentiate from pregnancy sx’s

DVT:

Unilateral leg pain and swelling, especially left leg

≥ 2 cm calf circumference difference

1st trimester

Homan’s sign


Diagnosis tree

Diagnosis tree

Dresand et al. aafp,77:1709-16, 2008


Diagnostic tools for dtv

Diagnostic tools for DTV

VCUS ( venous compression ultrasonagraphy)

Sensitivity : 89 - 97%

Specificity : 94 - 99%

Less accurate for isolated calf and iliac vein thrombosis

D-Dimer

Levels increase during pregnancy

Usually positive and hence of little use

Negative test with low clinical probability has a NPV of 99.5 % when highly sensitive assay used.

positive test sensitivity is 100% & specificity is 60% hence additional testing is needed

MRI and ct can be done in high probability pts


Presentation

presentation

Difficult to differentiate from pregnancy sx’s

PE:

Dyspnea

Chest pain

Unexplained tachycardia


Pe diagnosis tree

PE diagnosis tree

Dresand et al. aafp,77:1709-16, 2008


Diagnostic tools for pe

Diagnostic tools for PE

v/q scan

PPV when combined with high clinical pretest is 96%

Only 56% with low clinical pretest

Radiation dose : 0.003 -.077 mGY

ct

In one study PPV’s in

Lobar: 97%

segmental:68%

Subsegmental: 25%

False positive rates: 30% , detected incorrectly in segmental/ subsegmental

Radiation dose: 0.02 -0.06 gy


Case 12

Case 1

AK is a 24 yr old obese AA G2P0010, who comes for an initial prenatal visit. She is very sure of her lmp which places her at about 8wk 3d GA. She states this a planned pregnancy and that she has been taking pnv’s.

Pmhx: DVT in her left leg 4yrs ago,

Pshx: none

Fhx: DM, cHTN

Meds: pnv

Shx: married, employed, no smoking, no etoh, hx of thc in college with occasional addition of other substances which she denies using once she graduated

Obhx: SAB 2 yrs ago at 6 wks different partner


Case 1 extra stuff

Case 1 : extra stuff

On further examination you find

BP: 140/85

BMI of 32

A few varicose veins on her right calf

On US she is 10wk with twin gestation


Case 1 management

Case 1 management

Identify the risk factors

prenatal management

What do do during labor and delivery

Identify risk factor for post partum management


Vte and pregnancy

Rcog Green- top guideline 37, 2009


Management

management

prophylaxis in pregnancy

Marik & Plante nejm,359:2025-33, 2008


Vte and pregnancy

Therapeutic dosing in pregnancy

Vena caval filters

Marik & Plante nejm,359:2025-33, 2008


Which heparin

UFH

Which heparin???

LMWH

  • More predictable dose response

  • More dose independent mechanisms of clearance

  • Long plasma half life

  • Once or twice daily dosing

  • No lab visits

  • Lower risk of bleeding, HIT & fractures

  • Not easily reversed

  • Dose dependent response

  • Clearance is dependent on renal / liver function

  • Half life is short and dose dependent

  • Multiple dosing

  • Labs for PLTS

  • High risk of bleeding and HIT

  • Easily reversed by protamine sulphate


Why not warfarin

Why notWarfarin ?!

Crosses placenta

Increases miscarriage, stillbirth, embryopathy (midface hypoplasia,stippled epiphyses) if exposed in 1st trimester

In 2nd and 3rd trimester causes CNS abnormalities and hemorrhage

It is compatible with breast feeding


During labor and delivery

During labor and delivery

Switch to UFH several wks before

stop all anticoagulation with onset of labor

If planned IOL or c-section then stop 24 hrs prior to

Management varies based on prophylaxis /treatment doses


Anticoagulation anesthesia

Anticoagulation & Anesthesia

neuroaxial anesthesia contra-indicated in spontaneous labor with full anticoagulation

Spinal anesthesia placed

12 hrs after prophylactic dose of LMWH

24 hrs after therapeutic dose of LMWH

6 hrs after UFH dose and confirmed normal activated partial-thromboplastin time

General preferred if emergent c-section

Anticipate larger blood loss


Reversal of ufh and lmwh

reversal of UFH and LMWH

Bourjeily et al. lancet 375:500-12, 2010


After birth

After birth

Post partum thromboprophylaxis not routinely indicated

ASA not used

Thromboprophylaxis for 6-12 wks

Warfarin can be used


Post op

Post OP

Incidence of PE higher by a factor of 2.5 to 20

Incidence of fatal PE by a factor of 10

Thromboprophylaxis highly effective in reducing the high incidence

Duration is 3-7 days for intermediate risk

Up to 6 wks for high risk.


Vte and pregnancy

Rcog Green- top guideline 37, 2009


Thank you

Thank you


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