Venous thromboembolism (VTE) in obstetrics Dr.Roaa H. Gadeer MD.

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Transcript of Venous thromboembolism (VTE) in obstetrics Dr.Roaa H. Gadeer MD.

Venous thromboembolism (VTE) Venous thromboembolism (VTE) in obstetricsin obstetrics

Dr.Roaa H. GadeerMD

ObjectivesObjectives

IncidencePathogenesisPredisposing factorsClinical PresentationsProphylaxisManagement choices

– Antepartum– Postpartum

IncidenceIncidence

Deep venous thrombosis– antepartum: 0.5-3 per 1000 pregnancies– postpartum: 0.5-18 per 1000 pregnancies

High recurrent risk: 7-13%pulmonary embolus

– untreated DVT: 24% have PE, 15% mortality

– treated DVT: 5% have PE, 1-2% mortality

Number of pregnancy deaths from 1982-1992 in Canada

0

2

4

6

8

10

12

14 PE

postpartumhemorrhage

amniotic fluidemboli

preeclampsia

anesthetics

ectopicpregnancy

septicemia

undetermined

Pathogenesis of VTE in pregnancyPathogenesis of VTE in pregnancy

Stasis Hypercoagulation

Vessel wall abnormality

Predisposing factors associated Predisposing factors associated with pregnancywith pregnancy

Hypercoagulability Stasis Endothelial damage

Increased factors: II, V, VII, VIII, IX, X, XII, fibrinogen

Increased venous distensibility and decreased tone

Vascular damage at delivery (CS or operative vaginal deliveries)

Increased platelet aggregation 50% decrease in venous flow in lower extremity by 3rd trimester

Decreased protein S, tissue plasminogen activator, factor XI, XIII

Uterus is mechanical impediment to venous return

Increased resistance to activated protein C

Decreased or normal antithrombin

Major risk factorsMajor risk factors previous hx of DVT/PE: 7-13% risk of recurrence thrombophilias trauma or infection age > 35 obesity long hospitalization dehydration/shock immobility before the operation >4 dayschemotherapy

ThrombophiliasThrombophilias

Congenital:– resistance to activated protein C (factor V

leiden)– hyperhomocysteinemia (controversial)– protein S, C deficiency: 2-4% risk, 18-20%

risk during postpartum – antithrombin III deficiency: 25-55% risk– Prothrombin G20210A

ThrombophiliasThrombophilias

Acquired:– antiphospholipid syndrome (APLS): role

to cause VTE is uncertain

Prevalence in population Prevalence in population

General population Thrombosis

Factor V leiden 5-9% 20-40%

Prothrombin G20210A

3% 6-15%

Protein C def 0.3% 1-2%

Protein S 0.2% 1-2%

ATIII def 0.07% <1%

Hyperhomocystin-emia

5% 5-10%

Clinical PresentationsClinical Presentations

1. Superficial venous thrombosis Typically associated with

superficial varicosities and IV catheterization

DX and management similar to non-pregnant women

Clinical PresentationsClinical Presentations

2. DVT Presentations largely depends on

the degree of occlusion Lt>Rt (80%) Early puerperium (why?)

Symptoms of DVT– calf pain, tenderness, swelling,

cord, + Homan’s sign– discoloration– 50% thought to have DVT have

negative U/S

Clinical PresentationsClinical Presentations

Clinical PresentationsClinical Presentations

3. PE Leading cause of perinatal

maternal loss in developed countries

Declining incidence

Symptoms of PE and DVTSymptoms of PE and DVT

Symptoms of PE:– tachypnea 80%– dyspnea 81%– pleuritic pain 72%– apprehension 60%– cough 54%– tachycardia 43%– T > 37.5C 35%* in those with

proven PE

Investigations for PE:Investigations for PE:

– CXR nondiagnostic, excludes other causes of hypoxemia

– ABG’s A-a gradient, maybe normal in >20%

– Doppler & US– Ventilation/perfusion Lung (V/Q) scan 0.2

rads to fetus– 95% correlation with venography– Spiral CT (non invasive)

– contrast venography,gold standard, 0.25 rads to fetus for legs

– pulmonary angiography, gold standard, 0.25 rads to fetus, 1% maternal

morbidity, 1/2000 mortality

Investigations for PE:Investigations for PE:

DiagnosisDiagnosis

Use US plus V/Q scanNo known human effects for fetal

exposure < 5 radsIf therapy will be altered by an

invasive diagnostic procedure, the benefit far overweighs the risk to mother and fetus given 15-40% mortality for untreated PE

PE Prevalence PE Prevalence

Reports suggest equal distribution between antenatal and postnatal period

Higher mortality in the post partum period

Can be asymptomatic DVT until embloization develop

Recommendations for Recommendations for thromboprophylaxisthromboprophylaxis Antepartum all pregnant women who had previous VTE should

be tested for thrombophilia factors; for single episode of prior VTE with transient risk

factors: surveillance (1C) for single episode of idiopathic VTE: surveillance or

UFH or prophylactic LMWH dose (1C) for single episode of VTE and thrombophilia (except

protein S): surveillance (except decreased antithrombin) or UFH or prophylactic LMWH dose (1C)

Antepartum continues:Antepartum continues:

known thrombophilia: surveillance (except decreased antithrombin) or UFH or prophylactic LMWH dose (1C)

recurrent episodes of VTE: adjusted dose of UFH or adjusted dose of LMWH (1C)

> 3 moderate risk factors: surveillance or UFH or prophylactic LMWH dose (1C)

PostpartumWarfarin should be offered to all

postpartum women who had previous VTE (1C)

Recommendations for Recommendations for thromboprophylaxisthromboprophylaxis

Low molecular weight heparinLow molecular weight heparin

Adjusted dose LMWH: enoxaparin 1 mg/kg sc q12h, dalteparin 200 IU/kg sc q24h

Advantages:

• possibly less risk of– thrombocytopenia– osteoporosis

more predictable therapeutic effect OD or BID administration monitor anti-Xa levels in third trimester

Disadvantages:

more difficult to reverse

drug cost higher but no need for hospitalization

Low molecular weight heparinLow molecular weight heparin

IV HeparinIV Heparin

– inhibits thrombin by activating AT-III, prevents conversion of fibrinogen to fibrin

– need baseline CBC, INR PTT– initial 5000 IU bolus, then 1000-1500 IU/hr,

INR & PTT q6hr PTT therapeutic level 1.5-2.5, then INR/PTT q24h

Advantages:– doesn’t cross placenta– not excreted in breast milk

IV HeparinIV Heparin

– rapidly reversible (protamine sulfate 1mg/100units)

– no increase in perinatal mortality or morbidity over control

Disadvantages:– bleeding in 4-8%– osteoporosis (15,000U/d > 5 months)– thrombocytopenia (by day 4)– Cost and compliance

Warfarin Warfarin

easily crosses placenta up to 70% fetal complications if in 1st

trimester– IUGR, chondrodysplasia punctata– multiple congenital anomalies

20-30% complication rate in 2nd-3rd trimester

Long half life

Management during peripartumManagement during peripartum

Therapy throughout pregnancy and 8-12 weeks post partum

IV Heparin and LMWH should be held once labor is established in order to use local anesthesia

If therapeutic PTT is required in labor, patient should be switched to IV heparin

Therapeutic PTT may increase the incidence of hematomas but not PPH

Avoid trauma or C/S at delivery–midline episiotomy if necessary–avoid tears

Resume heparin 6 hrs postpartum Start Warfarin when oral intake tolerated Avoid OCP, estrogen Consult!

Management during peripartumManagement during peripartum

Take home messageTake home message Thromboprophylaxis is recommended for previous

VTE hx and a known thrombophilia; idiopathic VTE, recurrent VTE, and more than 3 major risk factors for VTE (II B)

Diagnosis of VTE is clinical suspicion + lab tests, never hesitate to order V/Q scan spiral CT or angiography if the result will change management

Treatment is long term: till postpartum 8-12 weeks. Considering side effects of different drugs, cost, local anesthesia, avoiding instrument delivery