VENOUS

THROMBOEMBOLIS
M
DURING
PREGNANCY
Dr. Novia Fransiska, SpOG
SMF Obgin RSU A.Wahab Sjahranie
SAMARINDA

What is DVT?
Deep vein thrombosis or DVT involves
abnormal clotting of the blood in a deep
vein, most commonly in the veins of the leg
or pelvis
Left untreated, DVT can cause serious health
problems and even death

What is PE?
Pulmonary embolism or PE occurs when a
clot (DVT) breaks free from its original site
in a vein, and travels through the
bloodstream and into the lungs
DVT and PE are common, potentially
life-threatening, but treatable and generally
preventable conditions

Incidence of Venous
Thrombosis

5-fold increased risk

0.5 3.0 per 1,000 women
Diagnosis
Antepartum
Postpartum
Most common site: left lower extremity

BLOOD CLOTTING
XII XIIa
XI XI a
IX IX a + VIIIa
X

Xa + Va
Prothrombin ---- thrombin
Fibrinigen fibrin
XIIIa

fibrin clot FDP

plasminogen

plasmin

Thrombosis :
1) Alteration in vessel wall
2) slowing of the blood flow (or stasis)
3) Changes in the blood components

DVT VTE Risk factors

Malignancy
Surgery
Trauma
Pregnancy
Oral contraceptives or hormonal therapy
Immobilization
Inherited thrombophillia
Presence of venous catheter
Congestive failure
Antiphospholipid antibody syndrome
Hyperviscosity
Nephrotic syndrome
Inflammatory bowel disease

How are DVT and PE Diagnosed?

Venous duplex ultrasound

D - dimer assay
Ventilation/perfusion scan
Computerized tomography (CT) scan
Magnetic resonance imaging (MRI)
Venogram
Pulmonary angiogram

Venous Thrombosis
If postpartum thrombosis occurs, it is more
commonly diagnosed on the second or third
postpartum day.
However, it can occur for up to 4 weeks
postpartum
Current findings reflect equal distribution of
thromboembolism throughout each trimester
and the postpartum period, with as many as
16-33% of cases occurring in the 1st trimester

Venous Thrombosis

In addition, research has identified that

greater than 90% of deep vein thromboses
(DVTs) during pregnancy will occur in the left
lower extremity
This is thought to be due to an exaggerated
compressive effect from the gravid uterus on
the left iliac vein.

Risk of Venous Thrombosis and

Thromboembolic Disorders
Thrombophilias (inherited or acquired

coagulation disorders)
Factor V Leiden mutation
Antithrombin III deficiency
Protein C and Protein S deficiencies
Prothrombin gene mutation

THROMBOPHILIAS

a group of inherited or acquired coagulation disorders

that may predispose an individual to the formation of
thromboses
Hereditary thrombophilias affect 15% of Western
populations
40%-50% of patients with thromboembolic disease
during pregnancy have a hereditary thrombophilia due
to the normal physiologic changes that affect
coagulation,
pregnancy is considered a hypercoagulable state

THROMBOPHILIAS

Fibrinogen levels double during pregnancy in

preparation for placental separation
There is also an increase in Clotting Factors V,
VII, VIII, IX, X, and XII manifest symptoms of
thrombophilia for the first time in pregnancy

Factor V Leiden mutation:

Factor V is a proenzyme that is activated by Factor Va,
which helps to activate prothrombin to thrombin in the
formation of a clot
autosomal dominant disorder seen in 5%-9% of White
Europeans,rare in women of Asian and African descent
present in 40% of pregnant women with VTEs
associated with late 1sttrimester loss, 2nd 3rd tms loss,
severe IUGR, abruption,preterm delivery, and severe
preeclampsia

Antithrombin III (AT-III):

the rarest inherited thrombophilia

AT-III is synthesized in the liver and endothelial cells.
acts as an anticoagulant by directly binding to Factors
XIa, IXa, Xa, and thrombin
Deficiency of AT-III causes a 60% risk of thrombosis
during pregnancy and 33% risk during the puerperium
associate with risk of stillbirth and early fetal loss

Protein C And Protein S Deficiencies:

relatively rare deficiencies of endogenous anticoagulant
proteins, both of which are produced by the liver
The risk during pregnancy is an increased incidence of
stillbirth

Prothrombin gene mutation:

present in 2%-3% of ethnic European populations
causes increased circulating levels of prothrombin,
which increases the patients risk for VTE
accounts for 17% of VTEs in pregnancy and associated
with fetal risk factors listed previously

Testing for venous hypercoagulability

Antithrombin III deficiency

Protein C deficiency
Protein S deficiency
Factor V Leiden
Protrombin mutation
Hyperhomocysteinemia
Elevated factors VIII, IX, XI
Antiphospholipid syndrome, anticardiolipin antibody

TREATMENT
Anticoagulant treatment
Heparin activates antithrombin III to bind
rapidly to thrombin and faktor Xa
LMWH actions primarily against factor Xa
Warfarin prevents completion of synthesis
of vitamin K-dependent clotting
factors (II,VII, IX, X)

VTE Other therapy issues

Anticoagulation same for DVT & PE
Compression stockings prevent post-phlebitic
syndrome
Thrombolysis - risk/benefit uncertain;
clinical outcomes generally not improved
Vena cava filters - limited evidence and
modest benefit

VTE Prophylaxis in Medical Patients

Indications
CHF or severe respiratory disease
Bedrest with additional risk factor
Cancer
Prior VTE
Most ICU patients
Options
Low dose unfractionated heparin or LMWH
Sequential compression devices
Graduated compression stockings

Overall Goal of Treatment

Stop the clot from getting bigger or extending
Stop the clot from breaking free in the vein and
traveling to the lungs
Decrease your chance of having another DVT
Decrease the long-term complications such as
post thrombotic syndrome (PTS)

TROMBOFLEBITIS FEMORALIS