This document discusses hemostasis and coagulation during pregnancy. It explains that during pregnancy, several coagulation factors increase by 50% and platelet activity increases to prevent blood loss during delivery when the placenta separates from the uterine wall. Pregnancy is also considered a hypercoagulable state to quickly stop bleeding when the placenta detaches. The document further discusses thromboembolism in pregnancy, describing superficial thrombophlebitis, deep vein thrombosis, pulmonary embolism, and thrombophilias as potential risks. It provides details on signs, symptoms, and treatments for venous thromboembolism during pregnancy.

1. Ms. Milan Sawant

2. Physiologyof Hemostasis:
 The term hemostasis means prevention of blood
loss.
 Whenever a vessel is severed or ruptured,
hemostasis is achieved by several mechanisms:
(1) vascular constriction,
(2) formation of a platelet plug,
(3)formation of a blood clot as a result of blood
coagulation, and
(4) eventual growth of fibrous tissue into the blood
clot to close the hole in the vessel permanently.
(1)

4.  The extrinsic pathway
begins with a traumatized
vascular wall.
 The intrinsic pathway
begins with trauma to the
blood itself or exposure of
the blood to collagen from
a traumatized blood vessel
wall. (1)

6. Coagulation During Pregnancy:
 Plasma Fibrinogen concentration by ~
50%.
 Factors: V, VII, VIII, IX, X and XII.

 Platelet reactivity in 2nd and 3rd TMs till
12wk post partum.
Fibrinolytic activity.
 Protein S (an inhibitor of coagulation). (2)

7.  Pregnancy is a hypercoagulable statethat
return to normal 4 weeks after delivery. (3)
WHY???

8.  Thishypercoagulability isparticularly relevant at
delivery, with placental separation…
 At term,around 500ml blood flows through the
placental bed everyminute…
 Without effective andrapid hemostasis,awoman
couldrapidly die from bloodloss…
 Myometrial contraction FIRSTcompressBV
supplying placentalbed…
 ThenFIBRINdeposition on pl. bed.(10%of blood
fibrinogen isusedfor this process!).(3)

9. Thromboembolism in Pregnancy:
1. Superficial Thrombophlebitis
2. Deep Vein Thrombosis.
3. Pulmonary Embolism.
4. Thrombophilias.

10. VenousThromboembolism (VTE)
 Venous thromboembolism (VTE) is the leading
direct cause of maternal death throughout
pregnancy.
 The incidence of thromboembolic complications,
pulmonary TE and DVT presented during
pregnancy is around 1/1000, with a further
2/1000 women presented in puerperium.
 VTE is up to 10 times more common in
pregnancy than in comparable non-pregnant
subject. (2)

11. Vascular
Damage
Hyper-
coagulabili
ty
Venous
Stasis
Pathogenesisof VTEin Pregnancy

13. RiskFactorsfor VTEin Pregnancy (4)
Timeframe Risk Factors
Previous venous thromboembolism
Thrombophilia
Medical comorbidities (e.g. heart or lung disease, SLE,
cancer, inflammatory conditions , nephrotic syndrome ,
sickle cell disease,
Age > 35 years
Obesity (BMI > 30 kg/m2)
Parity ≥ 3
Smoking
Gross varicose veins
Paraplegia
Pre-existing
Multiple pregnancy, assisted reproductive therapy
Pre-eclampsia
Caesarean section
Prolonged labour, mid-cavity rotational operative delivery
PPH (> 1 litre) requiring transfusion
Obstetric
Surgical procedure in pregnancy or puerperium
Hyperemesis, dehydration
Potentially
Reversible

14. 1* Superficial Thrombophlebitis
Clinical Features:
 Swelling and tenderness of the involved extremity.
 On physical examination, there is erythema,
tenderness, warmth, and a palpable cord over the
course of the involved superficial veins.
Treatment:
 Bed rest, pain medications, and local application of
heat are often sufficient treatment.
 There is no need for anticoagulants, but anti-
inflammatory agents may be considered. (5)

16. 2* Deep VeinThrombosis:
Clinical Features:
 50% of cases are
asymptomatic.
 DVT is much more common in
the left than the right leg.
 Pain in the calf in association
with dorsiflexion of the foot
(positive Homans’ sign) .
 Dull ache, tingling, tightness,
especially when walking.(5)

18. Investigations (6) :

19. 3* PulmonaryEmbolism:
Clinical Features:
Symptoms: - Pleuritic chest pain,
- Shortness of breath,
- Air hunger,
- Palpitations,
- Hemoptysis
Signs: º T
achypnea,
º Tachycardia,
º Pleural friction rub,
º Pulmonary rales,
º Signs of right ventricular failure. (5)

20. Investigations (6)
Other
investigations:
ECG
Arterial blood
gases
*CUS=
Compression
Ultrasound.
*CTPA=CT
pulmonary
Angiography.
*V/Q=
Ventilation
Perfusion Scan

22. Perfusion Ventilation

23. Treatment of VTEinPregnancy:
Acute Phase Treatment:
• Thrombolytic Therapy:
• Streptokinase and TPA.
• Cannot be
recommended in
pregnancy except in life
saving procedures:
• Skocked patient with
massive PE.
• Iliofemoral venous
thrombosis.
• Anticoagulants:
• Unfractionated Heparin:
• 40.000 IU/day
• IV infusion
• For (3-7) days
• Monitor by APTT (1.5-
2.5)x normal.
• Fractionated or LMWH:
• Surgery.

25. Chronic Phase
Treatment:
• Warfarin:
• Cross placenta
• If given in pregnancy it
must be stopped at 36
wk.
• Monitor by PT and INR
(target 2.0 – 3.0).
• Duration of action: 3 days
• S.E: bleeding tendency &
teratogenecity.
Teratogenic Effects of
Warfarin:
• Embryopathy.
• CNS abnormalities.
• ↑abortion and premature
labour.
• Chondroplasia punctata.
• Nasal hypoplasia.

27. 4* Thrombophilias
 Congenital
• Anti-thrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Factor V Leiden
• Prothrombin gene variant
 Acquired
• Antiphospholipid syndrome (2)

28. Antiphospholipid syndrome (APS)
 Antiphospholipid antibodies are circulating
antibodies to negatively charged phospholipids.
 They include lupus anticoagulant and
anticardiolipin antibodies.
 Antiphospholipid antibody syndrome is defined
as the presence of at least one antibody in
association with arterial or venous thrombosis with
or without one or more obstetric complication
(unexplained fetal demise after 10 weeks’
gestation or severe preeclampsia or fetal growth
restriction before 34 weeks’ gestation).
 Treatment: LMWH and Aspirin. If Hx of