By: Hanaa Adnan Rasheed
6th stage Group B1
Supervised by: Prof.Dr. Ayla K. Ghalib
Points to Discuss:
1) Physiology of hemostasis.
2) Coagulation during pregnancy.
3) Thromboembolism in pregnancy:
• Superf...
Physiology of Hemostasis:
 The term hemostasis means prevention of blood
loss.
 Whenever a vessel is severed or ruptured...
 The extrinsic pathway
begins with a traumatized
vascular wall.
 The intrinsic pathway
begins with trauma to the
blood i...
Coagulation During Pregnancy:
 Plasma Fibrinogen concentration by ~
50%.
 Factors: V, VII, VIII, IX, X and XII.
 Platel...
 Pregnancy is a hypercoagulable state that
return to normal 4 weeks after delivery. (3)
WHY???
 This hypercoagulability is particularly relevant at
delivery, with placental separation…
 At term, around 500ml blood f...
Thromboembolism in Pregnancy:
1. Superficial Thrombophlebitis
2. Deep Vein Thrombosis.
3. Pulmonary Embolism.
4. Thromboph...
Venous Thromboembolism (VTE)
 Venous thromboembolism (VTE) is the leading
direct cause of maternal death throughout
pregn...
Hyper-
coagulabili
ty
Vascular
Damage
Venous
Stasis
Pathogenesis of VTE in Pregnancy
Risk Factors for VTE in Pregnancy (4)
Risk FactorsTimeframe
Previous venous thromboembolism
Thrombophilia
Medical comorbid...
1* Superficial Thrombophlebitis
Clinical Features:
 Swelling and tenderness of the involved extremity.
 On physical exam...
2* Deep Vein Thrombosis:
Clinical Features:
 50% of cases are
asymptomatic.
 DVT is much more common in
the left than th...
Investigations (6) :
3* Pulmonary Embolism:
Clinical Features:
Symptoms: - Pleuritic chest pain,
- Shortness of breath,
- Air hunger,
- Palpita...
Investigations (6)
Other
investigations:
ECG
Arterial blood
gases
*CUS=
Compression
Ultrasound.
*CTPA=CT
pulmonary
Angiogr...
Perfusion Ventilation
Treatment of VTE in Pregnancy:
Acute Phase Treatment:
• Thrombolytic Therapy:
• Streptokinase and TPA.
• Cannot be
recomme...
Chronic Phase
Treatment:
• Warfarin:
• Cross placenta
• If given in pregnancy it
must be stopped at 36
wk.
• Monitor by PT...
4* Thrombophilias
 Congenital
• Anti-thrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Factor V Lei...
Antiphospholipid syndrome (APS)
 Antiphospholipid antibodies are circulating
antibodies to negatively charged phospholipi...
References:
1. Arthur C. Guyton. Guyton Textbook of Medical
Physiology. Elsevier Saunders. 11th edition.
2006. pages (419-...
4. Reducing the Risk of Thrombosis and
Embolism During Pregnancy and Puerperium.
RCOG green top guideline. American Colleg...
6. Cunningham F. Gary, Kenneth J. Levendo,
Steven L. Bloom et al. Williams Obstetrics.
Mc Graw Hill. 24th edition. 2014. P...
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
Thromboembolism in pregnancy
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Thromboembolism in pregnancy

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Thromboembolism in pregnancy

  1. 1. By: Hanaa Adnan Rasheed 6th stage Group B1 Supervised by: Prof.Dr. Ayla K. Ghalib
  2. 2. Points to Discuss: 1) Physiology of hemostasis. 2) Coagulation during pregnancy. 3) Thromboembolism in pregnancy: • Superficial thrombophlebitis. • Deep vein thrombosis. • Pulmonary embolism. • Thrombophilias. 4) Thromboprophylaxis.
  3. 3. Physiology of 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. 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)
  5. 5. 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)
  6. 6.  Pregnancy is a hypercoagulable state that return to normal 4 weeks after delivery. (3) WHY???
  7. 7.  This hypercoagulability is particularly relevant at delivery, with placental separation…  At term, around 500ml blood flows through the placental bed every minute…  Without effective and rapid hemostasis, a woman could rapidly die from blood loss…  Myometrial contraction FIRST compress BV supplying placental bed…  Then FIBRIN deposition on pl. bed.(10% of blood fibrinogen is used for this process!). (3)
  8. 8. Thromboembolism in Pregnancy: 1. Superficial Thrombophlebitis 2. Deep Vein Thrombosis. 3. Pulmonary Embolism. 4. Thrombophilias.
  9. 9. Venous Thromboembolism (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)
  10. 10. Hyper- coagulabili ty Vascular Damage Venous Stasis Pathogenesis of VTE in Pregnancy
  11. 11. Risk Factors for VTE in Pregnancy (4) Risk FactorsTimeframe 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
  12. 12. 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)
  13. 13. 2* Deep Vein Thrombosis: 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)
  14. 14. Investigations (6) :
  15. 15. 3* Pulmonary Embolism: Clinical Features: Symptoms: - Pleuritic chest pain, - Shortness of breath, - Air hunger, - Palpitations, - Hemoptysis Signs: º Tachypnea, º Tachycardia, º Pleural friction rub, º Pulmonary rales, º Signs of right ventricular failure. (5)
  16. 16. Investigations (6) Other investigations: ECG Arterial blood gases *CUS= Compression Ultrasound. *CTPA=CT pulmonary Angiography. *V/Q= Ventilation Perfusion Scan
  17. 17. Perfusion Ventilation
  18. 18. Treatment of VTE in Pregnancy: 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.
  19. 19. 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.
  20. 20. 4* Thrombophilias  Congenital • Anti-thrombin III deficiency • Protein C deficiency • Protein S deficiency • Factor V Leiden • Prothrombin gene variant  Acquired • Antiphospholipid syndrome (2)
  21. 21. 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
  22. 22. References: 1. Arthur C. Guyton. Guyton Textbook of Medical Physiology. Elsevier Saunders. 11th edition. 2006. pages (419-468). 2. Edmonds D. Keith. Dewhurst’s Textbook of Obstetrics and Gynecology. Blackwell publishing. 7th edition. 2007. pages (270-281). 3. Philip N. Baker. Obstetrics by Ten Teachers. Hodder Arnold. 18th edition. 2006. Pages (286- 299).
  23. 23. 4. Reducing the Risk of Thrombosis and Embolism During Pregnancy and Puerperium. RCOG green top guideline. American College of Obstetricians and gynecologists. No.37a. November 2009. pages (1-35). 5. Neville F. Hacker, Josephe C. Gambone and Calvin J. Hobel. Hacker and Moore’s Essentials of Obstetrics and Gynecology. Elseviers Saunders. 5th edition. 2010. pages (191-218).
  24. 24. 6. Cunningham F. Gary, Kenneth J. Levendo, Steven L. Bloom et al. Williams Obstetrics. Mc Graw Hill. 24th edition. 2014. Pages (1028-1047).

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