Dr. Mohammed Abdalla Egypt, Domiat General Hospital

1. Primary Postpartum haemorrhage Dr. Mohammed Abdalla Egypt, Domiat General Hospital

2. Hemorrhage is the underlying causative factor in at least 25% of maternal deaths in industrialized and underdeveloped countries

3. Maternal physiology is well prepared for hemorrhage: • increase in blood volume . • hypercoagulable state. • the “tourniquet” effect of uterine contractions.

4. vital signs may remain near normal until more than 30% of blood volume is lost . • tachycardia can be attributed to pregnancy, stress, pain, and delivery.

5. blood supply to the pelvis

6. blood supply to the pelvis • internal iliac (hypogastric) a. • ovarian arteries . Are The main vascular supply to the pelvis . connected in a continuous arcade on the lateral borders of the vagina, uterus, and adnexa.

7. blood supply to the pelvis • /The ovarian arteries : are direct branches of the aorta beneath the renal arteries. They traverse bilaterally and retroperitoneally to enter the infundibulopelvic ligaments.

8. blood supply to the pelvis • /The hypogastric artery: retroperitoneally posterior to the ureter it divides into an anterior and posterior divisions.

9. The hypogastric artery anterior division 5 visceral branches • Uterine • superior vesical • middle hemorrhoidal • inferior hemorrhoidal • vaginal 3 parietal branches • Obturator • inferior gluteal • internal pudendal

10. The hypogastric artery posterior division • important collateral to the pelvis. • Iliolumbar • lateral sacral • superior gluteal

11. PHYSIOLOGY OF COAGULATION

12. PHYSIOLOGY OF COAGULATION The four components of coagulation that continuously interrelate are (1) the vasculature, (2) platelets, (3) plasma-clotting proteins, (4) fibrinolysis.

13. the vasculature A disruption in the vessel wall removes the protective covering of the endothelial cells and releases tissue thromboplastin, which activates the clotting mechanism.

14. platelets Activation of surface receptors causes morphologic changes in the platelets (changing first to a sphere and then to a spiderlike structure with pseudopods) and the generation of thromboxane A2 These lead to platelet aggregation and eventual formation of a platelet plug.

15. plasma-clotting proteins Activation of the clotting system is initiated in two ways: the intrinsicor extrinsicpathway.

16. Intrinsic Pathway requires no extravascular component for initiation and begins with Factor XII, which is activated by contact with injured epithelium.

17. Extrinsic Pathway is activated by the tissue factor thromboplastin (which subsequently activates Factor VII) when vascular disruption occurs. Prothrombin is converted to thrombin, which catalyzes the conversion of fibrinogen to fibrin. A clot is eventually formed at the site of vascular injury.

18. fibrinolysis plasma substrate plasminogen is activated This substrate is converted to the active enzyme plasmin, which lyses fibrin clots and destroys fibrinogen and Factors XII and VII.

19. Etiology of PPH

20. Etiology of PPH The causes of postpartum hemorrhage can be thought of as the four Ts: • tone, • tissue, • trauma, • thrombin

21. Etiology of PPH Uterine atony • Multiple gestation, • high parity, • prolonged labor • chorioamnionitis, • augmented labor, • tocolytic agents

22. Etiology of PPH Retained uterine contents • Products of conception, • blood clots

23. Etiology of PPH Placental abnormalities Congenital Bicornuate uterus Location Placenta previa Attachment Acquired structural Leiomyoma, previous surgery Peripartum Uterine inversion, uterine rupture, placental abruption Accreta

24. Etiology of PPH Lacerations and trauma • Unplanned • Vaginal/cervical tear, • surgical trauma •  Planned • Cesarean section, • episiotomy

25. Etiology of PPH Coagulationdisorders Acquired DIC, dilutionalcoagulopathy, heparin Congenital Von Willebrand's disease

26. prevention

27. Women in whom these factors have been identified should be advised to deliver in a specialist obstetric unit( GRADE B )

28. The following factors, becoming apparent during labour and delivery are associated with an increased risk of PPH. (GRADE B)

29. Prophylactic oxytocics should be offered routinely in the management of the third stage of labour as they reduce the risk of PPH by about 60%. (GRADE A)

30. Women considered at high risk of thromboembolism may be receiving prophylaxis in the form of Unfractionated Heparin (UH) or Low Molecular Weight Heparin (LMWH) antenatally. • Women with a lower level of increased risk of thromboembolism may be receiving aspirin (75mg daily) antenatally and may begin intrapartum prophylaxis with the above agents. In prophylactic dosage, these agents do not present a haemorrhagic hazard and should be continued intrapartum. (ALL GRADE C)

31. GRADE C In the event of a woman coming to delivery while receiving therapeutic heparin, the infusion should be stopped. Heparin activity will fall to safe levels within an hour. Protamine sulphate will reverse activity more rapidly, if required.

32. UH and LMWH in prophylactic dosage are not felt to present a haemorrhagic hazard. However, in overdosage there can be bleeding problems and protamine sulphate is less effective at reversing the effects of these agents (particularly LMWH) than of therapeutic heparin administered by infusion. Letsky EA. Peripartum prophylaxis of thromboembolism. In: Greer IA, ed. Thromboembolic disease in obstetrics and gynaecology. 1997

33. If women with inherited bleeding disorders present for preconceptual counselling, they should be tested for immunity against hepatitis B ,and immunised if required (as a safeguard should blood products be required at delivery). Immunisation during pregnancy is also safe. GRADE C

34. Antenatal assessmenthistory The existence of some of the obstetric risk factors may be known early in pregnancy from historyand examination.

35. Antenatal assessmentanemia Detection of anemia more than physiologic anemia of pregnancy is important, because anemia at delivery increases the likelihood of a woman requiring blood transfusion.

36. Antenatal assessmentCoagulation studies Coagulation studies may be required in the presence of congenital or acquired coagulation defects.

37. Antenatal assessmentImaging investigations Imaging investigations are useful in the detection of placental abnormalities, with placenta previa and placenta accreta the most important identifiable risk factors for massive hemorrhage.

38. Antenatal assessmentImaging investigations Conventional gray-scale assessment has a sensitivity of 93%, a specificity of 79%, and a positive predictive value of 78% in the diagnosis of placenta accreta when previa and previous cesarean scar are present Finberg HJ, Williams JW. Placenta accreta: prospective sonographic diagnosis in patients with placenta previa and prior cesarean section. J Ultrasound Med 1992;11:333-43.  

39. Antenatal assessmentImaging investigations Certain characteristics, such as the ”Swiss cheese appearance” with placenta previa, are associated with a threefold increase in mean blood loss during cesarean section Guy GP, Peisner DB, Timor-Tritsch IE. Ultrasonographic evaluation of uteroplacental blood flow patterns of abnormally located and adherent placenta. Am J Obstet Gynecol 1990;163:723-7.  

40. Antenatal assessmentImaging investigations Color Doppler may increase the specificity to 96%, which gives a positive predictive value in high-risk patients of 87% and a negative predictive value of 95% and allows better assessment of the depth of placental myometrial or serosal invasion Chou MM, Ho ESC, Lee YH. Prenatal diagnosis of placenta previa accreta by transabdominal color Doppler ultrasound. Ultrasound Obstet Gynecol 2000;15:28-35.  

41. Antenatal assessmentImaging investigations Further imaging by MRI is recommended to assess bladder involvement in percreta and assess high-risk cases Thorp Jr. JM, Councell RB, Sandridge DA, et al. Antepartum diagnosis of placenta previa percreta by magnetic resonance imaging. Obstet Gynecol 1992;80:506-8.  

42. management

43. Guidelines by the Scottish Executive Committee of the RCOG • COMMUNICATE. • RESUSCITATE. • MONITOR / INVESTIGATE. • STOP THE BLEEDING.

44. COMMUNICATEcall 6 • Callexperienced midwife • Callobstetric registrar & alert consultant • Callanaesthetic registrar , alert consultant • Alerthaematologist • Alert Blood Transfusion Service • Callporters for delivery of specimens / blood

45. RESUSCITATE • IV access with 14 G cannula X 2 • Head down tilt • Oxygen by mask, 8 litres / min • Transfuse • Crystalloid (eg Hartmann’s) • Colloid (eg Gelofusine) • once 3.5 litres infused, GIVE ‘O NEG’ If no cross-matched blood available OR give uncross-matched own-group blood, as available • Give up to 1 liter Fresh Frozen Plasma and 10 units cryoprecipitate if clinically indicated

46. MONITOR / INVESTIGATE • Cross-match 6 units • Full blood count • Clotting screen • Continuous pulse / BP / • ECG / Oximeter • Foley catheter: urine output • CVP monitoring • Discuss transfer to ITU

47. STOP THE BLEEDING • Exclude causes of bleeding other than uterine atony • Ensure bladder empty • Uterine compression • IV syntocinon 10 units • IV ergometrine 500 mg • Syntocinon infusion (30 units in 500 ml) • IM Carboprost (500 mg) • Surgery earlier rather than late • Hysterctomy early rather than late (GRADE B)

48. If conservative measures fail to control haemorrhage, initiate surgical haemostasisSOONER RATHER THAN LATER • At laparotomy, direct intramyometrial injection of Carboprost (Haemabate) 0.5mg • Bilateral ligation of uterine arteries • Bilateral ligation of internal iliac (hypogastric arteries) • Hysterectomy (GRADE C)

49. Resort to hysterectomy SOONER RATHER THAN LATER (especially in cases of placenta accreta or uterine rupture)(GRADE C)

50. Whole blood frequently is used for rapid correction of volume loss because of its ready availability, but component therapy is ideal. A general practice has been to transfuse 1 unit of fresh-frozen plasma for every 3 to 4 units of red cells given to patients who are bleeding profusely