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DR. FIROUZABADI

Primary Postpartum haemorrhage. DR. FIROUZABADI. Postpartum Hemorrhage. EBL > 500 cc 10% of deliveries If within 24 hrs. pp = 1  pp hemorrhage If 24 hrs. - 6 wks. pp = 2 pp hemorrhage. Postpartum Hemorrhage. Incidence 3% of all births 6.4% of cesarean deliveries

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DR. FIROUZABADI

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  1. Primary Postpartum haemorrhage DR. FIROUZABADI

  2. Postpartum Hemorrhage • EBL > 500 cc • 10% of deliveries • If within 24 hrs. pp = 1 pp hemorrhage • If 24 hrs. - 6 wks. pp = 2 pp hemorrhage

  3. Postpartum Hemorrhage Incidence • 3% of all births • 6.4% of cesarean deliveries • 3rd most common cause of maternal mortality

  4. Postpartum Hemorrhage • Definition • greater than 500cc blood loss (vaginal delivery) or 1000cc blood loss (cesarean) • decrease in HCT of 10 or greater • obstetrical emergency that can follow vaginal or cesarean delivery with clinical instability leading to transfusion, shock, renal failure, acute respiratory distress, and coagulopathy

  5. Hemorrhage is the underlying causative factor in at least 25% ofmaternal deaths in industrialized and underdeveloped countries

  6. Peripartum Hemorrhage • Causes of maternal death in US (9.1/100,000) • hemorrhage: 28.7% (*) • embolism: 19.7% (*) • PIH: 17.6% (*) • infection: 13.1% (*) • anesthesia: 2.5% (*)

  7. Hospitalization for delivery and Availability of blood for transfusion have reduced the maternal mortality rate death from hemorrhage . • It remains a cause of maternal mortality.

  8. Hemorrhageis a reason for admission of pregnant women to intensive care units. • Hemorrhage has been identified as the single most important cause of maternal death, accounting for almost half of all post partum death in developing countries.

  9. Incidence of obstetrical hemorrhage can not be determined precisely • Defined by a post partum HCT drop of 10 volumes percent or need for transfusion. • 3.9% NVD • 6-8% C/S

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

  11. 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.

  12. 5% of women delivering vaginally last more than 1000 ml of blood. Estimated blood loss is commonly only about half the actual loss. The effect of hemorrhage depend to a degree on the non pregnant blood volume, magnitude of PIH, degree of anemia at the time of delivery.

  13. blood supply to the pelvis

  14. 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.

  15. 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.

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

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

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

  19. PHYSIOLOGY OF COAGULATION

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

  21. 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.

  22. 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.

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

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

  25. 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.

  26. 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.

  27. Etiology of PPH

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

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

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

  31. 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

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

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

  34. prevention

  35. Women in whom these factors have been identified should be advised to deliver in a specialist obstetric unit

  36. The following factors, becoming apparent during labour and delivery are associated with an increased risk of PPH.

  37. 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.

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

  39. management

  40. Guideline by the RCOG • COMMUNICATE. • RESUSCITATE. • MONITOR / INVESTIGATE. • STOP THE BLEEDING.

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

  42. RESUSCITATE • IV access with 14 G cannula X 2 • Head down tilt • Oxygen by mask, 8 litres / min • Transfuse • Crystalloid • Colloid • 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

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

  44. 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) • prostaglandins • Surgery earlier rather than late • Hysterctomy early rather than late

  45. If conservative measures fail to control haemorrhage, initiate surgical haemostasisSOONER RATHER THANLATER • laparotomy • Bilateral ligation of uterine arteries • Bilateral ligation of internal iliac (hypogastric arteries) • Hysterectomy

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

  47. 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

  48. Genital tract lacerations Genital trauma always must be eliminated first if the uterus is firm.

  49. Management of uterine atony • Explore the uterine cavity. • Inspect vagina and cervix for lacerations. • If the cavity is empty, Massage and give methylergonovine 0.2 mg, the dose can be repeated every 2 to 4 hours. • Rectal 800mcg. Misoprostol is beneficial.

  50. Uterine Atony:Prostaglandins •  myometrial intracellular free Ca++, enhance action of other oxytocics • Side effects: fever, nausea/vomiting, diarrhea • 15-methyl PG F2 (Carboprost, Hemabate) • may cause bronchospasm, altered VQ,  shunt, hypoxemia, HTN • 250 g IM or intramyometrially q 15-30 min, up to max 2 mg. • contraindications: asthma, hypoxemia

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