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Edit Comment Close By: manish.singh400 (56 month(s) ago) please send me this presentation Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Slide 1: Dr. Mohammed Abdalla Egypt, Domiat General Hospital Primary Postpartum haemorrhage Slide 2: Hemorrhage is the underlying causative factor in at least 25% of maternal deaths in industrialized and underdeveloped countries Slide 3: Maternal physiology is well prepared for hemorrhage: increase in blood volume . hypercoagulable state. the “tourniquet” effect of uterine contractions. Slide 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. Slide 5: blood supply to the pelvis blood supply to the pelvis : 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. 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. blood supply to the pelvis Slide 8: /The hypogastric artery: retroperitoneally posterior to the ureter it divides into an anterior and posterior divisions. blood supply to the pelvis Slide 9: The hypogastric artery anterior division 3 parietal branches 5 visceral branches Obturator inferior gluteal internal pudendal Uterine superior vesical middle hemorrhoidal inferior hemorrhoidal vaginal Slide 10: The hypogastric artery posterior division important collateral to the pelvis. Iliolumbar lateral sacral superior gluteal Slide 11: PHYSIOLOGY OF COAGULATION PHYSIOLOGY OF COAGULATION : PHYSIOLOGY OF COAGULATION The four components of coagulation that continuously interrelate are (1) the vasculature, (2) platelets, (3) plasma-clotting proteins, (4) fibrinolysis. the vasculature : 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. platelets : 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. plasma-clotting proteins : plasma-clotting proteins Activation of the clotting system is initiated in two ways: the intrinsic or extrinsic pathway. Intrinsic Pathway : Intrinsic Pathway requires no extravascular component for initiation and begins with Factor XII, which is activated by contact with injured epithelium. Extrinsic Pathway : 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. fibrinolysis : 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. Slide 19: Etiology of PPH Etiology of PPH : The causes of postpartum hemorrhage can be thought of as the four Ts: Etiology of PPH tone, tissue, trauma, thrombin Etiology of PPH : Etiology of PPH Uterine atony Multiple gestation, high parity, prolonged labor chorioamnionitis, augmented labor, tocolytic agents Etiology of PPH : Etiology of PPH Retained uterine contents Products of conception, blood clots Etiology of PPH : Placental abnormalities Congenital Bicornuate uterus Location Placenta previa Attachment Accreta Acquired structural Leiomyoma, previous surgery Peripartum Uterine inversion, uterine rupture, placental abruption Etiology of PPH Etiology of PPH : Lacerations and trauma Planned Cesarean section, episiotomy Unplanned Vaginal/cervical tear, surgical trauma Etiology of PPH Etiology of PPH : Coagulation disorders Etiology of PPH Congenital Von Willebrand's disease Acquired DIC, dilutional coagulopathy, heparin Slide 26: prevention Women in whom these factors have been identified should be advised to deliver in a specialist obstetric unit( GRADE B ) : Women in whom these factors have been identified should be advised to deliver in a specialist obstetric unit( GRADE B ) The following factors, becoming apparent during labour and delivery are associated with an increased risk of PPH. (GRADE B) : The following factors, becoming apparent during labour and delivery are associated with an increased risk of PPH. (GRADE B) Slide 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) Slide 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) Slide 31: 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. Slide 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 Slide 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 Antenatal assessment history : The existence of some of the obstetric risk factors may be known early in pregnancy from history and examination. Antenatal assessment history Antenatal assessment anemia : Antenatal assessment anemia Detection of anemia more than physiologic anemia of pregnancy is important, because anemia at delivery increases the likelihood of a woman requiring blood transfusion. Antenatal assessment Coagulation studies : Coagulation studies may be required in the presence of congenital or acquired coagulation defects. Antenatal assessment Coagulation studies Antenatal assessment Imaging 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. Antenatal assessment Imaging investigations Antenatal assessment Imaging 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 Antenatal assessment Imaging investigations 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. Antenatal assessment Imaging 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. Antenatal assessment Imaging investigations Antenatal assessment Imaging 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 Antenatal assessment Imaging investigations Chou MM, Ho ESC, Lee YH. Prenatal diagnosis of placenta previa accreta by transabdominal color Doppler ultrasound. Ultrasound Obstet Gynecol 2000;15:28-35. Antenatal assessment Imaging 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. Antenatal assessment Imaging investigations Slide 42: management Guidelines by the Scottish Executive Committee of the RCOG : Guidelines by the Scottish Executive Committee of the RCOG COMMUNICATE. RESUSCITATE. MONITOR / INVESTIGATE. STOP THE BLEEDING. COMMUNICATEcall 6 : COMMUNICATEcall 6 Call experienced midwife Call obstetric registrar & alert consultant Call anaesthetic registrar , alert consultant Alert haematologist Alert Blood Transfusion Service Call porters for delivery of specimens / blood RESUSCITATE : 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 MONITOR / INVESTIGATE : 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 STOP THE BLEEDING : 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) If conservative measures fail to control haemorrhage, initiate surgical haemostasis SOONER RATHER THAN LATER : If conservative measures fail to control haemorrhage, initiate surgical haemostasis SOONER 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) Slide 49: Resort to hysterectomy SOONER RATHER THAN LATER (especially in cases of placenta accreta or uterine rupture)(GRADE C) Slide 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 Genital tract lacerations : Genital tract lacerations Genital trauma always must be eliminated first if the uterus is firm. 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. Management of uterine atony Slide 53: During the administration of uterotonic agents, bimanual compression may control hemorrhage. The physician places his or her fist in the vagina and presses on the anterior surface of the uterus while an abdominal hand placed above the fundus presses on the posterior wall. This while the Blood for transfusion made available. Management of uterine atony Retained placenta : Retained placenta Retained placental fragments are a leading cause of early and delayed postpartum hemorrhage. Treatment is manual removal, General anesthesia with any volatile agent (1.5–2 minimum alveolar concentration (MAC)) may be necessary for uterine relaxation On rare occasions, a retained placenta is an undiagnosed placenta accreta, and massive bleeding may occur during attempted manual removal. Placenta accreta : Placenta accreta Placenta accreta is defined as an abnormal implantation of the placenta in the uterine wall, of which there are three types: (1) accreta vera, in which the placenta adheres to the myometrium without invasion into the muscle. (2) increta, in which it invades into the myometrium. (3) percreta, in which it invades the full thickness of the uterine wall and possibly other pelvic structures, most frequently the bladder. Placenta accreta : In a patient with a previous cesarean section and a placenta previa: Placenta accreta Previous one has 14% risk of placenta accreta. Previous two has 24% risk of placenta accreta. Previous three has 44% risk of placenta accreta. UTERINE RUPTURE : UTERINE RUPTURE Rupture of the uterus is described as complete or incomplete and should be differentiated from dehiscence of a cesarean section scar. UTERINE RUPTURE : UTERINE RUPTURE The reported incidence for all pregnancies is 0.05%, After one previous lower segment cesarean section 0.8% After two previous lower segment cesarean section is 5% all pregnancies following myomectomy may be complicated by uterine rupture. UTERINE RUPTURE : Complete rupture describes a full-thickness defect of the uterine wall and serosa resulting in direct communication between the uterine cavity and the peritoneal cavity. UTERINE RUPTURE UTERINE RUPTURE : Incomplete rupture describes a defect of the uterine wall that is contained by the visceral peritoneum or broad ligament. In patients with prior cesarean section, UTERINE RUPTURE UTERINE RUPTURE : dehiscence describes partial separation of the scar with minimal bleeding, with the peritoneum and fetal membranes remaining intact. UTERINE RUPTURE Management of Rupture Uterus : The identification or suspicion of uterine rupture must be followed by an immediate and simultaneous response from the obstetric team. Surgery should not be delayed owing to hypovolemic shock because it may not be easily reversible until the hemorrhage is controlled. Management of Rupture Uterus Management of Rupture Uterus : Upon entering the abdomen, aortic compression can be applied to decrease bleeding. Oxytocin should be administered to effect uterine contraction to assist in vessel constriction and to decrease bleeding. Hemostasis can then be achieved by ligation of the hypogastric artery, uterine artery, or ovarian arteries. Management of Rupture Uterus Management of Rupture Uterus : At this point, a decision must be made to perform hysterectomy or to repair the rupture site. In most cases, hysterectomy should be performed. In selected cases, repair of the rupture can be attempted. When rupture occurs in the body of the uterus, bladder rupture must be ruled out by clearly mobilizing and inspecting the bladder to ensure that it is intact. This avoids injury on repair of the defect as well. Management of Rupture Uterus Management of Rupture Uterus : A lower segment lateral rupture can cause transection of the uterine vessels. The vessels can retract toward the pelvic side wall, and the site of bleeding must be isolated before placing clamps to avoid injury to the ureter and iliac vessels. Typically, longitudinal tears, especially those in a lateral position, should be treated by hysterectomy, whereas low transverse tears may be repaired. Management of Rupture Uterus Uterine Artery Ligation : Uterine Artery Ligation Uterine artery ligation involves taking large purchases through the uterine wall to ligate the artery at the cervical isthmus above the bladder flap . Hypogastric Artery Ligation : Hypogastric Artery Ligation The hypogastric artery is exposed by ligating and cutting the round ligament and incising the pelvic sidewall peritoneum cephalad, parallel to the infundibulopelvic ligament The ureter should be visualized and left attached to the medial peritoneal reflection to prevent compromising its blood supply. Slide 68: . The common, internal, and external iliac arteries must be identified clearly. The hypogastric vein, which lies deep and lateral to the artery, may be injured as instruments are passed beneath the artery, resulting in massive, potentially fatal bleeding. Hypogastric Artery Ligation Slide 69: The hypogastric artery should be completely visualized. A blunt-tipped, right-angle clamp is gently placed around the hypogastric artery, 2.5 to 3.0 cm distal to the bifurcation of the common iliac artery. Passing the tips of the clamp from lateral to medial under the artery is crucial in preventing injuries to the underlying hypogastric vein . Hypogastric Artery Ligation Slide 71: the artery is double-ligated with a nonabsorbable suture, with 1-0 silk, but not divided .The ligation is then performed on the contralateral side in the same manner. Hypogastric Artery Ligation Slide 72: Dr. Mohammed Abdalla Egypt , Domiat G. Hospital Thank you You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.