Advances in the Treatment of Postpartum Hemorrhage

Alison M El Ayadi; Nuriya Robinson; Stacie Geller; Suellen Miller

Disclosures

Expert Rev of Obstet Gynecol. 2013;8(6):525-537. 

In This Article

Diagnosis of Hemorrhage Etiology & Management of Non-atonic PPH

Treatment of PPH is specific to cause of bleeding, and appropriate etiologic management must be implemented. Identification of bleeding source and subsequent repair can rectify bleeding attributable to genital tract lacerations.[35] If bleeding is so severe, hematoma formation so rapid or vaginal tissue so friable that suturing is not feasible, mechanical and conservative surgical intervention may be warranted.

Manual removal of retained placenta is the definitive treatment, and should be performed after attempting gentle CCT with counter pressure upwards on the uterus (skilled provider only), and administration of IM or IV oxytocin but avoidance of ergometrine and prostaglandin E2 alpha (dinoprostone or sulprostone).[6] A Cochrane review of nine trials suggested that intra-umbilical vein injection of prostaglandins or plasma expander may reduce the need for manual removal of placenta; however, further research is necessary to determine the effect on requirement for blood transfusion or therapeutic uterotonics.[36]

Abnormal placentation (i.e., placenta accreta, increta, and percreta) should be suspected if manual extraction of retained placenta is unsuccessful. Antenatal diagnosis via ultrasonography, supplemented by magnetic resonance imagery (MRI), will minimize maternal and neonatal mortality and morbidity and is particularly important among women with prior cesarean section.[22,37] Lower blood loss and fewer complications are observed in planned versus emergent cesarean hysterectomies; thus, planned cesarean delivery is favorable.[38] Scheduled cesarean at 34–35 weeks balances the increased risks associated with an emergency cesarean section with advancing gestational age while maximizing fetal maturity.[39] Optimal delivery management includes antenatal optimization of maternal hemoglobin level, early assessment by anesthesiologist, placement of pneumatic compression stockings, administration of prophylactic antibiotics, performance of pre-operative cystoscopy, alerting the blood bank for potential massive hemorrhage and ensuring availability of blood products in the operating theater.[37] Where women strongly desire future fertility, conservative approaches to the management of placenta accreta have been attempted such as ligation, suturing, uterine artery embolization (UAE) and methotrexate to accelerate placental regression; however, the evidence base is low for these methods.[40–42]

Uterine rupture and uterine inversion are rare yet serious obstetrical complications, which may result in PPH. The most common etiology of uterine rupture is a prior uterine scar from a cesarean section or other uterine surgery;[43] however, it is often due to prolonged obstructed labor or use of herbal preparations to induce or augment labor in low-resource countries.[44] Rupture may extend superiorly toward the uterine fundus, inferiorly toward the bladder and vagina or laterally toward the broad ligaments thus increasing the risk of substantial blood loss and associated maternal morbidity and mortality. Labor induction/augmentation is implicated in uterine rupture, with greater evidence for prostaglandins than for oxytocin.[45] The American College of Obstetricians and Gynecologists (ACOG) and the Society of Obstetricians and Gynaecologists of Canada (SOGC) acknowledge the potential increased risk of uterine rupture with induction, but support its rational use in conjunction with appropriate patient counseling.[46] ACOG and RCOG recommend vaginal birth after cesarean (VBAC) be undertaken in a suitably staffed and equipped delivery facility capable of providing emergency care. SOGC indicates that laparotomy be available within 30 minutes. Signs and symptoms of rupture include abdominal pain and tenderness, vaginal or intra-abdominal bleeding, chest pain, fetal de-oxygenation, cessation of uterine contractions and palpation of the fetus outside of the uterus. Early recognition or suspicion of rupture allows for timely surgical evaluation, fetal delivery and surgical repair of the uterus. Delays in diagnosis or management may otherwise result in fetal and/or maternal death.[43] Uterine inversion may result from forceful placental cord traction at placental delivery, especially where the uterus is not well contracted, or spontaneously with Valsalva maneuver.[43] Manual return of the uterus to its proper anatomical position will correct the inversion and the resulting PPH.[43] Tocolytics, halogenated anesthetics or nitroglycerine may be administered to relax the uterus and aid in reversal.[47] If the inversion is resistant to manual efforts, surgical intervention may be required.[47]

Bleeding due to inherited or acquired coagulopathy is an uncommon cause of PPH; however, it should be considered with a family history of bleeding defects or personal history of menorrhagia.[48] More common is development of DIC, a consumptive coagulopathy caused by severe PPH. In DIC, the clotting cascade is activated and fibrin-rich thrombi are deposited intra-vascularly. This process causes rapid depletion of platelets and clotting factors, and severe bleeding develops due to the body's inability to continue forming clots as factors V and VII, platelets, prothrombin and fibrinogen quickly become depleted.[49] The hemorrhage that ensues from factor depletion is managed by factor replacement and transfusion of blood products.[50] Treatment with fibrinogen concentrate within the obstetric population suggests rapid and efficient treatment of hypofibrinogenemia in the absence of severe adverse effects.[51,52] Clinical trials of fibrinogen concentrate conducted among elective and cardiac surgery patients have found improved hemostasis and reduced need for other blood products;[53] however, the first RCT focusing specifically PPH is still underway.[54]

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