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POSTPARTUM HEMORRHAGE & OTHER COMPLICATIONS OF THIRD STAGE OF LABOR

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Presentation on theme: "POSTPARTUM HEMORRHAGE & OTHER COMPLICATIONS OF THIRD STAGE OF LABOR"— Presentation transcript:

1 POSTPARTUM HEMORRHAGE & OTHER COMPLICATIONS OF THIRD STAGE OF LABOR
Dr Samar Sarsam

2 Definition Postpartum hemorrhage denotes excessive bleeding (> 500 mL in vaginal delivery) following delivery. Hemorrhage may occur before, during, or after delivery of the placenta. Types: *Blood lost during the first 24 hours after delivery is early or primary postpartum hemorrhage. * Blood lost between 24 hours and 6 weeks after delivery is late or secondary postpartum hemorrhage. Incidence The incidence of excessive blood loss following vaginal delivery is 5–8%. it is the third leading cause of maternal mortality in the U.S. In less-developed countries, hemorrhage is among the leading obstetric causes of maternal death.

3 Morbidity & Mortality - women already compromised by anemia or intercurrent illness are more likely to demonstrate serious deterioration of condition, excessive blood loss may predispose to subsequent puerperal infection. -Major morbidity associated with transfusion therapy (e.g. hepatitis, human immunodeficiency virus infection, transfusion reactions) -Postpartum hypotension may lead to partial or total necrosis of the anterior pituitary gland and cause postpartum panhypopituitarism, or Sheehan's syndrome, which is characterized by failure to lactate, amenorrhea, decreased breast size, loss of pubic and axillary hair, hypothyroidism, and adrenal insufficiency. The condition is rare (< 1 in 10,000 deliveries).. - acute renal failure and other organ system injury. -In extreme hemorrhage, sterility will result from hysterectomy

4 Etiology A. UTERINE ATONY Postpartum bleeding is physiologically controlled by constriction of interlacing myometrial fibers that surround the blood vessels supplying the placental implantation site. Uterine atony exists when the myometrium cannot contract. Atony is the most common cause of postpartum hemorrhage (50% of cases). Predisposing factors: include excessive manipulation of the uterus. general anesthesia (particularly with halogenated compounds). uterine overdistention (twins or polyhydramnios). prolonged labor. grand multiparity. uterine leiomyomas. operative delivery oxytocin induction or augmentation of labor. previous hemorrhage in the third stage. uterine infection. extravasation of blood into the myometrium (Couvelaire uterus). intrinsic myometrial dysfunction.

5 B. OBSTETRIC LACERATIONS
Excessive bleeding from an episiotomy, lacerations, or both causes about 20% of postpartum hemorrhages. C. RETAINED PLACENTAL TISSUE Retained placental tissue and membranes cause 5–10% of postpartum hemorrhages. Retention of placental tissue in the uterine cavity occurs: in placenta accrete. in manual removal of the placenta. in mismanagement of the third stage of labor. and in unrecognized succenturiate placenta. Ultrasonographic findings of an echogenic uterine mass strongly support a diagnosis of retained placental products. Transvaginal duplex Doppler imaging is also effective in evaluating these patients. There is some evidence that sonohysterography may aid in the diagnosis of residual trophoblastic tissue.

6 D. COAGULATION DEFECTS Coagulopathies in pregnancy may be acquired coagulation defects seen in association with several obstetric disorders including: 1. abruptio placentae 2.excess thromboplastin from a retained dead fetus 3. amniotic fluid embolism 4. severe preeclampsia 5. eclampsia 6.and sepsis. *These coagulopathies may present as: hypofibrinogenemia, thrombocytopenia, and disseminated intravascular coagulation. Transfusion of more than 8 U of blood may in itself induce a dilutional coagulopathy. Von Willebrand's disease, autoimmune thrombocytopenia, and leukemia may also occur in pregnant women.

7 Management A. PREDELIVERY PREPARATION All obstetric patients should have blood typed and screened on admission. Patients identified as being at risk for postpartum hemorrhage should have their blood typed and cross-matched immediately. A large-bore intravenous catheter should be securely taped into place after insertion. Delivery room personnel should be alerted to the risk of hemorrhage. Severely anemic patients should be transfused as soon as cross-matched blood is ready. With concerns associated with blood transfusion, autologous blood donation in obstetric patients at risk for postpartum hemorrhage has been advocated. Despite careful evaluation for risk factors, with the exception of cases of placenta previa, our ability to predict which patients will have hemorrhage and require blood transfusion remains poor.

8 B. DELIVERY Following delivery of the infant, the uterus is massaged in a circular or back-and-forth motion until the myometrium becomes firm and well contracted. Excessive and vigorous massage of the uterus before, during, or after delivery of the placenta may interfere with normal contraction of the myometrium and instead of hastening contraction may lead to excessive postpartum blood loss. C. THIRD STAGE OF NORMAL LABOR; PLACENTAL SEPARATION The placenta typically separates from the uterus and is delivered within 5 minutes of delivery of the infant. Signs of separation of the placenta: sudden gush of blood comes from the vagina the uterus seems to rise in the abdomen and the umbilical cord lengthen. The placenta can then be removed from the vagina by gentle traction on the umbilical cord.

9 Prior to placental separation, gentle steady traction on the cord combined with upward pressure on the lower uterine segment (Brandt-Andrews maneuver) ensures that the placenta can be removed as soon as separation occurs and provides a means of monitoring the consistency of the uterus. Adherent membranes can be removed by gentle traction with ring forceps. The placenta is inspected for completeness immediately after delivery.

10 Separation of Amniotic and Chorionic Membranes

11 Circumvallate Placenta

12 Battledore Insertion - Fetal Surface

13 Succinturiate Lobes

14 Manual Removal of the Placenta
Opinion is divided about the timing of manual removal of the placenta. In the presence of hemorrhage, it is obviously unreasonable to wait for spontaneous separation, and manual removal of the placenta should be undertaken without delay. In the absence of bleeding, many would advocate removal of the placenta 30 minutes after delivery of the infant. Manual removal of the placenta may be a risk factor for postpartum endometritis. prophylactic antibiotics given. Uterotonic agents may be administered as soon as the infant's anterior shoulder is delivered. (Routine administration of oxytocics during the third stage reduces the chances of postpartum hemorrhage by 40%). Manual removal of placenta is done under general anesthesia using the right hand for evacuation and the left hand applied on the abdomen to support the position of the uterus. Repair of Lacerations The entire birth canal is carefully inspected to make sure that there are no bleeding sites.

15 Evaluation of Persistent Bleeding
If vaginal bleeding persists after delivery of the placenta, aggressive treatment should be initiated. The following steps should be undertaken without delay: (1) Manually compress the uterus. (2) Obtain assistance. (3) If not already done, obtain blood for typing and cross-matching. (4) Observe blood for clotting to rule out coagulopathy. (5) Begin fluid or blood replacement. (6) Carefully explore the uterine cavity. (7) Completely inspect the cervix and vagina. (8) Insert a second intravenous catheter for administration of blood or fluids.

16 A. MEASURES TO CONTROL BLEEDING
1. Manual exploration of the uterus— (1) when vaginal delivery follows previous cesarean section (2) when intrauterine manipulation. (3) when malpresentation has occurred during labor and delivery (4) when a premature infant has been delivered (5) when an abnormal uterine contour has been noted prior to delivery (6) when there is a possibility of undiagnosed multiple pregnancy—to rule out twins. 2. Bimanual compression and massage— Immediate bimanual uterine compression, which may have to be continued for 20–30 minutes or more. 3. Curettage— 4. Uterine packing—

17 5. Uterotonic agents— Oxytocin 20–40 U/L Methylergonovine, 0.2 mg, can be given intramuscularly, but is contraindicated if the patient is hypertensive. Intramyometrial injection of prostaglandin F2a (PGF2a) to control bleeding was initially described in Intravaginal or rectal prostaglandin suppositories, intrauterine irrigation with prostaglandins, and intramyometrial injection of prostaglandins have also been reported to control hemorrhage from uterine atony.. 6. Radiographic embolization of pelvic vessels— 7. Operative management— a. Pressure occlusion of the aorta—

18 Uterine artery ligation

19 b. Uterine artery ligation— During pregnancy, 90% of the blood flow to the uterus is supplied by the uterine arteries. Direct ligation of these easily accessible vessels can successfully control hemorrhage in 75–90% of cases, particularly when the bleeding is uterine in origin. Recanalization can occur. Bilateral utero-ovarian artery ligation can also be performed. c. Internal iliac artery ligation—

20 b. Uterine artery ligation— During pregnancy, 90% of the blood flow to the uterus is supplied by the uterine arteries. Direct ligation of these easily accessible vessels can successfully control hemorrhage in 75–90% of cases, particularly when the bleeding is uterine in origin. Recanalization can occur. Bilateral utero-ovarian artery ligation can also be performed. c. Internal iliac artery ligation—

21 d. B-Lynch brace suture—

22 B. MANAGEMENT OF DELAYED POSTPARTUM HEMORRHAGE
e. Hysterectomy— 8. Blood replacement—Component therapy is advocated, with transfusion of packed cells, platelets, fresh frozen plasma, and cryoprecipitate when indicated. B. MANAGEMENT OF DELAYED POSTPARTUM HEMORRHAGE Delayed postpartum hemorrhage (bleeding 2 weeks or more after delivery) is almost always due to: -subinvolution of the placental bed -or retained placental fragments. Involution of the placental site is normally delayed when compared with that of the rest -of the endometrium, but for unknown reasons, in subinvolution, the adjacent endometrium and the decidua basalis have not regenerated to cover the placental implantation site. The involutional processes of thrombosis and hyalinization have failed to occur in the underlying blood vessels, so bleeding may occur cause of subinvolution: Is unknown, faulty placental implantation, implantation in the poorly vascularized lower uterine segment, and infection. transvaginal ultrasound for diagnosis Uterine compression and bimanual massage control this type of bleeding. If imaging studies suggest intracavitary tissue: curettage is warranted. Broad-spectrum antibiotics Oxytocic agents.

23 Complications of third stage of labor
1-Retained placenta: has been discussed before 2-Placenta Accreta A layer of decidua normally separates the placental villi and the myometrium at the site of placental implantation. A placenta that directly adheres to the myometrium without an intervening decidual layer is termed placenta accreta. Classification BY DEGREE OF ADHERENCE 1. Placenta accreta vera— Villi adhere to the superficial myometrium. 2. Placenta increta— Villi invade the myometrium. 3. Placenta percreta— Villi penetrate the full thickness of the myometrium. Classification BY AMOUNT OF PLACENTAL INVOLVEMENT 1. Focal adherence— A single cotyledon is involved. 2. Partial adherence— One or several cotyledons are involved. 3. Total adherence— The entire placenta is involved

24 Incidence vary from 1 in 2000 to 1 in 7000 deliveries. Morbidity & Mortality postpartum hemorrhage. uterine perforation and infection. Sterility may occur as a result of hysterectomy performed to control bleeding. Recurrence may be common with lesser degrees of adherence. Etiology Both excessive penetrability of the trophoblast and defective or missing decidua basalis Histologic examination of the placental implantation site usually demonstrates the absence of the decidua and Nitabuch's layer. Associated factors: Previous cesarean section, placenta previa, grand multiparity, previous uterine curettage, and previously treated Asherman's syndrome.

25 Diagnosis *the diagnosis is usually being made at laparotomy. *The diagnosis of placenta increta prior to delivery based on the lack of the sonolucent area normally seen beneath the implantation site during ultrasonographic examination is a finding confirmed in several reports. *Color Doppler imaging. *MRI. Management Fluid and blood replacement Conservative treatment of placenta accreta in women of low parity has occasionally succeeded. resection of the area with the adherent placenta hysterectomy may be required. In anticipated cases of severe placenta accreta, preoperative balloon occlusion and embolization of the internal iliac arteries may minimize intraoperative blood losses. the risk of recurrence of placenta accreta may be high.

26 3-UTERINE INVERSION Definition Uterine inversion is the prolapse of the fundus to or through the cervix so that the uterus is turned inside out. Almost all cases of uterine inversion occur after delivery and may be worsened by excess traction on the cord before placental separation. Nonpuerperal uterine inversion is very rare and is usually associated with tumors (eg, polypoid leiomyomas). Classification Incomplete inversion; If the uterus is inverted but does not protrude through the cervix complete inversion; the fundus has prolapsed through the cervix. Occasionally, the entire uterus may prolapse out the vagina. Puerperal inversion has also been classified on the basis of its duration: Acute inversion occurs immediately after delivery and before the cervix constricts. Once the cervix constricts, the inversion is termed subacute. Chronic inversion is noted more than 4 weeks after delivery.

27 Incidence 1 in 20,000. Morbidity & Mortality The morbidity and mortality associated with uterine inversion correlate with the degree of hemorrhage, the rapidity of diagnosis, and the effectiveness of treatment, postpartum hemorrhage; endomyometritis. The intestines and uterine appendages may be injured if they are entrapped by the prolapsed uterine fundus. Death Etiology The exact cause of uterine inversion is unknown, and the condition is not always preventable. Conditions that may predispose women to uterine inversion include: fundal implantation of the placenta, abnormal adherence of the placenta, congenital or acquired weakness of the myometrium, uterine anomalies, protracted labor, previous uterine inversion, intrapartum therapy with magnesium sulfate, strong traction exerted on the umbilical cord, and fundal pressure. Many cases of uterine inversion result from mismanagement of the third stage of labor.

28 Diagnosis Shock and hemorrhage are prominent, as is considerable pain. A dark red-blue bleeding mass is palpable and often visible at the cervix, in the vagina, or outside the vagina. A depression in the uterine fundus or even an absent fundus is noted on abdominal examination. Treatment prompt recognition and treatment. Hemorrhage can be massive, and hypovolemia should be vigorously treated with fluid and blood replacement. A. MANUAL REPOSITIONING OF THE UTERUS Treatment should begin as soon as the diagnosis of uterine inversion is made. An initial attempt should be made to reposition the fundus. The inverted fundus, along with the placenta if it is still attached, is slowly and steadily pushed upward in the axis of the uterus. If the initial attempt fails, induce general anesthesia. tocolytics may be used effectively. The placenta can then be removed. Antibiotics Oxytocics or ergot alkaloids are continued for at least 24 hours. B. SURGICAL REPOSITIONING OF THE UTERUS Surgical repositioning of the uterus is rarely necessary.


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