Presentation on theme: "POSTPARTUM HEMORRHAGE “PPH” Postpartum hemorrhage is defined as blood loss in excess of 500 mL at the time of vaginal delivery. There is normally a greater."— Presentation transcript:
POSTPARTUM HEMORRHAGE “PPH” Postpartum hemorrhage is defined as blood loss in excess of 500 mL at the time of vaginal delivery. There is normally a greater blood loss following delivery by cesarean section; therefore, blood loss in excess of 1000 mL is considered a postpartum hemorrhage in such patients. The excessive blood loss usually occurs in the immediate postpartum period but can occur slowly over the first 24 hours”Primary post partum hemorrhage”.
Delayed postpartum hemorrhage can occasionally occur, with the excessive bleeding commencing more than 24 hours after delivery” Secondary PPH”. This is usually a result of subinvolution of the uterus and disruption of the placental site "scab" several weeks postpartum or of the retention of placental fragments that separate several days after delivery. Postpartum hemorrhage occurs in about 4% of deliveries.
Etiology Most of the blood loss occurs from the myometrial spiral arterioles and decidual veins that previously supplied and drained the intervillous spaces of the placenta. As the contractions of the partially empty uterus cause placental separation, bleeding occurs and continues until the uterine musculature contracts around the blood vessels and acts as a physiologic-anatomic ligature.
The four T’s’ *Tone Atony (over-distension/exhaustion/infection/distortion) *Tissue Retained POC *Trauma genital tract trauma (inversion/rupture/lacerations) *Thrombin Coagulation abnormalities (hereditary/acquired)
Failure of the uterus to contract after placental separation (uterine atony) leads to excessive placental site bleeding. Other causes of postpartum hemorrhage are list below. Causes of postpartum hemorrhage 1-Uterine atony 2- Genital tract trauma 3- Retained placental tissue 4- Low placental implantation 5- Uterine inversion 6- Coagulation disorders ◦ Abruptio placentae ◦ Amniotic fluid embolism ◦ Retained dead fetus ◦ Inherited coagulopathy
UTERINE ATONY The majority of postpartum hemorrhages (75% to 80%) are due to uterine atony. The factors predisposing to postpartum uterine atony are shown below; *Factors predisposing to postpartum uterine atony; Overdistention of the uterus Multiple gestations Polyhydramnios Fetal macrosomia Prolonged labor Oxytocic augmentation of labor Grand multiparity (a parity of 5 or more) Precipitous labor (one lasting <3 hr) Magnesium sulfate treatment of preeclampsia Chorioamnionitis Halogenated anesthetics Uterine leiomyomata
GENITAL TRACT TRAUMA Trauma during delivery is the second most common cause of postpartum hemorrhage. During vaginal delivery, lacerations of the cervix and vagina may occur spontaneously, but they are more common following the use of forceps or a vacuum extractor. The vascular beds in the genital tract are engorged during pregnancy, and bleeding can be profuse. Lacerations are particularly prone to occur over the perineal body, in the periurethral area, and over the ischial spines along the posterolateral aspects of the vagina. The cervix may lacerate at the two lateral angles while rapidly dilating in the first stage of labor.
Uterine rupture may occasionally occur. At the time of delivery by low transverse cesarean section, an inadvertent lateral extension of the incision can damage the ascending branches of the uterine arteries; an extension inferiorly can damage the cervical branches of the uterine artery. Continued vaginal bleeding with a contracted uterus is either due to retained placenta/membrane/clot or due to trauma and needs to be managed actively while the patient is stable.
RETAINED PLACENTAL TISSUE Normally, a layer of fibrinoid material, called Nitabuch's layer, is found at the base of the placenta. When the partially empty uterus contracts, the placenta cleanly separates through this layer. If the placental anchoring villi grow down into the myometrium and disrupt this fibrinoid layer, placental separation will be incomplete or may not occur at all. In about half of the patients with delayed postpartum hemorrhage, placental fragments are present when uterine curettage is performed with a large curette.
LOW PLACENTAL IMPLANTATION Low implantation of the placenta can predispose to postpartum hemorrhage because the relative content of musculature in the uterine wall decreases in the lower uterine segment, which may result in insufficient control of placental site bleeding. COAGULATION DISORDERS Peripartum coagulation disorders are high-risk factors for postpartum hemorrhage but fortunately are quite rare. Patients with coagulation problems, such as occur with thrombotic thrombocytopenic purpura, amniotic fluid embolism, abruptio placentae, idiopathic thrombocytopenic purpura, or von Willebrand's disease, may develop postpartum hemorrhage because of their inability to form a stable blood clot in the placental site.
DIFFERENTIAL DIAGNOSIS Identification of the cause of postpartum hemorrhage requires a systematic approach. The fundus of the uterus should be palpated through the abdominal wall to determine the presence or absence of uterine atony. Next, a quick but thorough inspection of the vagina and cervix should be performed to ascertain whether any lacerations may be compounding the bleeding problem. Any uterine inversion or pelvic hematoma should be excluded during the pelvic examination. If the cause of bleeding has not been identified, manual exploration of the uterine cavity should be performed, under general anesthesia if necessary. With fingertips together, a gloved hand is slipped through the open cervix, and the endometrial surface is palpated carefully to identify any retained products of conception, uterine wall lacerations, or partial uterine inversion. If no cause for the bleeding is found, a coagulopathy must be sought.
MANAGEMENT OF POSTPARTUM HEMORRHAGE The first steps toward good management are the identification of patients at risk for postpartum hemorrhage and the institution of prophylactic measures during labor to minimize the possibility of maternal mortality. Patients with any predisposing factors for postpartum hemorrhage, including a history of postpartum hemorrhage, should be screened for anemia and atypical antibodies to ensure that an adequate supply of type-specific blood is on hand in the blood bank. An intravenous infusion via a large-bore needle or catheter should be commenced prior to delivery, and blood should be held in the laboratory for possible crossmatching.
**2 major components Resuscitation Identification and management of the underlying cause(s) **Simultaneously and systematically
During the diagnostic workup of an established hemorrhage, **the patient's vital signs must be monitored closely. Hypotension is a very late sign and tachycardia, peripheral perfusion, skin colour and urine output should be noted. If the lower segment of the uterus or the cervix fills up with blood or clot it can cause vagal stimulation producing a bradycardia – this can mislead when there is no visible vaginal bleeding and a vaginal examination should be done. **Four units of packed red blood cells must be typed and cross- matched. **Intravenous crystalloids (such as normal saline or lactated Ringer's solution) infused to restore intravascular volume. Resuscitation with normal saline usually requires a volume of three times the estimated blood loss.
UTERINE ATONY If uterine atony is determined to be the cause of the postpartum hemorrhage, continuous massage of the uterus with a rapid continuous intravenous infusion of dilute oxytocin (40 to 80 U in 1 L of normal saline) should be given to increase uterine tone. If the uterus remains atonic and the placental site bleeding continues during the oxytocic infusion, ergonovine maleate or methylergonovine, 0.2 mg, may be given intramuscularly. The ergot drugs are contraindicated in patients with hypertension, because the pressor effect of the drug may increase blood pressure to dangerous levels.
Analogues of prostaglandin F 2α given intramuscularly are quite effective in controlling postpartum hemorrhage caused by uterine atony. The 15-methyl analogue (Hemabate) has a more potent uterotonic effect and longer duration of action than the parent compound. The expected time of onset of the uterotonic effect when the 15-methyl analogue (0.25 mg) is given intramuscularly is 20 minutes, whereas when injected into the myometrium it may take up to 4 minutes. Failing these pharmacologic treatments, a bimanual compression and massage of the uterine corpus may control the bleeding and cause the uterus to contract.
Although packing the uterine cavity is not widely practiced, it may occasionally control postpartum hemorrhage and obviate the need for surgical intervention. The vital signs, hematocrit, and fundal height should be monitored frequently while the packing is in place, because continued bleeding will not be initially evident through the packing. The packing may be removed in 1 to 24 hours. Usually, the bleeding will be controlled. Recently rather than using a gauze pack, an inflatable balloon has the advantage of being quick and expandable. Various balloon catheters have been reported for this technique including the Sengstaken-Blakemore, but the urological Rusch balloon catheter is cheaper and effective.
Whatever is used to pack the uterus, antibiotic cover should be given for the procedure and until the pack/balloon is removed; and similarly the bladder should be catheterized until the pack is removed.
If uterine bleeding persists in an otherwise stable patient, she could be transported to the angiocatheterization laboratory, where radiologists can place an angiocatheter into the uterine arteries for injection of thrombogenic materials to control blood flow and hemorrhaging. Operative intervention is a last resort. If the patient has completed her childbearing, a supracervical or total abdominal hysterectomy is definitive therapy for intractable postpartum hemorrhage caused by uterine atony.
Aortic compression If bleeding is out of control and the anaesthetist needs to stabilize the patient, it is worth trying aortic compression while waiting for senior or specialist help to arrive. The effect is dramatic and can be life-saving. **If reproductive potential is important to the patient,then Brace suture The B-Lynch brace suture, first described in 1997 can avoid hysterectomy in cases of bleeding from uterine atony. It aims to exert longitudinal lateral compression to the uterus combined with a tamponade effec t
ligation of the uterine arteries adjacent to the uterus will lower the pulse pressure distal to the ligatures. This procedure is more successful in controlling uterine placental site hemorrhage and is easier to perform than bilateral hypogastric artery “internal iliac artery” ligation. Cell salvage This technique of contemporary peri-operative autologous blood salvage and retransfusion. It has an excellent safety record, is acceptable to Jehovah’s witnesses and avoids the risks associated with homologous blood transfusion. With the impending blood shortages and the risk of post-transfusion infection, it is likely to be adopted in an increasing number of obstetric units.
Activated factor VIIa The use of this novel, prohaemostatic agent has potential for treating severe obstetric haemorrhage. Its use is limited to patients with complicated coagulation disorders and should only be considered in life-threatening bleeding.
GENITAL TRACT TRAUMA When postpartum hemorrhage is related to genital tract trauma, surgical intervention is necessary. Repair of genital tract lacerations requires the implementation of an important principle: The first suture must be placed well above the apex of the laceration to incorporate any retracted bleeding arterioles into the ligature. Repair of vaginal lacerations requires good light and good exposure, and the tissues should be approximated without dead space. A running lock suture technique provides the best hemostasis.
**Cervical lacerations need not be sutured unless they are actively bleeding. Large, expanding hematomas of the genital tract require surgical evacuation of clots and a search for bleeding vessels that can be ligated, then packed for hemostasis. Stable hematomas can be observed and treated conservatively. A retroperitoneal hematoma generally begins in the pelvis. If the bleeding cannot be controlled from a vaginal approach, a laparotomy and bilateral hypogastric artery ligation may be necessary.