Sarah B.H. Poggi, MD
POSTPARTUM HEMORRHAGE
ESSENTIALS OF DIAGNOSIS
Postpartum hemorrhage denotes excessive bleeding (>500 mL in vaginal delivery) following delivery. Hemorrhage may occur before, during, or after delivery of the placenta. Actual measured blood loss during uncomplicated vaginal deliveries averages 700 mL, and blood loss often may be underestimated. Nevertheless, the criterion of a 500-mL loss is acceptable on historical grounds.
Blood lost during the first 24 hours after delivery is early postpartum hemorrhage; blood lost between 24 hours and 6 weeks after delivery is late postpartum hemorrhage.
Pathogenesis
The incidence of excessive blood loss following vaginal delivery is 5–8%. Postpartum hemorrhage is the most common cause of excessive blood loss in pregnancy, and most transfusions in pregnant women are performed to replace blood lost after delivery. Hemorrhage is the third leading cause of maternal mortality in the United States and is directly responsible for approximately one-sixth of maternal deaths. In less developed countries, hemorrhage is among the leading obstetric causes of maternal death.
Causes of postpartum hemorrhage include uterine atony, obstetric lacerations, retained placental tissue, and coagulation defects.
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 causes include excessive manipulation of the uterus, general anesthesia (particularly with halogenated compounds), uterine overdistention (twins or polyhydramnios), prolonged labor, grand multi-parity, uterine leiomyomas, operative delivery and intrauterine manipulation, oxytocin induction or augmentation of labor, previous hemorrhage in the third stage, uterine infection, extravasation of blood into the myometrium (Couvelaire uterus), and intrinsic myometrial dysfunction.
B. Obstetric Lacerations
Excessive bleeding from an episiotomy, lacerations, or both causes approximately 20% of postpartum hemorrhages. Lacerations can involve the uterus, cervix, vagina, or vulva. They usually result from precipitous or uncontrolled delivery or operative delivery of a large infant; however, they may occur after any delivery. Laceration of blood vessels underneath the vaginal or vulvar epithelium results in hematomas. Bleeding is concealed and can be particularly dangerous because it may go unrecognized for several hours and become apparent only when shock occurs.
Episiotomies may cause excessive bleeding if they involve arteries or large varicosities, if the episiotomy is large, or if a delay occurred between episiotomy and delivery or between delivery and repair of the episiotomy.
Persistent bleeding (especially bright red) and a well-contracted, firm uterus suggest bleeding from a laceration or from the episiotomy. When cervical or vaginal lacerations are identified as the source of postpartum hemorrhage, repair is best performed with adequate anesthesia.
Spontaneous rupture of the uterus is rare. Risk factors for this complication include grand multiparity, malpresentation, previous uterine surgery, and oxytocin induction of labor. Rupture of a previous caesarean section scar after vaginal delivery may be an increasingly important cause of postpartum hemorrhage.
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 accreta, which is an increasingly frequent diagnosis in this era of multiple caesarean deliveries. Retained placental tissue may also develop in cases managed by 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. The technique probably is better used in cases of hemorrhage occurring a few hours after delivery or in late postpartum hemorrhage. Transvaginal duplex Doppler imaging also is effective in evaluating these patients. Some evidence indicates that sonohysterography may aid in the diagnosis of residual trophoblastic tissue. If the endometrial cavity appears empty, unnecessary dilatation and curettage may be avoided.
D. Coagulation Defects
Coagulopathies in pregnancy may be acquired coagulation defects seen in association with several obstetric disorders, including abruptio placentae, excess thromboplastin from a retained dead fetus, amniotic fluid embolism, severe preeclampsia, eclampsia, and sepsis. These coagulopathies may present as hypofibrinogenemia, thrombocytopenia, and disseminated intravascular coagulation. Transfusion of more than 8 U of blood in itself may induce a dilutional coagulopathy.
Von Willebrand’s disease, autoimmune thrombocytopenia, and leukemia may occur in pregnant women.
Prevention
Prevention of hemorrhage is preferable to even the best treatment. All patients in labor should be evaluated for risk of postpartum hemorrhage. Risk factors include coagulopathy, hemorrhage, or blood transfusion during a previous pregnancy; anemia during labor; grand multiparity; multiple gestation; large infant; polyhydramnios; dysfunctional labor; oxytocin induction or augmentation of labor; rapid or tumultuous labor; severe preeclampsia or eclampsia; vaginal delivery after previous caesarean birth; general anesthesia for delivery; forceps delivery; and delay in placental delivery after vaginal delivery of the infant.
Complications
Although any woman may suffer excessive blood loss during delivery, women already compromised by anemia or intercurrent illness are more likely to demonstrate serious deterioration of condition, and anemia and excessive blood loss may predispose to subsequent puerperal infection. Major morbidity associated with transfusion therapy (eg, viral infection, transfusion reactions) is infrequent but is not insignificant. Moreover, other types of treatment for anemia may involve some risk.
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). A woman who has been hypotensive postpartum and who is actively lactating probably does not have Sheehan’s syndrome. Hypotension also can lead to acute renal failure and other organ system injury. In extreme hemorrhage, sterility will result from hysterectomy performed to control intractable postpartum hemorrhage.
Treatment
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. The blood should be reserved in the blood bank for 24 hours after delivery. 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; therefore, the cost of such an approach may not be justified.
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 in 50% of cases and within 15 minutes in 90% of cases. Attempts to speed separation are of no benefit and may cause harm. Spontaneous placental separation is impending if the uterus becomes round and firm, a sudden gush of blood comes from the vagina, the uterus seems to rise in the abdomen, and the umbilical cord moves down out of the vagina.
The placenta then can be removed from the vagina by gentle traction on the umbilical cord. 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.
Manual Removal of the Placenta
Opinion is divided about the timing of manual removal of the placenta. In the presence of hemorrhage, it is unreasonable to wait for spontaneous separation, and manual removal of the placenta should be undertaken without delay. Traditionally, in the absence of bleeding, many have advocated removal of the placenta 30 minutes after delivery of the infant. Newer evidence suggests that to prevent postpartum hemorrhage, a placenta that has not been delivered by 18 minutes should be removed.
Efforts to promote routine manual removal of the placenta were often made in the past. The rationale includes shortening the third stage of labor, decreasing blood loss, developing experience in manual removal as practice for dealing with placenta accreta, and providing a way to simultaneously explore the uterus. Evidence now indicates that manual removal of the placenta may be a risk factor for postpartum endometritis. These real or potential benefits must be weighed against the discomfort caused to the patient, the risk of infection, and the risk of causing more bleeding by interfering with normal mechanisms of placental separation.
Technique: The uterus is stabilized by grasping the fundus with a hand placed over the abdomen. The other hand traces the course of the umbilical cord through the vagina and cervix into the uterus to palpate the edge of the placenta. The membranes at the placental margin are perforated, and the hand is inserted between the placenta and the uterine wall, palmar side toward the placenta. The hand is then gently swept from side to side and up and down to peel the placenta from its attachments to the uterus. When the placenta has been completely separated from the uterus, it is grasped and pulled from the uterus.
The fetal and maternal sides of the placenta should be inspected to ensure that it has been removed in its entirety. On the fetal surface, incomplete placental removal is manifested as interruption of the vessels on the chorionic plate, usually shown by hemorrhage. On the maternal surface, it is possible to see where cotyledons have been detached. If evidence of incomplete removal is observed, the uterus must be re-explored and any small pieces of adherent placenta removed. The uterus should be massaged until a firm myometrial tone is achieved. Depending on the patient’s other risk factors for postpartum endometritis, prophylactic antibiotics can be given at the time of manual removal of the placenta.
Immediate Postpartum Period
Uterotonic agents can be administered as soon as the infant’s anterior shoulder is delivered. There is a significantly lowered incidence of postpartum hemorrhage in patients receiving oxytocin (either low-dose intravenous [IV] or intramuscular [IM]) at the time of delivery of the anterior shoulder and controlled cord traction compared to patients receiving IV oxytocin after placental delivery. There was no greater incidence of placental retention. However, populations without ultrasound screening for twins have a potential risk for entrapment of an undiagnosed second twin, and oxytocin should only be given after placental delivery. Routine administration of oxytocics during the third stage reduces the blood loss of delivery and decreases the chances of postpartum hemorrhage by 40%. Oxytocin, 10–20 U/L of isotonic saline, or other IV solution by slow IV infusion or 10 U IM can be used. Bolus administration should not be used because large doses (>5 U) can cause hypotension. Recently, sublingual misoprostol (800 μg) has been found to be clinically as effective as oxytocin (40 U/L) for treatment of postpartum hemorrhage. This information is particularly useful for low-resource areas because misoprostol does not have to be refrigerated or require specialized equipment for administration, but regardless of setting, misoprostol is a useful adjunct to treatment of postpartum hemorrhage. Ergot alkaloids (eg, methylergonovine maleate 0.2 mg IM) also can be routinely used, but they are not more effective than oxytocin and pose more risk because they rarely cause marked hypertension. This occurs most commonly with IV administration or when regional anesthesia is used. Ergot alkaloids should not be used in hypertensive women or in women with cardiac disease.
Repair of Lacerations
If bleeding is excessive before placental separation, manual removal of the placenta is indicated. Otherwise, excessive manipulation of the uterus should be avoided.
The vagina and cervix should be carefully inspected immediately after delivery of the placenta, with adequate lighting and assistants available. The episiotomy is quickly repaired after massage has produced a firm, tightly contracted uterus. A pack placed in the vagina above the episiotomy helps to keep the field dry; attaching the free end of the pack to the adjacent drapes reminds the operator to remove it after the repair is completed.
The tendency of bleeding vessels to retract from the laceration site is the reason for one of the cardinal principles of repair. Begin the repair above the highest extent of the laceration. The highest suture is also used to provide gentle traction to bring the laceration site closer to the introitus. Hemostatic ligatures are then placed in the usual manner, and the entire birth canal is carefully inspected to ensure that no additional bleeding sites are present. Extensive inspection also provides time to confirm that prior hemostatic efforts have been effective.
A cervical or vaginal laceration extending into the broad ligament should not be repaired vaginally. Laparotomy with evacuation of the resultant hematoma and hemostatic repair or hysterectomy are required.
Large or expanding hematomas of the vaginal walls require operative management for proper control. The vaginal wall is first exposed by an assistant. If a laceration accompanies the hematoma, the laceration is extended so that the hematoma can be completely evacuated and explored. When the bleeding site is identified, a large hemostatic ligature can be placed well above the site. This ensures hemostasis in the vessel, which is likely to retract when lacerated. The hematoma cavity should be left open to allow drainage of blood and ensure that bleeding will not be concealed if hemostasis cannot be achieved.
If no laceration is present on the vaginal side wall when a hematoma is identified, then an incision must be made over the hematoma to allow treatment to proceed as outlined.
Following delivery, recovery room attendants should frequently massage the uterus and check for vaginal bleeding.
Evaluation of Persistent Bleeding
If vaginal bleeding persists after delivery of the placenta, aggressive treatment should be initiated. It is not sufficient to perform perfunctory uterine massage, for instance, without searching for the cause of the bleeding and initiating definitive treatment. 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 IV catheter for administration of blood or fluids.
A. Measures to Control Bleeding
1. Manual exploration of the uterus—The uterus should be explored immediately in women with postpartum hemorrhage. Manual exploration also should be considered after delivery of the placenta in the following circumstances: (1) when vaginal delivery follows previous caesarean section; (2) when intrauterine manipulation, such as version and extraction, has been performed; (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; and (6) when there is a possibility of undiagnosed multiple pregnancy—to rule out twins.
Ensure that all placental parts have been delivered and that the uterus is intact. This should be done even in the case of a well-contracted uterus. Exploration performed for reasons other than evaluation of hemorrhage also should confirm that the uterine wall is intact and should attempt to identify any possible intrauterine structural abnormalities. Manual exploration of the uterus does not increase febrile morbidity or blood loss.
Technique: Place a fresh glove over the glove on the exploring hand. Form the hand into a cone and gently introduce it by firm pressure through the cervix while stabilizing the fundus with the other hand. Sweep the backs of the first and second fingers across the entire surface of the uterus, beginning at the fundus. In the lower uterine segment, palpate the walls with the palmar surface of 1 finger. Uterine lacerations will be felt as an obvious anatomic defect. All exploration should be gentle because the postpartum uterus is easily perforated.
Uterine rupture detected by manual exploration in the presence of postpartum hemorrhage requires immediate laparotomy. A decision to repair the defect or proceed with hysterectomy is made on the basis of the extent of the rupture, the patient’s desire for future childbearing, and the degree of the patient’s clinical deterioration.
2. Bimanual compression & massage—The most important step in controlling atonic postpartum hemorrhage is immediate bimanual uterine compression, which may have to be continued for 20–30 minutes or more. Fluid replacement should begin as soon as a secure IV line is in place. Typed and cross-matched blood is given when it is available. Manual compression of the uterus will control most cases of hemorrhage due to uterine atony, retained products of conception (once the products are removed), and coagulopathies.
Technique: Place a hand on the patient’s abdomen and grasp the uterine fundus; bring it down over the symphysis pubis. Insert the other hand into the vagina, and place the first and second fingers on either side of the cervix and push it cephalad and anteriorly. The pulsating uterine arteries should be felt by the fingertips. Massage the uterus with both hands while maintaining compression. Prolonged compression (20–30 minutes) may be required but almost always is successful in controlling bleeding.
Insert a Foley catheter into the bladder during compression and massage because vigorous fluid and blood replacement will cause diuresis. A distended bladder will interfere with compression and massage, will contribute to the patient’s discomfort, and may itself be a major contributor to uterine atony.
3. Curettage—Curettage of a large, soft postpartum uterus can be a formidable undertaking because the risk of perforation is high and the procedure commonly results in increased rather than decreased bleeding. The suction curette, even with a large cannula, covers only a small area of the postpartum uterus, and its size and shape increase the likelihood of perforation. A large blunt curette, the “banjo” curette, probably is the safest instrument for curettage of the postpartum uterus. It can be used when manual exploration fails to remove fragments of adherent placenta.
Curettage should be delayed unless bleeding cannot be controlled by compression and massage alone. Overly vigorous puerperal curettage can result in focal complete removal of the endometrium, particularly if the uterus is infected, with subsequent healing characterized by formation of adhesions and Asherman’s syndrome (amenorrhea and secondary sterility due to intrauterine adhesions and uterine synechiae). If circumstances permit, ultrasonic evaluation of the postpartum uterus may distinguish those patients who will benefit from curettage from those who should be managed without it.
4. Uterine packing—Although once widely used for control of obstetric hemorrhage, uterine packing is no longer favored. The uterus may expand to considerable size after delivery of the placenta, thus accommodating both a large volume of packing material and a large volume of blood. The technique also demands considerable technical expertise because the uterus must be packed uniformly with 5 yards of 4-inch gauze, sometimes with the aid of special instrumentation (Torpin packer). However, this method has been used successfully, avoiding conversion to laparotomy in 9 reported cases. As a last resort, uterine packing may be particularly appropriate in centers where an interventional radiologist is not immediately available.
An alternative for uterine packing that relies on the same principle of uterine tamponade is the Bakri balloon. This device is an inflatable balloon that inflates up to 800 mL. Due to a double lumen port, drainage of blood can still occur so that concealed hemorrhage does not occur. The balloon can easily be moved after deflation vaginally. An advantage of the device is that it can be inserted at time of hemorrhage from a vaginal approach or at time of laparotomy; in either case, it can be removed vaginally. The success of the device has been described in case series.
5. Uterotonic agents—Oxytocin 20–40 U/L of crystalloid should be infused, if not already running, at a rate of 10–15 mL/min. Methylergonovine 0.2 mg can be given IM but is contraindicated if the patient is hypertensive. Intramyometrial injection of prostaglandin F2α (PGF2α) to control bleeding was initially described in 1976. Intravaginal or rectal prostaglandin suppositories, intrauterine irrigation with prostaglandins, and intramyome-trial injection of prostaglandins also have been reported to control hemorrhage from uterine atony. IM administration of 15-methylprostaglandin analogue was successful in treating 85% of patients with postpartum hemorrhage due to atony. Failures in these series occurred in women who had uterine infections or unrecognized placenta accreta. Side effects usually are minimal but may include transient oxygen desaturation, bronchospasm, and, rarely, significant hypertension. Transient fever and diarrhea may occur. Rectal misoprostol (800 μg), a prostaglandin E1 analogue, has been found to be effective in the treatment of primary postpartum hemorrhage secondary to atony. As mentioned earlier, sublingual misoprostol (800 μg) has been found to be clinically as effective as oxytocin (40 U/L) for treatment of postpartum hemorrhage due to atony. This information is particularly useful for low-resource areas because misoprostol does not have to be refrigerated or require specialized equipment for administration.
6. Radiographic embolization of pelvic vessels—Embolization of pelvic and uterine vessels by angiographic techniques is increasingly common and has success rates that range from 85–95% in experienced hands. In institutions with trained interventional radiologists, the technique is worth considering in women of low parity as an alternative to hysterectomy. With the patient under local anesthesia, a catheter is placed in the aorta and fluoroscopy is used to identify the bleeding vessel. Pieces of absorbable gelatin sponge (Gelfoam) or coil are injected into the damaged vessel (most typically the uterine artery) or into the internal iliac vessels if no specific site of bleeding can be identified. If bleeding continues, further embolization can be performed. This technique has the advantage of being effective even when the cause of hemorrhage is extrauterine and in the presence or absence of uterine atony. Many authors recommend embolization before internal iliac ligation, because ligation obstructs the access route for angiography. Adequate recanalization can occur to maintain fertility, although at this point, there are only limited case series demonstrating maintenance of fertility with pelvic artery embolization in this setting (as opposed to use for uterine fibroids). Although pelvic artery embolization is clearly preferable to hysterectomy in a patient desiring fertility, it is important to remember that the procedure does have an inherent complication rate, about 3–5%, with reports in the medical literature of loss of circulation to the lower extremities, labial and buttock necrosis, and vesicovaginal fistula.
7. Operative management—The patient’s wishes regarding further childbearing should be made clear as soon as laparotomy is contemplated for the management of postpartum hemorrhage. If the patient’s wishes cannot be ascertained, the operator should assume that the childbearing function is to be retained. Whenever possible, the spouse or family members should also be consulted prior to laparotomy.
A. PRESSURE OCCLUSION OF THE AORTA—Immediate temporary control of pelvic bleeding may be obtained at laparotomy by pressure occlusion of the aorta, which will provide valuable time to treat hypotension, obtain experienced assistants, identify the source of bleeding, and plan the operative procedure. In the young and otherwise healthy patient, pressure occlusion can be maintained for several minutes without permanent sequelae.
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, and subsequent pregnancies have been reported.
Technique: The uterus is lifted upward and away from the side to be ligated. Absorbable suture on a large needle is placed around the ascending uterine artery and vein on 1 side of the uterus, passing through the myometrium 2–4 cm medial to the vessels and through the avascular area of the broad ligament. The suture includes the myometrium to fix the suture and to avoid tearing the vessels. The same procedure is then performed on the opposite side. If the ligation is performed during caesarean section, the sutures can be placed just below the uterine incision under the bladder flap. It is not necessary to mobilize the bladder otherwise. Bilateral utero-ovarian artery ligation can also be performed in an attempt to reduce blood flow to the uterus. This technique should be performed with absorbable suture near the point of anastomoses between the ovarian artery and the ascending uterine artery at the utero-ovarian ligament.
C. B-LYNCH BRACE SUTURE—An alternative to the vessel ligation techniques is placement of a brace suture to compress the uterus in cases of diffuse bleeding from atony or percreta (Fig. 21–1). This technique, initially described in 1997, and in multiple small cases series since, has become increasing popular due to the simplicity of the procedure.
Figure 21–1. B-Lynch brace suture
Technique: Laparotomy is made in the standard way for caesarean section, and a low-transverse uterine incision is made after the bladder is taken down. The uterus is exteriorized. To test the effectiveness of the method, the uterus is compressed manually, and another operator checks the vagina for decreased bleeding. Using no. 2 catgut, the uterus is punctured 3 cm from the right lower incision and 3 cm from the right lateral border. The suture is threaded to emerge 3 cm above the upper incision margin and 4 cm from the lateral border. The catgut is now visible anteriorly as it is passed over to compress the uterine fundus approximately 34 cm from the right cornual border. The suture is fed posteriorly and vertically to enter the posterior wall of the uterine cavity at the same level as the previous entry point. After manual compression, the suture is tightened and then passed posteriorly on the left side and passed around the uterine fundus again, this time on the left. The suture is brought anteriorly to puncture the uterus at the upper part of the left uterine incision and then reemerge below the lower incision in a symmetric fashion. With 1 operator providing compression, the other throws the knot. The hysterotomy is closed in the standard fashion for a caesarean section.
D. INTERNAL ILIAC ARTERY LIGATION—Bilateral internal iliac (hypogastric) artery ligation is the surgical method most often used to control severe postpartum bleeding (Fig. 21–2). Exposure can be difficult, particularly in the presence of a large boggy uterus or hematoma. Failure rates of this technique can be as high as 57% but may be related to the skill of the operator, the cause of the hemorrhage, and the patient’s condition before ligation is attempted.
Figure 21–2. Location of ligatures for right internal iliac (hypogastric) artery ligation.
Technique: The peritoneum lateral to the infundibulopelvic ligament is incised parallel with the ligament, or the round ligament is transected. In either case, the peritoneum to which the ureter will adhere is dissected medially, which removes the ureter from the operative field. The pararectal space is then enlarged by blunt dissection. The internal iliac artery on the lateral side of the space is isolated and doubly ligated (but not cut) with silk ligatures at its origin from the common iliac artery. The operator must be careful not to tear the adjacent thin veins. Blood flow distally to the uterus, cervix, and upper vagina is not occluded, but the pulse pressure is sufficiently diminished to allow hemostasis to occur by in situ thrombosis. Fertility is preserved, and subsequent pregnancies are not compromised.
E. HYSTERECTOMY—Hysterectomy is the definitive method of controlling postpartum hemorrhage. Simple hemostatic repair of a ruptured uterus with or without tubal ligation in a woman of high parity or in poor condition for more extensive surgery may be preferred unless she has intercurrent uterine disease. The procedure is undoubtedly lifesaving.
8. Blood replacement—Blood and fluid replacement are required for successful management of postpartum hemorrhage. Massive transfusions may be necessary in patients with severe hemorrhage. Component therapy is advocated, with transfusion of packed cells, platelets, fresh-frozen plasma, and cryoprecipitate when indicated. Blood products should be obtained and given without delay when needed, because postponing transfusion may only contribute to the development of disseminated intravascular coagulation. In specialized settings, there may be a role for off-label use of recombinant activated factor VII, which was originally developed for hemophilia patients, but has been used successfully in several cases of fulminant postpartum hemorrhage.
B. Management of Delayed Postpartum Hemorrhage
Delayed postpartum hemorrhage (bleeding ≥2 weeks 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. However, 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 with only minimal trauma or other (unknown) stimuli. Although the cause of subinvolution is unknown, faulty placental implantation, implantation in the poorly vascularized lower uterine segment, and persistent infection at the implantation site have been suggested as possible factors. Uterine compression and bimanual massage, as previously described, control this type of bleeding, but it may be necessary to continue compression and massage for 30–45 minutes or longer. As previously mentioned, transvaginal ultrasound may aid in diagnosis of retained placental products. If imaging studies suggest intracavitary tissue, curettage is warranted.
Broad-spectrum antibiotics should be started when resuscitation allows. Oxytocin 10 U IM every 4 hours or 10–20 U/L IV solution by slow continuous infusion, 15-methyl PGF2α (Prostin 15M) 0.25 mg IM every 2 hours, or ergot alkaloids, such as methylergonovine maleate 0.2 mg orally every 6 hours, should be administered for at least 48 hours.
Prognosis
Postpartum hemorrhage has a recurrence rate of approximately 10% in future pregnancies. There are limited data on outcomes of pregnancies after uterine artery embolization or B-Lynch suture. It is unknown if these procedures put future pregnancies at increased risk of complications, although there are case reports and series of uneventful pregnancy outcomes after these procedures.
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PLACENTA ACCRETA
ESSENTIALS OF DIAGNOSIS
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
A. 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.
B. 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.
Pathogenesis
Estimates of the incidence of placenta accreta (all forms) vary from 1 in 2000 to 1 in 7000 deliveries. Placenta accreta vera accounts for approximately 80% of abnormally adherent placentas, placenta increta accounts for 15%, and placenta percreta accounts for 5%. The rate has risen over the last 2 decades, paralleling the increasing caesarean section rate. The condition has emerged as the major cause of peripartum hysterectomy in high-resource countries.
Both excessive penetrability of the trophoblast and defective or missing decidua basalis have been suggested as causes of placenta accreta. Histologic examination of the placental implantation site usually demonstrates the absence of the decidua and Nitabuch’s layer. Cases of placenta accreta have been seen in the first trimester, suggesting that the process may occur at the time of implantation and not later in gestation.
Although the exact cause is unknown, several clinical situations are associated with placenta accreta, such as previous caesarean section, placenta previa, grand multiparity, previous uterine curettage, and previously treated Asherman’s syndrome.
These conditions share a common possible defect in formation of the decidua basalis. The incidence of placenta accreta in the presence of placenta previa after 1 prior uterine incision is between 14% and 24%, after 2 is 23–48%, and after 3 is 35–50%. The incidence of placenta accreta after successful treatment of Asherman’s syndrome may be as high as 15%.
Clinical Findings
Adverse effects from placenta accreta in pregnancy or during the course of labor and delivery are uncommon. Rarely, intraabdominal hemorrhage or placental invasion of adjacent organs prior to labor has occurred, with the diagnosis 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. Sonographic antenatal diagnosis of the less invasive placental accreta also has been reported. Color Doppler imaging appears to be particularly helpful in diagnosis. Magnetic resonance imaging has also aided in the diagnosis of placenta accreta. The diagnosis is more often established when no plane of cleavage is found between the placenta or parts of the placenta and the myometrium in the presence of postpartum hemorrhage. Retained placental parts prevent the myometrium from contracting and thereby achieving hemostasis. Bleeding can be brisk. Inspection of the already separated placenta shows that portions are missing, and manual exploration may produce additional placental fragments.
Delayed spontaneous separation of the placenta is also an indication of an unusually adherent placenta. Focal or partial involvement may be manifested as difficulty in establishing a cleavage plane during manual removal of the placenta. Removal of a totally adherent placenta is difficult. Persistent efforts to manually remove a totally adherent placenta are futile and waste time, and they result in even more blood loss. Preparation for hysterectomy should begin as soon as the diagnosis is suspected.
Complications
The immediate morbidity associated with an abnormally adherent placenta is that associated with any type of postpartum hemorrhage. Massive blood loss and hypotension can occur. Intrauterine manipulation necessary to diagnose and treat placenta accreta may result in uterine perforation and infection. Sterility may occur as a result of hysterectomy performed to control bleeding. Perhaps due to diagnosis prior to delivery and preparation of the obstetric team, the condition is not a leading cause of mortality in the United States.
Recurrence may be common with lesser degrees of adherence.
Treatment
Fluid and blood replacement should begin as soon as excessive blood loss is diagnosed. Insertion of a second large-bore IV catheter may be necessary. Evaluation of puerperal hemorrhage should be performed as outlined earlier in Evaluation of Persistent Bleeding.
Conservative treatment of placenta accreta in women of low parity is increasingly attempted. A recent series described success in 131 of 167 women managed with serial IM methotrexate injections after pelvic artery embolization. The placenta (or portions of it) is left in situ if bleeding is minimal and will later slough off. Successful subsequent pregnancies have been reported, although the risk of recurrence of placenta accreta may be high.
Successful conservative treatment of placenta percreta is rare, but the conservative approach may be a reasonable option if only focal defects are present, blood loss is not excessive, and the patient wishes to preserve fertility. In anticipated cases of severe placenta accreta, preoperative balloon occlusion and embolization of the internal iliac arteries may minimize intraoperative blood losses. Successful embolization in unpredicted cases of placenta accreta has been reported. However, additional resection of adjacent organs, such as partial cystectomy, may be necessary in placenta percreta.
Prognosis
For women who were successfully treated with conservative management and uterine preservation, subsequent pregnancies have been reported, although the risk of recurrence of placenta accreta may be high.
Sentilhes L, Ambroselli C, Kayem G, et al. Maternal outcomes after conservative treatment for placenta accreta. Obstet Gynecol 2010;115:526–534. PMID: 20177283.
UTERINE INVERSION
ESSENTIALS OF DIAGNOSIS
Uterine inversion is prolapse of the fundus to or through the cervix so that the uterus is in effect 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 rare and usually is associated with tumors (eg, polypoid leiomyomas).
Pathogenesis
In series reported within the past 30 years, the incidence of uterine inversion has varied from 1 in 4000 to 1 in 100,000 deliveries; an incidence of 1 in 20,000 is frequently cited. One worker reported no inversions in more than 10,000 personally conducted deliveries. More recent reviews indicate a greater incidence of uterine inversion, approximately 1 in 2000 to 1 in 2500 deliveries.
The exact cause of uterine inversion is unknown, and the condition is not always preventable. The cervix must be dilated, and the uterine fundus must be relaxed for inversion to occur. Rapid uterine emptying may contribute to uterine relaxation.
Conditions that may predispose women to uterine inversion include fundal implantation of the placenta, abnormal adherence of the placenta (partial placenta accreta), 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.
Prevention
Many cases of uterine inversion result from mismanagement of the third stage of labor in women who already are at risk for developing uterine inversion. The following maneuvers are to be avoided: excessive traction on the umbilical cord, excessive fundal pressure, excessive intraabdominal pressure, and excessively vigorous manual removal of the placenta.
Clinical Findings
The diagnosis of uterine inversion usually is obvious. 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. Partial inversion in which the fundus stays within the vagina can escape immediate notice if the attendant is not aware of this complication.
If the uterus is inverted but does not protrude through the cervix, the inversion is incomplete. In complete inversion, the fundus has prolapsed through the cervix. Occasionally, the entire uterus may prolapse out of 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. Today, nearly all cases of uterine inversion are of the acute variety and are recognized and treated immediately after delivery.
Differential Diagnosis
In some cases, a prolapsed fibroid may have clinical findings similar to uterine inversion; however, with a prolapsed fibroid, the uterine fundus should be palpable on abdominal examination.
Complications
The morbidity and mortality associated with uterine inversion correlate with the degree of hemorrhage, the rapidity of diagnosis, and the effectiveness of treatment.
The immediate morbidity is that associated with any postpartum hemorrhage; however, endomyometritis frequently follows uterine inversion. The intestines and uterine appendages may be injured if they are entrapped by the prolapsed uterine fundus. Death has occurred from uterine inversion, although with prompt recognition, definitive treatment, and vigorous resuscitation, the mortality rate in this condition should be quite low.
Treatment
Successful management of patients with uterine inversion depends on prompt recognition and treatment. If initial measures fail to relieve the condition, it may progress to the point at which operative treatment or even hysterectomy is necessary. Shock associated with uterine inversion typically is profound. 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. Assistance is vital. 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 (Fig. 21–3). If the placenta has not separated, do not remove it until an adequate IV infusion has been established.
Figure 21–3. Replacement of an inverted uterus.
If the initial attempt fails, induce general anesthesia, preferably with a halogenated agent (eg, halothane) to provide uterine relaxation. Alternatively, 50 μg of IV nitroglycerin can be given as a bolus to relax the uterus and avoid intubation. The dose can be repeated at least once. While awaiting anesthesiology assistance, easily available tocolytics may be used effectively. Either IV magnesium sulfate or terbutaline 0.25 mg given as a bolus dose IV has been used successfully to achieve uterine relaxation in subacute inversion, and neither has been associated with bleeding.
Technique: The operator’s fist is placed on the uterine fundus, and the fundus is gradually pushed back into the pelvis through the dilated cervix. The general anesthetic or uterine relaxant is discontinued. Infusion of oxytocin or ergot alkaloids is started and fluid and blood replacement continued. Alternatively, prostaglandins can be used to effect uterine contraction after repositioning. Bimanual uterine compression and massage are maintained until the uterus is well contracted and hemorrhage has ceased. The placenta can then be removed.
Antibiotics should be started as soon as is practical. Oxytocics or ergot alkaloids are continued for at least 24 hours. Frequent determinations of the hematocrit level should be made to ascertain the need for further blood replacement. Iron supplements should begin with resumption of oral intake.
B. Surgical Repositioning of the Uterus
Surgical repositioning of the uterus is rarely necessary in contemporary medical practice in the United States. However, when all other efforts have failed to reposition the everted uterus, operative intervention may be lifesaving. This is generally accomplished by a vertical incision through the lower uterine segment directly posterior. The uterus is repositioned by either pulling from above or, very rarely, pushing from below (using a sterile glove). The incision is then repaired as would be any uterine incision. Blood replacement, antibiotics, and careful monitoring are necessary for successful perioperative management.
Prognosis
It is not clear whether uterine inversion is at increased risk of recurrence in future pregnancies. The prognosis for women with uterine inversion in whom the uterus was successfully restored to its normal anatomic position is generally considered to be excellent.
POSTPARTUM & PUERPERAL INFECTIONS
General Considerations
Infections are among the most prominent puerperal complications. An improved understanding of the natural history of female genital infections and the availability of powerful antibiotics may have produced a complacent attitude toward puerperal infections that is unrealistic. Postpartum infections still are costly to both patients and society, and they are associated with an admittedly small but not negligible threat of serious disability and death.
Puerperal morbidity due to infection has occurred if the patient’s temperature is higher than 38°C (100.4°F) on 2 separate occasions at least 24 hours apart following the first 24 hours after delivery. Overt infections can and do occur in the absence of these criteria, but fever of some degree remains the hallmark of puerperal infection, and the patient with fever can be assumed to have a genital infection until proved otherwise.
Incidence
Puerperal infectious morbidity affects 2–8% of pregnant women and is more common in those of low socioeconomic status, who have undergone operative delivery, with premature rupture of the membranes, with long labors, or who have multiple pelvic examinations.
Morbidity & Mortality
Postpartum infections are responsible for much of the morbidity associated with childbirth, and they either are directly responsible for or contribute to the death of approximately 7% of all pregnant women who die each year in the United States. The costs are considerable, not only in additional days of hospitalization and medications but also in time lost from work.
Sterility may result from the sequelae of postpartum infections, such as periadnexal adhesions. Hysterectomy occasionally is required in patients with serious postpartum or postoperative infection.
Pathogenesis
The flora of the birth canal of pregnant women is essentially the same as that of nonpregnant women, although variations in culture techniques and in the study populations have produced markedly different results. The vaginal flora typically includes aerobic and anaerobic organisms that are commonly considered pathogenic (Table 21–1). Several mechanisms appear to prevent overt infection in the genital tract, such as the acidity of the normal vagina; thick, tenacious cervical mucus; and maternal antibodies to most vaginal flora.
Table 21–1. Percentage of organisms isolated from the vagina or cervix in normal pregnant and nonpregnant women.
During labor and particularly after rupture of the membranes, some of the protective mechanisms are no longer present. Examinations and invasive monitoring apparatus probably facilitate the introduction of vaginal bacteria into the uterine cavity. Bacteria can be cultured from the amniotic fluid of most women undergoing intrauterine pressure monitoring, but overt postpartum infection is seen in fewer than 10% of these cases. Contractions during labor may spread bacteria present in the amniotic cavity to the adjacent uterine lymphatics and even into the bloodstream.
The postpartum uterus initially is devoid of mechanisms that keep it sterile, and bacteria may be recovered from the uterus in nearly all women in the postpartum period. Whether or not disease is clinically expressed depends on the presence of predisposing factors, the duration of uterine contamination, and the type and amount of microorganisms involved. The necrosis of decidua and other intrauterine contents (lochia) promotes an increase in the number of anaerobic bacteria, heretofore limited by lack of suitable nutrients and other factors necessary for growth.
Sterility of the endometrial cavity returns by the third or fourth postpartum week. Granulocytes that penetrate the endometrial cavity and the open drainage of lochia are effective in preventing infection in most patients.
Etiology
Almost all postpartum infections are caused by bacteria normally present in the genitalia of pregnant women. The lochia is an excellent culture medium for organisms ascending from the vagina. In women who have undergone caesarean section, more devitalized tissue and foreign bodies (sutures) are present, providing additional fertile ground for possible contamination and subsequent infection. Approximately 70% of puerperal soft tissue infections are mixed infections consisting of both aerobic and anaerobic organisms; infections occurring in women undergoing caesarean section are more likely to be serious.
General Evaluation
The source of infection should be identified, the likely cause determined, and the severity assessed. Most women with fever in the postpartum period have endometritis. Urinary tract infection is the next most common infection. Neglected or virulent endomyometritis may progress to more serious infection. Generalized sepsis, septic pelvic thrombophlebitis, or pelvic abscess may be the end result of an initial infection of the endometrial cavity.
1. Endometritis
ESSENTIALS OF DIAGNOSIS
Infection of the endometrium
Fever and a soft, tender uterus on physical examination
Pathogenesis
All of the following circumstances have led to higher than normal postpartum infection rates: prolonged rupture of the membranes (>24 hours), chorioamnionitis, an excessive number of digital vaginal examinations, prolonged labor (>12 hours), toxemia, intrauterine pressure catheters (>8 hours), fetal scalp electrode monitoring, preexisting vaginitis or cervicitis, operative vaginal deliveries, caesarean section, intrapartum and postpartum anemia, poor nutrition, obesity, low socioeconomic status, and coitus near term.
Caesarean section and low socioeconomic class are consistently associated with higher rates of postpartum infection, and caesarean section is easily the most common identifiable risk factor for development of puerperal infection. Some series report an infection rate of 40–80% following caesarean section delivery. Postpartum infection is more likely to be serious after caesarean section than after vaginal delivery. A history of bacterial vaginosis is associated with a higher risk of postcaesarean endometritis.
Clinical Findings
A. Symptoms & Signs
Fever and a soft, tender uterus are the most prominent signs of endometritis. The lochia may or may not have a foul odor. Leukocytosis is seen. In more severe disease, high fever, malaise, abdominal tenderness, ileus, hypotension, and generalized sepsis may be seen. Movement of the uterus causes increased pain.
1. Fever—Although the puerperium is a period of high metabolic activity, this factor should not raise the temperature above 37.2°C (99°F) and then only briefly in the first 24 hours postpartum. Modest temperature elevations may occur with dehydration. Any woman with a fever over 38°C (100.4°F) at any time in the puerperium should be evaluated.
Endometritis results in temperatures ranging from 38°C to over 40°C (100.4°F to >104°F), depending on the patient, the causative microorganism, and the extent of infection. The lower range of temperatures is more common. Endometritis usually develops on the second or third postpartum day. Early fever (within hours of delivery) and hypotension are almost pathognomonic for infection with β-hemolytic streptococci.
2. Uterine tenderness—The uterus is soft and exquisitely tender. Motion of the cervix and uterus may cause increased pain.
Abdominal tenderness is generally limited to the lower abdomen and does not lateralize. A carefully performed baseline examination should include an adnexal evaluation. Adnexal masses palpable on abdominal or pelvic examination are not seen in uncomplicated endometritis, but tubo-ovarian abscess may be a later complication of an infection originally confined to the uterus. Bowel sounds may be decreased and the abdomen distended and tympanitic.
Pelvic examination confirms the findings disclosed by abdominal examination.
B. Laboratory Findings
1. Hematologic findings—Leukocytosis is a normal finding during labor and the immediate puerperal period. White blood cell counts may be as high as 20,000/μL in the absence of infection, so higher counts can be anticipated in infection. Bacteremia is present in 5–10% of women with uncomplicated endometritis. Mycoplasma is frequently recovered from the blood of patients with postpartum fever. Infections with Bacteroides as the predominant organism are frequently associated with positive blood cultures.
2. Urinalysis—Urinalysis should be routinely performed in patients thought to have endometritis because urinary tract infections are often associated with a clinical picture similar to that of mild endometritis. If pyuria and bacteria are noted in a properly collected specimen, appropriate antibiotic therapy for urinary tract infections should be started and a portion of the specimen sent for culture.
3. Lochia cultures—Bacteria colonizing the cervical canal and ectocervix almost always can be recovered from lochia cultures, but they may not be the same organisms causing endometritis. Accurate cultures can be achieved only if specimens obtained transcervically are free from vaginal contamination. Material should be obtained using a speculum to allow direct visualization of the cervix and a gloved culture device (a swab that is covered while it is passed through a contaminated area, then uncovered to obtain a culture from the desired area). Transabdominal aspiration of uterine contents does secure an uncontaminated specimen, but routine use of this technique probably is not justified, and confirmation of placement within the uterine cavity may be difficult. Unless special means are taken to prevent cervical contamination and to ensure the recovery of anaerobic species, results of lochia cultures must be interpreted with great care.
4. Bacteriologic findings—Although the organisms responsible for puerperal infections vary considerably among hospitals, most puerperal infections are due to anaerobic streptococci, gramnegative coliforms, Bacteroides spp., and aerobic streptococci. Chlamydia and Mycoplasma are also implicated in many postpartum infections, but clinical isolates are rare because of the difficulty in culturing these organisms. Gonococci are recovered in varying degrees. The percentage of representative microorganisms recovered from women with endometritis is given in Table 21–2.
Table 21–2. Percentage of organisms recovered from women with postpartum endomyometritis.
Patterns of bacterial isolates in puerperal infections in the patient’s hospital are more important in guiding selection of appropriate antibiotics than are studies from the literature.
A. AEROBIC BACTERIA—Group A streptococci are no longer a major cause of postpartum infection, but infection with these organisms still occurs occasionally, often associated with rapid progression of toxic shock syndrome. If more than an isolated instance of infection due to these streptococci occurs, immediate measures should be taken to halt a potential epidemic. Penicillin is highly effective.
In as many as 30% of women with clinically recognized endometritis, group B streptococci are partly or wholly responsible for the infection. Classic presenting signs are high fever and hypotension shortly after delivery. However, group B streptococci are commonly recovered from the vaginas of pregnant women whether or not they have endometritis. Why some women with positive cultures develop serious illness whereas others do not undoubtedly depends on the presence of predisposing factors as well as other, as yet unknown, elements. It is interesting that positive cultures in women do not correlate well with the incidence of streptococcal infection in their newborns. Penicillin is the treatment of choice for patients with endometritis.
Group D streptococci, which include Streptococcus faecalis, are common isolates in endometritis. Ampicillin in high doses is the treatment of choice. Aminoglycosides are also effective against this group.
Staphylococcus aureus is not commonly seen in cultures from women with postpartum infections of the uterus. Staphylococcus epidermidis is frequently recovered from women with postpartum infections. These organisms are typically not seen in pure culture. When established staphylococcal infections require treatment, nafcillin, cloxacillin, or cephalosporins should be used.
Among the gramnegative aerobic organisms likely to be recovered in postpartum uterine infections, Escherichia coli is the most common. In postpartum uterine infections, E coli is more likely to be isolated from seriously ill patients, whereas in urinary tract infections, it is the most commonly isolated organism but is not necessarily found in the sickest patients. Hospital-acquired E coli is most susceptible to aminoglycosides and cephalosporins.
The incidence of Neisseria gonorrhoeae is 2–8% in pregnant women antepartum. Unless repeat screening examinations and treatment of patients with positive cultures are undertaken in women near term, the incidence of asymptomatic endocervical gonorrhea at delivery probably is only slightly less, and it is reasonable to believe that some cases of puerperal endometritis are gonococcal in origin.
Gardnerella vaginalis, a cause of vaginitis, is seen in isolates from women with postpartum infections, usually in those with a polymicrobial cause, although pure isolates have been reported.
Other gramnegative bacilli that are commonly encountered on medical and surgical wards (eg, Klebsiella pneumoniae, Enterobacter, Proteus, and Pseudomonas spp.) are uncommon causes of endometritis.
B. ANAEROBIC BACTERIA—Anaerobic bacteria are involved in puerperal infections of the uterus in at least 50% and perhaps as many as 95% of cases. They are much less commonly seen in urinary tract infections. Anaerobic peptostreptococci and peptococci are commonly recovered in specimens from women with postpartum infection, particularly with other anaerobic species. Clindamycin, chloramphenicol, and the newer cephalosporins are active against these organisms.
Bacteroides spp., particularly Bacteroides fragilis, are commonly found in mixed puerperal infections. These are likely to be the more serious infections (eg, puerperal pelvic abscess, caesarean section wound infections, and septic pelvic thrombophlebitis). When infection with this organism is suspected or confirmed, clindamycin, chloramphenicol, or third-generation cephalosporins should be used.
Gram-positive anaerobic organisms are represented only by Clostridium perfringens, which is not infrequently isolated from an infected uterus but which is a rare cause of puerperal infection.
C. OTHER ORGANISMS—Mycoplasma and Ureaplasma spp. are common genital pathogens that have been isolated from the genital tract and blood of postpartum women both with and without overt infection. These pathogens are frequently found in the presence of other bacteria. The role of these organisms in puerperal infections is unknown.
Chlamydia trachomatis is now thought to be the leading cause of pelvic inflammatory disease in some populations. Because the population most at risk for pelvic inflammatory disease is the same as that most likely to become pregnant, it is not surprising that Chlamydia is in some way involved in puerperal infections, but it is infrequently isolated as a cause of early postpartum endometritis. Chlamydia is more frequently associated with mild late-onset endometritis, so cultures for this organism should be obtained from patients with endometritis diagnosed several days after delivery. Chlamydia is difficult to culture, and it is possible that as more effective culture techniques become available, the place of this organism in the morbidity associated with postpartum infections will be clarified.
Differential Diagnosis
In the immediate postpartum period, involuntary chills are common and are not necessarily an indication of overt infection. Lower abdominal pain is common as the uterus undergoes involution with continuing contractions.
Extragenital infections are much less common than endometritis and urinary tract infections. Most of these infections can be effectively ruled out by history and examination alone. Patients should be asked, at a minimum, about coughing, chest pain, pain at the insertion site of IV catheters, breast tenderness, and leg pain. Examination of the breasts, chest, IV catheter insertion site, and leg veins should determine whether these areas might be the source of the postpartum fever. Chest x-ray films are rarely of benefit unless signs and symptoms point to a possible pulmonary cause of the fever.
Treatment
The choice of antibiotics for treatment of endometritis depends on the suspected causative organisms and the severity of the disease. If the illness is serious enough to require antibiotics, initial therapy should consist of IV antibiotics in high doses. Factors reinforcing the need for this approach include the large volume of the uterus, the expanded maternal blood volume, the brisk diuresis associated with the puerperium, and the difficulty in achieving adequate tissue concentrations of the antibiotic distal to the thrombosed myometrial blood vessels. Clindamycin plus an aminoglycoside is a standard first-line regimen. Good evidence now indicates that once-a-day dosing of gentamicin is as effective as the traditional thrice-daily regimen. Single-agent therapy with second- or third-generation cephalosporins is an acceptable alternative.
The response to therapy should be carefully monitored for 24–48 hours. Deterioration or failure to respond determined both clinically and by laboratory test results requires a complete reevaluation. Ampicillin is added when the patient has a less than adequate response to the usual regimen, particularly if Enterococcus spp. are suspected.
IV antibiotics are continued until the patient has been afebrile for 24–48 hours. Randomized and prospective trials have shown that additional treatment with oral antibiotics after IV therapy is unnecessary. Patients with documented concurrent bacteremia can be treated similarly, unless they have persistently positive blood cultures or a staphylococcal species cultured. If the patient remains febrile despite the standard antibiotic regimens, further evaluation should be initiated to look for abscess formation, hematomas, wound infection, and septic pelvic thrombophlebitis.
For patients known to be infected or at extremely high risk for infection at the time of delivery, initial therapy with 2- or 3-drug regimens in which 1 of the agents is clindamycin is prudent. Single-agent IV infusion of broad-spectrum agents such as piperacillin or cefoxitin appears to be equally effective.
Costantine MM, Rahman M, Ghulmiyah L, et al. Timing of perioperative antibiotics for cesarean delivery: A meta-analysis. Am J Obstet Gynecol 2008;301.e1–301.e6. PMID: 18771991.
Thurman AR. Post-cesarean delivery infectious morbidity: Focus on preoperative antibiotics and methicillin-resistant Staphylococcus aureus. Am J Infect Control 2010;38:612–616. PMID: 20627452.
2. Urinary Tract Infection
ESSENTIALS OF DIAGNOSIS
Urine culture demonstrating the presence of bacteria in the urine in a patient symptomatic for urinary tract infection
Pyelonephritis typically presents with symptoms of flank pain and/or systemic signs of fever, chills, and nausea/vomiting
Pathogenesis
Approximately 2–4% of women develop a urinary tract infection postpartum. After delivery, the bladder and lower urinary tract remain somewhat hypotonic, and residual urine and reflux result. This altered physiologic state, in conjunction with catheterization, birth trauma, conduction anesthesia, frequent pelvic examinations, and nearly continuous contamination of the perineum, is sufficient to explain the high incidence of lower urinary tract infections postpartum. In many women, preexisting asymptomatic bacteria, chronic urinary tract infections, and anatomic disorders of the bladder, urethra, and kidneys contribute to urinary tract infection postpartum.
Clinical Findings
A. Symptoms & Signs
Urinary tract infection usually presents with dysuria, frequency, urgency, and low-grade fever; however, an elevated temperature is occasionally the only symptom. White blood cells and bacteria are seen in a centrifuged sample of catheterized urine. A urine culture should be obtained. The history should be reviewed for evidence of chronic antepartum infections. If a woman had an antepartum urinary tract infection, then her postpartum infection likely is caused by the same organism. Repeated urinary tract infections call for careful postpartum evaluation. Urethral diverticulum, kidney stones, and upper urinary tract anomalies should be ruled out.
Urinary retention postpartum in the absence of regional anesthesia or well after its effects have worn off almost always indicates urinary tract infection.
Pyelonephritis may be accompanied by fever, chills, malaise, and nausea and vomiting. Characteristic signs of kidney involvement associated with pyelonephritis include costovertebral angle tenderness, dysuria, pyuria, and, in the case of hemorrhagic cystitis, hematuria.
B. Laboratory Findings
E coli is easily the most common organism isolated from infected urine in postpartum women (approximately 75% of cases). Other gramnegative bacilli are much less likely to be recovered. E coli is less likely to be the causative organism in women who had repeated urinary tract infections in the recent past.
Treatment
Antibiotics with specific activity against the causative organism are the cornerstone of therapy in uncomplicated cystitis. These drugs include sulfonamides, nitrofurantoin, trimethoprim-sulfamethoxazole, oral cephalosporins (cephalexin, cephradine), and ampicillin. Some hospitals report a high incidence of microbial resistance to ampicillin. The oral combination of amoxicillin-clavulanic acid provides a better spectrum of bacterial sensitivity. Sulfa antibiotics can be used safely in women who are breastfeeding if the infants are term without hyperbilirubinemia or suspected glucose-6-phosphate dehydrogenase deficiency. High fluid intake should be encouraged.
Pyelonephritis requires initial therapy with high doses of IV antibiotics, such as ampicillin 8–12 g/d or first-generation cephalosporins (cefazolin 3–6 g/d, cephalothin 4–8 g/d). An aminoglycoside can be added when resistant organisms are suspected or when the patient has clinical signs of sepsis. A long-acting third-generation cephalosporin, such as ceftriaxone 1–2 g every 12 hours, also can be used. The response to therapy may be rapid, but some women respond with gradual defervescence over 48 hours or longer. Urine cultures should be obtained to guide any necessary modifications in drug therapy if the patient’s response is not prompt. Even with prompt resolution of fever, antibiotic therapy should be continued IV or orally for a total of 10 days. Urine for culture should be obtained at a postpartum visit after therapy has been completed.
3. Pneumonia
ESSENTIALS OF DIAGNOSIS
Pneumonia typically presents with fever, chills, and productive cough.
Women with obstructive lung disease, smokers, and those undergoing general anesthesia have an increased risk for developing pneumonia postpartum.
Clinical Findings
A. Symptoms & Signs
Symptoms and signs are the same as those of pneumonia in nonpregnant patients: productive cough, chest pain, fever, chills, rales, and infiltrates on chest x-ray film. In some cases, careful differentiation from pulmonary embolus is required.
B. X-Ray & Laboratory Findings
Chest x-ray film confirms the diagnosis of pneumonia. Gram-stained smears of sputum and material for culture should be obtained.
Streptococcus pneumoniae and Mycoplasma pneumoniae are the 2 most likely causative organisms. S pneumoniae can easily be identified on gram-stained smears. Infection with M pneumoniae can be suspected on clinical grounds.
Treatment
Appropriate antibiotics, oxygen (if the patient is hypoxic), IV hydration, and pulmonary toilet are the mainstays of therapy.
4. Caesarean Section Wound Infection
ESSENTIALS OF DIAGNOSIS
Wound erythema and tenderness +/− drainage from the wound
The patient may also demonstrate systemic signs of infection such as fever or malaise
Pathogenesis
Wound infection occurs in 4–12% of patients after caesarean section. The following risk factors predispose to subsequent wound infection in women undergoing caesarean section: obesity, diabetes, prolonged hospitalization before caesarean section, prolonged rupture of the membranes, chorioamnionitis, endomyometritis, prolonged labor, emergency rather than elective indications for caesarean section, and anemia.
Prevention
The high rate of infection (averaging 35–40%) after caesarean section is sufficient reason to consider prophylactic perioperative antibiotic administration. A major difference in practice in terms of prophylactic antibiotic administration prior to caesarean delivery has recently been advocated. While historically antimicrobial prophylaxis has been given after umbilical cord clamping, due to concerns regarding the masking of a neonatal infection, reductions in postcaesarean wound infection as great as 50% can be attributed to a single dose of cefazolin (1 g) given IV prior to skin incision.
Clinical Findings
A. Symptoms & Signs
Fever with no apparent cause that persists to the fourth or fifth postoperative day strongly suggests a wound infection. Wound erythema and tenderness may not be evident until several days after surgery. Occasionally, wound infections are manifested by spontaneous drainage, often accompanied by resolution of fever and relief of local tenderness. Rarely, a deep-seated wound infection becomes apparent when the skin overtly separates, usually after some strenuous activity by the patient.
B. Laboratory Findings
Gram-stained smears and culture of material from the wound may be helpful in guiding selection of the initial antibiotic. Blood cultures may be positive in the patient with systemic sepsis due to wound infection. The organisms responsible for most wound infections originate on the patient’s skin. S aureus is the organism most commonly isolated. Streptococcus species, E coli, and other gramnegative organisms that may originally have colonized the amniotic cavity are also seen. Occasionally, Bacteroides, which comes only from the genital tract, is isolated from material taken from serious wound infections. In addition, methicillin-resistant S aureus (MRSA) is an emerging isolate from caesarean delivery wound infections. At this point, prophylactic antibiotic regimens have not addressed this particular organism.
Rarely, necrotizing fasciitis and the closely related synergistic bacterial gangrene can involve caesarean section incisions. They are recognized by their intense tissue destruction, lack of sensation in the involved tissues, and rapid extension. Radical debridement of necrotic and infected tissue is the cornerstone of treatment.
Treatment
A. Initial Evaluation
The incision should be opened along its entire length and the deeper portion of the wound gently explored to determine whether fascial separation has occurred. If the fascia is not intact, the wound is dissected to the fascial level, debrided, and repaired. Wound dehiscence has a high mortality rate and should be treated aggressively. Dehiscence is uncommon in healthy patients and with Pfannenstiel incisions. The skin can be left open to undergo delayed closure or to heal by primary intention.
If the fascia is intact, the wound infection can be treated by local measures.
B. Definitive Measures
Mechanical cleansing of the wound is the mainstay of therapy for caesarean wound infection. Opening the wound encourages drainage of infected material. The wound can be packed with saline-soaked gauze 2–3 times per day, which will remove necrotic debris each time the wound is unpacked. The wound can be left open to heal, or it can be closed secondarily when granulation tissue has begun to form.
Costantine MM, Rahman M, Ghulmiyah L, et al. Timing of perioperative antibiotics for cesarean delivery: A meta-analysis. Am J Obstet Gynecol 2008;301.e1–301.e6. PMID: 18771991.
Thurman AR. Post-cesarean delivery infectious morbidity: Focus on preoperative antibiotics and methicillin-resistant Staphylococcus aureus. Am J Infect Control 2010;38:612–616. PMID: 20627452.
5. Episiotomy Infection
ESSENTIALS OF DIAGNOSIS
Pain at the episiotomy site
Physical examination demonstrates disruption of the episiotomy wound
Pathogenesis
It is surprising that infected episiotomies do not occur more often than they do, because contamination at the time of delivery is universal. Subsequent contamination during the healing phase also should be common, yet infection and disruption of the wound are infrequent (0.5–3%). The excellent local blood supply is suggested as an explanation for this phenomenon.
In general, the more extensive the laceration or episiotomy, the greater are the chances for infection and breakdown of the wound. More tissue is devitalized in a large episiotomy, thereby providing greater opportunity for contamination. Women with infections elsewhere in the genital area probably are at greater risk for infection of the episiotomy.
Clinical Findings
A. Symptoms & Signs
Pain at the episiotomy site is the most common symptom. Spontaneous drainage is frequent, so a mass rarely forms. Incontinence of flatus and stool may be the presenting symptom of an episiotomy that breaks down and heals spontaneously.
Inspection of the episiotomy site shows disruption of the wound and gaping of the incision. A necrotic membrane may cover the wound and should be debrided if possible. A careful rectovaginal examination should be performed to determine whether a rectovaginal fistula has formed. The integrity of the anal sphincter should be evaluated.
B. Laboratory Findings
Infection with mixed aerobic and anaerobic organisms is common. Staphylococcus may be recovered from cultures of material from these infections. Culture results frequently are misleading because the area of the episiotomy typically is contaminated with a wide variety of pathogenic bacteria.
Treatment
Initial treatment should be directed toward opening and cleaning the wound and promoting the formation of granulation tissue. Warm sitz baths or Hubbard tank treatments help the debridement process. Attempts to close an infected, disrupted episiotomy are likely to fail and may make ultimate closure more difficult. Surgical closure by perineorrhaphy should be undertaken only after granulation tissue has thoroughly covered the wound site. There is an increasing trend toward early repair of episiotomy wound dehiscence, in contrast to conventional wisdom, which suggests a 3- to 4-month delay. Several large case series show excellent results once initial infection is treated.
6. Mastitis
ESSENTIALS OF DIAGNOSIS
One or both breasts are tender, erythematous, and engorged on physical examination.
With infectious mastitis or breast abscess, the patient commonly demonstrates fever and malaise.
Pathogenesis
Congestive mastitis, or breast engorgement, is more common in primigravidas than in multiparas. Infectious mastitis and breast abscesses also are more common in women pregnant for the first time and are seen almost exclusively in nursing mothers.
Infectious mastitis and breast abscesses are uncommon complications of breastfeeding. They almost certainly occur as a result of trauma to the nipple and the subsequent introduction of organisms from the infant’s nostrils to the mother’s breast. S aureus contracted by the infant while in the hospital nursery is the usual causative agent.
Clinical Findings
A. Symptoms & Signs
Breast engorgement usually occurs on the second or third postpartum day. The breasts are swollen, tender, tense, and warm. The patient’s temperature may be mildly elevated. Axillary adenopathy can be seen.
Mastitis presents 1 week or more after delivery. Usually only 1 breast is affected and often only 1 quadrant or lobule. It is tender, reddened, swollen, and hot. There may be purulent drainage, and aspiration may produce pus. The patient is febrile and appears ill.
B. Laboratory Findings
The organism responsible for infectious mastitis and breast abscess almost always is S aureus. Streptococcus spp. and E coli are occasionally isolated. Leukocytosis is evident.
Treatment
A. Congestive Mastitis
The form of treatment depends on whether or not the patient plans to breastfeed. If she does not, tight breast binding, ice packs, restriction of breast stimulation, and analgesics help to relieve pain and suppress lactation. Medical suppression of lactation probably does not hasten involution of congested breasts unless the drug is taken very early after delivery. Bromocriptine 2.5 mg twice daily orally for 10 days is an effective regimen, although concerns about its side effect profile have curtailed its use. For the woman who is breastfeeding, manually emptying the breasts following infant feeding is all that is necessary to relieve discomfort.
B. Infectious Mastitis
Infectious mastitis is treated in the same way as congestive mastitis. Local heat and support of the breasts help to reduce pain. Cloxacillin, dicloxacillin, nafcillin, or a cephalosporin—antibiotic with activity against the commonly encountered causative organisms—should be administered. Infants tolerate the small amount of antibiotics in breast milk without difficulty. It may be prudent to check the infant for possible colonization with the same bacteria present in the mother’s breast.
If an abscess is present, incision and drainage are necessary. The cavity should be packed open with gauze, which is then advanced toward the surface in stages daily. Most authorities recommend cessation of breastfeeding when an abscess develops. Antistaphylococcal antibiotics should be prescribed. Inhibition of lactation is also recommended.
POSTPARTUM DEPRESSION
ESSENTIALS OF DIAGNOSIS
Depression that begins in the 12 months after delivery
Criteria for diagnosis are the same as nonpregnancy-related depression
Symptoms must be present nearly every day for at least 2 weeks
Pathogenesis
Considering the excitement, anticipation, and tension associated with imminent delivery, the marked hormonal alterations after delivery, and the substantial new burdens and responsibilities that result from childbirth, it is not surprising that some women experience depression after delivery. The incidence of postpartum depression is difficult to estimate, but the disorder is common. The pathogenesis is not well understood; genetic susceptibility combined with a major life event and hormonal changes in the puerperium appears to underlie many cases of postpartum depression. The greatest risk factor for depression is a history of depression prior to pregnancy. In women who suffered from depression before they became pregnant and in those without effective support mechanisms, the severity of depression may be more profound and the consequences far more serious. An openly psychotic state may develop within a few days after delivery and render the woman incapable of caring for herself or her newborn. In some cases, she may harm her infant and herself.
Clinical Findings
A. Symptoms & Signs
Symptoms of postpartum depression include derangements in sleep patterns, energy level, appetite, weight, and libido. Women often complain of depressed mood and/or anxiety. Other symptoms include irritability, anger, feelings of guilt, a sense of feeling overwhelmed, feelings of inadequacy, and inability to bond emotionally with the baby. To meet a diagnosis of postpartum depression, the symptoms must be present nearly every day for at least 2 weeks.
B. Laboratory Tests
Several screening tools are available for evaluating postpartum women for depression. The Edinburgh Postnatal Depression Scale is one such questionnaire that is able to identify most women with postpartum depression. Hypothyroidism is emerging as a cause of some cases of postpartum depression, and screening for this disorder should be considered if suggested by clinical presentation.
Differential Diagnosis
The main differential diagnosis of postpartum depression is postpartum blues. Postpartum blues, however, is characterized by transient symptoms of depression, whereas postpartum depression requires that the characteristic symptoms be present nearly every day for at least 2 weeks.
Complications
Complications of postpartum depression include poor bonding with the infant, which can impact child development. Additionally, women with postpartum depression are at increased risk of suicide and infanticide.
Treatment
The first step in managing women with postpartum depression is an evaluation to determine the severity of her depression and whether she is a threat to herself or others. Psychiatric consultation should be obtained for the postpartum woman who shows symptoms of severe depression or overt psychosis. Initial treatment options include psychosocial therapy and pharmacotherapy. Some antidepressant medications are compatible with breastfeeding, although all antidepressants are transferred through the breast milk in some amount. For women unresponsive to pharmacotherapy, electroconvulsive therapy has been used with success.
American College of Obstetricians and Gynecologists. Use of Psychiatric Medications during Pregnancy and Lactation. ACOG Practice Bulletin No. 91. Washington, DC: American College of Obstetricians and Gynecologists; 2008.
Brockington I. Postpartum psychiatric disorders. Lancet 2004;363:303–310. PMID: 14751705.
Hoffbrand S, Howard L, Crawley H. Antidepressant drug treatment for postnatal depression. Cochrane Database Syst Rev 2001;2:CD002018. PMID: 11406023.