Obstetric Hemorrhage and Puerperal Sepsis

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Chapter 10 Obstetric Hemorrhage and Puerperal Sepsis

The most common causes of maternal death are hemorrhage, embolism, hypertensive disease, and infection. In this chapter, the problems of obstetric hemorrhage and infection are considered. These conditions are associated not only with potential maternal and fetal mortality but also with significant morbidity and prolonged hospitalization.

image Antepartum Hemorrhage

It is critical for the well-being of both the mother and the fetus that the patient who presents with third-trimester bleeding be evaluated and managed emergently. The differential diagnosis of third-trimester bleeding is listed in Box 10-1.

INITIAL EVALUATION

If a patient is bleeding profusely, a team approach to the assessment and management should be instituted to establish hemodynamic stability. This team should include an obstetrician, an anesthesiologist, and nurses who are knowledgeable about the management of the critically ill patient. At least two large-bore peripheral intravenous lines should be placed because this allows for the most rapid replacement of fluid and blood volume. A central venous pressure line, or preferably a Swan-Ganz catheter, is helpful in the management of hypovolemic shock.

The vital signs and amount of bleeding should be checked immediately, as should the patient’s mental status. Medical history should be checked for known bleeding disorders or liver disease, which predisposes to coagulopathy. A pelvic examination should not be performed until placenta previa has been excluded by ultrasonography. Once placenta previa has been excluded, a sterile speculum examination can be safely done to rule out genital tears or lesions (e.g., cervical cancer) that may be responsible for the bleeding. If none are identified, a digital examination may be performed to determine whether cervical dilation is present.

A complete blood count should be obtained and compared with previous evaluations to help assess the amount of blood loss, although acute blood loss may not be reflected in the hemoglobin level until homeostasis has been reestablished. An assessment of the patient’s coagulation profile should be done by obtaining a platelet count, serum fibrinogen level, prothrombin time, and partial thromboplastin time. Additionally the patient should be typed and crossmatched for at least 4 units of blood (packed cells). A rapid but subjective method to test for coagulopathy is to partially fill a red-topped tube with blood. If a clot does not form, or once formed does not stay clotted, the patient most likely has disseminated intravascular coagulopathy (DIC).

An important and accurate method for determining the cause of third-trimester bleeding is ultrasonography. This evaluation should include not only the location and extent of the placenta but also an assessment of gestational age, an estimate of fetal weight, a determination of the fetal presentation, and a screening for fetal anomalies. Uterine activity and the fetal heart rate should be assessed with a monitored strip to rule out labor and establish fetal well-being.

image Abnormal Placentation

The incidence of placenta previa, the most common type of abnormal placentation, is 0.5%. Bleeding from a placenta previa accounts for about 20% of all cases of antepartum hemorrhage. Seventy percent of patients with placenta previa present with painless vaginal bleeding in the third trimester, 20% have contractions associated with bleeding, and 10% have the diagnosis made incidentally by ultrasonography or at term.

CLASSIFICATION

Placenta previa is classified according to the relationship of the placenta to the internal cervical os (Figure 10-1). Complete placenta previa implies that the placenta totally covers the cervical os. A complete placenta previa may be central, anterior, or posterior, depending on where the center of the placenta is located relative to the os. Partial placenta previa implies that the placenta partially covers the internal cervical os. A marginal placenta previa is one in which the edge of the placenta extends to the margin of the internal cervical os.

MATERNAL-FETAL RISKS

The maternal mortality from placenta previa has dropped precipitously during the past 60 years from 30% to less than 1%. This has primarily been the result of the liberal use of cesarean delivery and careful expectant management. The rare maternal death is generally associated with complications of cesarean or uncontrolled hemorrhage from the placental site. The lower uterine segment does not contract well, especially after a lower uterine incision from cesarean delivery. DIC may also result if a massive hemorrhage or an associated abruption occurs.

The risk for antepartum or intrapartum hemorrhage, or both, is a constant threat to the patient with placenta previa. Bleeding may be exacerbated by an associated placenta accreta or uterine atony. Placenta accreta implies an abnormal attachment of the placenta through the uterine myometrium as a result of defective decidual formation (absent Nitabuch’s layer). This abnormal attachment may be superficial (accreta), or the placental villi may invade partially through the myometrium (increta) or extend to the uterine serosa (percreta). Two thirds of patients with this complication require hysterectomy. Patients with a history of uterine surgery are at greatest risk for developing an accreta. In fact, those with a prior cesarean delivery have a 25% risk.

Placenta previa predisposes to preterm delivery, which poses the greatest risk to the fetus. As a result of advances in obstetric and neonatal care, the perinatal mortality rate (PMR) for premature infants has declined over the past decade. The incidence of malpresentation with placenta previa is 30%, presumably owing to the mass effect and distortion of the lower uterine segment.

image Abruptio Placentae

Abruptio placentae, or premature separation of the normally implanted placenta, complicates 0.5% to 1.5% of all pregnancies (1 in 120 births). Abruption severe enough to result in fetal death occurs in 1 per 500 deliveries.

DIAGNOSIS AND MANAGEMENT

Clinically, the diagnosis of a placental abruption is entertained if a patient presents with painful vaginal bleeding in association with uterine tenderness, hyperactivity, and increased tone. The signs and symptoms of placental abruption are, however, variable. The most common finding is vaginal bleeding, seen in 80% of cases. Abdominal pain and uterine tenderness are present in 66% of cases, fetal distress in 60%, uterine hyperactivity and increased uterine tone in 34%, and fetal demise in 15%.

The diagnosis of placental abruption is made clinically. Ultrasonography may detect only 2% of abruptions. Because placental abruption may coexist with a placenta previa, the reason for doing an initial ultrasonic examination is to exclude the previa.

Management of the patient with an abruption includes careful maternal hemodynamic and fetal monitoring, serial evaluation of the hematocrit and coagulation profile, and delivery. Intensive monitoring of both the mother and the fetus is essential because rapid deterioration of the condition of either one can occur. Blood products for replacement should always be available, and a large-bore (16- to 18-gauge) intravenous line must be secured. Red blood cells should be given liberally if indicated. In the setting of placental abruption, the use of tocolytics or uterine relaxants is not advised. Uterine tone must be maintained to control bleeding following delivery, or at least to control the bleeding sufficiently to allow a safe hysterectomy to be performed, if necessary.

image Uterine Rupture

Uterine rupture implies complete separation of the uterine musculature through all of its layers, ultimately with all or a part of the fetus being extruded from the uterine cavity. The overall incidence is 0.5%.

Uterine rupture may be spontaneous, traumatic, or associated with a prior uterine scar, and it may occur during or before labor or at the time of delivery. A prior uterine scar is associated with 40% of cases. With a prior lower-segment transverse incision, the risk for rupture is less than 1%, whereas the risk with a high vertical (classical) scar is 4% to 7%. Sixty percent of uterine ruptures occur in previously unscarred uteri.

image Postpartum Hemorrhage

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 cesarean delivery; therefore, blood loss in excess of 1000 mL is considered a postpartum hemorrhage in these patients. The excessive blood loss usually occurs in the immediate postpartum period but can occur slowly over the first 24 hours. Delayed postpartum hemorrhage can occasionally occur, with the excessive bleeding commencing more than 24 hours after delivery. 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.

COAGULATION DISORDERS

Peripartum coagulation disorders are high-risk factors for postpartum hemorrhage but fortunately are quite rare.

Patients with thrombotic thrombocytopenia have a rare syndrome of unknown etiology characterized by thrombocytopenic purpura, microangiopathic hemolytic anemia, transient and fluctuating neurologic signs, renal dysfunction, and a febrile course. In pregnancy, the disease is usually fatal. An amniotic fluid embolus is also rare and is associated with an 80% mortality rate. This syndrome is characterized by a fulminating consumption coagulopathy, intense bronchospasm, and vasomotor collapse. It is triggered by an intravascular infusion of a significant amount of amniotic fluid during a tumultuous or rapid labor in the presence of ruptured membranes. During the process of placental abruption, a small amount of amniotic fluid may leak into the vascular system, and the thromboplastin in the amniotic fluid may trigger a consumption coagulopathy. Patients with idiopathic thrombocytopenic purpura have platelets with abnormal function or a shortened life span. This causes thrombocytopenia and a tendency to bleed. Circulating antiplatelet antibodies of the IgG type may occasionally cross the placenta and result in fetal and neonatal thrombocytopenia as well. Von Willebrand’s disease is an inherited coagulopathy characterized by a prolonged bleeding time due to factor VIII deficiency. During pregnancy, these patients are likely to have a decreased bleeding diathesis because pregnancy elevates factor VIII levels. In the postpartum period, they are susceptible to delayed bleeding as factor VIII levels fall.

image Obstetric Shock

Hypotension without significant external bleeding may occasionally develop in an obstetric patient. This condition is called obstetric shock. The causes of obstetric shock include concealed hemorrhage, uterine inversion, and amniotic fluid embolism.

An improperly sutured episiotomy can lead to a concealed postpartum hemorrhage. If the first suture at the vaginal apex of the episiotomy incision does not incorporate the cut and retracted arterioles, they can continue to bleed, creating a hematoma that can dissect cephalad into the retroperitoneal space. This may cause shock without external evidence of blood loss. A soft tissue hematoma, usually of the vulva, may occur following delivery in the absence of any laceration or episiotomy and may also contribute to occult blood loss.

image Management of Postpartum Hemorrhage and Obstetric Shock

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 available. An intravenous infusion through a large-bore needle or catheter should be started before delivery, and blood should be held in the laboratory for possible crossmatching.

During the diagnostic workup of an established hemorrhage, the patient’s vital signs must be monitored closely. Multiple units of packed red blood cells must be typed and crossmatched and 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 3 times the estimated blood loss.

UTERINE ATONY

If uterine atony is determined to be the cause of the postpartum hemorrhage, 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 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. Alternatively, a large-volume balloon catheter has been developed that performs a similar function while maintaining a channel into the uterine cavity, allowing further bleeding to be monitored.

If uterine bleeding persists in an otherwise stable patient, she can 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. When reproductive potential is important to the patient, ligation of the uterine arteries adjacent to the uterus will lower the pulse pressure. This procedure is more successful in controlling placental site hemorrhage and is easier to perform than bilateral hypogastric artery ligation.

GENITAL TRACT TRAUMA

When postpartum hemorrhage is related to genital tract trauma, surgical intervention is necessary. When repairing genital tract lacerations, 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 (Figure 10-2). 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.

The intraoperative laceration of the ascending branch of the uterine artery during delivery through a low transverse incision can be easily controlled by the placement of a large suture ligature through the myometrium and broad ligament below the level of the laceration. A uterine rupture usually necessitates subtotal or total abdominal hysterectomy, although small defects may be repaired.

RETAINED PRODUCTS OF CONCEPTION

When the placenta cannot be delivered in the usual manner, manual removal is necessary (Figure 10-3). This should be performed urgently if bleeding is profuse. Otherwise, it is reasonable to delay 30 minutes to await spontaneous separation. General anesthesia may be required. Following manual removal of the placenta or placental remnants, the uterus should be scraped with a large curette.

COAGULOPATHY

When postpartum hemorrhage is associated with coagulopathy, the specific defect should be corrected by the infusion of blood products, as outlined in Table 10-1 and Box 10-5. Patients with thrombocytopenia require platelet concentrate infusions; those with von Willebrand’s disease require factor VIII concentrate or cryoprecipitate.

TABLE 10-1 BLOOD PRODUCTS USED TO CORRECT COAGULATION DEFECTS

Blood Product Volume (mL) in 1 Unit Effect of Transfusion
Platelet concentrate 30-40 Increases platelet count by about 20,000 to 25,000
Cryoprecipitate 15-25 Supplies fibrinogen, factor VIII, and factor XIII (3-10 times more concentrated than the equivalent volume of fresh plasma)
Fresh-frozen plasma 200 Supplies all factors except platelets (1 g of fibrinogen)
Packed red blood cells 200 Raises hematocrit 3%-4%

Quantity obtained from 1 Unit (500 mL) of fresh whole blood.

A packed red cell infusion is given to a patient who has bled enough to drop the circulating red cell population sufficiently to compromise the delivery of oxygen to the tissues. Therefore, institution of blood transfusion is best judged by symptoms of oxygen deprivation rather than by some empirical hemoglobin level. No important physiologic impairment has been noted at hemoglobin levels as low as 6 to 8 g/dL (hematocrit, 18% to 24%). In general, a 1-U transfusion of packed red blood cells will increase the hemoglobin level by 1 g/dL (and the hematocrit by 3% to 4%).

Massive blood replacement (when total blood volume is replaced in a 24-hour period) may be associated with thrombocytopenia, prolonged prothrombin time (PT), and hypofibrinogenemia. Thrombocytopenia is the most common abnormality, so platelet transfusion following determination of a low platelet count is not an uncommon scenario. Fresh frozen plasma may be transfused for prolonged PT or hypofibrinogenemia.

image Puerperal Sepsis

Puerperal sepsis still accounts for significant postpartum maternal morbidity and mortality. Patients with a puerperal genital tract infection are susceptible to the development of septic shock, pelvic thrombophlebitis, and pelvic abscess.

Following a vaginal delivery, about 6% to 7% of women demonstrate febrile morbidity, defined as a temperature of 100.4°F (38°C) or higher that occurs for more than 2 consecutive days (exclusive of the first postpartum day) during the first 10 postpartum days. Following primary cesarean delivery, the incidence of febrile morbidity is about twice that following vaginal delivery. Most of these fevers are caused by endometritis.

ETIOLOGY

The pathophysiology of puerperal sepsis is closely related to the various microbial inhabitants of the vagina and cervix. The vaginal flora during gestation resembles the nonpregnant state, although there is a trend toward isolating more Mycoplasma genitalis and anaerobic streptococci in the last trimester. Potentially pathogenic organisms can be cultured from the vagina in about 80% of pregnant women. These organisms include enterococci, hemolytic and nonhemolytic streptococci, anaerobic streptococci, enteric bacilli, pseudodiphtheria bacteria, and Neisseria species other than N. gonorrhoeae. Excessive overgrowth of these organisms during pregnancy is inhibited by the acidity of the vagina (pH 4 to 5), primarily as a result of the production of lactic acid by the lactobacilli.

The uterine cavity is normally free of bacteria during pregnancy. After parturition, the pH of the vagina changes from acidic to alkaline because of the neutralizing effect of the alkaline amniotic fluid, blood, and lochia, as well as the decreased population of lactobacilli. This change in pH favors an increased growth of aerobic organisms. About 48 hours postpartum, progressive necrosis of the endometrial and placental remnants produces a favorable intrauterine environment for the multiplication of anaerobic bacteria.

About 70% of puerperal infections are caused by anaerobic organisms. Most of these are anaerobic cocci (Peptostreptococcus, Peptococcus, and Streptococcus), although mixed infections with Bacteroides fragilis are encountered in up to one third of cases. Of the aerobic organisms, Escherichia coli is the most common pathogen, followed by enterococci. Puerperal infection from clostridia is rare.

Intrauterine staphylococcal infection is rare. This organism is frequently responsible for infection of perineal wounds and abdominal incisions. Trichomonas vaginalis and Candida albicans are frequent inhabitants of the vagina, but no connection with puerperal sepsis has been established. Mycoplasma organisms have been shown to contribute to puerperal endometritis.

PREDISPOSING FACTORS

Predisposing factors for the development of a puerperal genital tract infection are shown in Box 10-6.

After delivery, the placental site vessels are clotted off, and there is an exudation of lymph-like fluid along with massive numbers of neutrophils and other white cells to form the lochia. Vaginal microorganisms readily enter the uterine cavity and may become pathogenic at the placental site, depending on such variables as the size of the inoculum, the local pH, and the presence or absence of devitalized tissue. The latter may include tissue incorporated in the suture line of a cesarean incision.

The normal body defense mechanisms usually prevent any progressive infection, but a breakdown of these defenses allows the bacteria to invade the myometrium. Further invasion into the lymphatics of the parametrium can cause lymphangitis, pelvic cellulitis, and the possibility of widespread infection from septic emboli.

Endomyoparametritis is a potentially life-threatening condition. It commonly begins with retention of secundines (placental and amniochorionic membrane fragments) that block the normal lochial flow, allowing accumulation of intrauterine lochia, which in turn changes the local pH and acts as a culture medium for bacterial growth. Unless normal lochial flow is established, bacterial invasion progresses.

MANAGEMENT

A febrile puerperal patient with cessation of lochial flow should undergo a pelvic examination and removal of any secundines that may be occluding the cervical os.

The antibiotic treatment of puerperal infection usually follows two major principles. First, early antibiotic treatment should be instituted to confine and then eliminate the infectious process. Second, the antibiotics should provide anaerobic coverage because these organisms are involved in 70% of puerperal infections. Antibiotics should be continued for at least 48 hours after the patient becomes afebrile. Anaerobic organisms especially require prolonged chemotherapy for elimination.

Broad-spectrum antibiotics, such as ampicillin and the cephalosporins, are effective first-line drugs for mild and moderate cases of puerperal infection. When the infection is moderate to severe, a penicillin-aminoglycoside combination has traditionally been used as first-line therapy. The major pelvic pathogen resistant to this combination is Bacteroides fragilis, which is usually sensitive to clindamycin. the use of clindamycin with either an aminoglycoside or ampicillin will provide the best first-line coverage.

When pelvic thrombophlebitis or thromboembolism is suspected or clinically diagnosed, unfractionated heparin therapy should be instituted to increase the clotting time (Lee-White method) or activated prothrombin time to 2 to 3 times normal. Only 2 to 3 weeks of anticoagulant therapy are needed for uncomplicated pelvic thrombophlebitis. Patients with femoral thrombophlebitis require 4 to 6 weeks of heparin therapy followed by the administration of oral anticoagulants for a few months.

If the patient does not respond to heparin therapy and the clinical course is one of unrelenting fever and pelvic tenderness, a diagnosis of pelvic abscess must be considered. Diagnosis is made by pelvic examination and confirmed by pelvic ultrasonography or computed tomography scan. The finding of a tender, pelvic parametrial mass suggests an abscess. Ultrasonography will confirm that the mass is fluid-filled rather than solid. The presence of a pelvic abscess requires surgical drainage.