Risk factors (17,20) for placental abruption include physical forces such as trauma and membrane rupture; exposures such as amphetamine, cocaine, methadone, and tobacco; comorbid conditions such as hypertension with superimposed preeclampsia, severe preeclampsia, uterine fibroids, chorioamnionitis, acute/chronic respiratory illnesses (21), advanced maternal age/parity (12), multiple gestation, and previous history of placental abruption (16). Preeclampsia is the commonest risk factor for placental abruption, accounting for 50% of patients (22).

The overall incidence for placental abruption is 5.9 to 6.5 per 1,000 singleton births and 12.2 per twin births (23,24). However, the incidence of placental abruption related to gestational age was found to be 60% for preterm gestation (20% before 34 weeks and 40% between 34 and 37 weeks) and 40% for after 37 weeks of gestation. This incidence was causally related to the low birth weight newborns seen in parturients with placental abruption as compared to parturients without placental abruption (25). The relative risk for delivering a low birth weight newborn in placental abruption is shown in Table 21-2. Recent data show that perinatal mortality rates have dropped from almost 80% several decades ago to 12% (19).

The typical clinical presentation of placental abruption is usually impressive and includes abdominal pain, vaginal bleeding, uterine tenderness, uterine irritability,
coagulopathy, preterm labor, and nonreassuring fetal heart rate. Vaginal bleeding may be profuse and is termed “revealed” or may be absent, if a sequestered retroplacental clot is formed, and is termed “concealed”. Unexplained maternal hypotension, in the absence of vaginal bleeding, may be the presenting feature in concealed placental abruption. In contrast to placenta previa where diagnosis is largely based on imaging, placental abruption has to be diagnosed clinically since Kleihauer–Betke assay and ultrasonography have a limited role (19,26).

However, ultrasonography may aid confirmation in the event of clinical suspicion of placental abruption (27), help determine the age of the hematoma (28), and rule out placenta previa (29). Normal placental thickness is up to 5 cm and if the placenta is more than 8 to 9 cm, one should consider placental abruption as part of the differential diagnosis (30).

Differential diagnosis for revealed vaginal hemorrhage should include placenta previa, genital tract trauma, marginal sinus rupture, hematuria, and vasa previa (17). Differential diagnosis for concealed hemorrhage should include acute appendicitis, chorioamnionitis, uterine fibroid degeneration, ovarian rupture and torsion, pyelonephritis, retroplacental abruption, and uterine rupture (17).

Placental abruption is also classified as mild, moderate, or severe (Table 21-3). Complications of severe placental abruption include hemorrhagic shock, disseminated intravascular coagulopathy (DIC), anemia, acute renal failure, uterine atony, pituitary necrosis, and fetal distress/demise (12,17).

DIC, in placental abruption, occurs in 20% of patients (31), increases with fetal demise, and is due to release of thromboplastin, a thrombogenic substance. Thromboplastin activates the extrinsic coagulation cascade and releases thrombin, converting fibrinogen to fibrin, and sets off massive intravascular coagulation resulting in consumption of clotting factors I, II, V, VIII, and platelets (17). Laboratory confirmation is in the form of elevated levels of prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), fibrin split products (FSP), thrombocytopenia, hypofibrinogenemia, and a typical thromboelastography (TEG) profile (17). Fibrin and thrombin plug the microcirculation and disrupt essential blood flow to critical organs. Simultaneously, secondary fibrinolysis occurs to break down the excessive fibrin (17). Rotational thromboelastometry (ROTEM) is being recommended to help with early diagnosis of fibrinolytic activity and to initiate intervention.

Uterine atony, in placental abruption, is due to the increased levels of FSP in maternal serum and lochia (32). FSP reduce myometrial contractility in vitro (32) and may predispose to ongoing hemorrhage in vivo (17). Also, antifibrinolytics have been shown to enhance myometrial contractility in placental abruption (33).

Obstetric management of placental abruption is best accomplished by delivery of the fetus and placenta. However, clinical considerations for route and timing of delivery should include the severity of placental abruption, gestational age, cardiovascular stability, coagulation profile, and fetal status (15,17). Electronic fetal heart rate monitoring (EFHR) and continuous tocodynamometry, with an intrauterine pressure catheter, are the mainstay of obstetric management.

Anesthetic management for placental abruption should involve early patient evaluation and preparation, including large-bore intravenous access; type and cross-match for 4 to 6 units of packed erythrocytes; laboratory analysis for complete blood count (with platelet count), coagulation profile (PT, PTT, and fibrinogen), arterial blood gas, and TEG (if available). Acute blood loss and the consequent hemodynamic response warrants
aggressive volume resuscitation; left uterine displacement; urinary catheterization; oxygen therapy based on pulse oximetry; and gastrointestinal prophylaxis in preparation for a general anesthetic (12,17).

An easy, inexpensive, and rapid bedside test for coagulation status is to monitor a red top glass test tube, filled with blood, to clot within 6 to 7 minutes or for the clot to break down within 60 minutes; if either does not occur, it suggests the presence of a coagulation abnormality (20). Obviously, the red top test tube examination is a crude surrogate to more specific coagulation tests such as PT, PTT, fibrinogen, platelet count, and TEG. Even though it may not be very reliable, the red top test tube examination may be of some value in situations and facilities where access to coagulation tests is not readily available.

An ominous and not so uncommon consumptive coagulopathy in placental abruption is hypofibrinogenemia, usually below 150 mg/dL (36), and is directly related to degree of placental separation (36). The TEG may show an increase in the K time (normal range, 2 to 4 minutes) and a decrease in the alpha angle (normal range, 50° to 75°). Both these parameters on the TEG are predominantly affected by fibrinogen levels and reflect the speed of clotting. Hypofibrinogenemia responds extremely well to cryoprecipitate transfusion, which is a rich source of fibrinogen, and contains three to ten times more fibrinogen per unit volume as compared to fresh frozen plasma (FFP) (17). Typically, a unit (10 to 15 mL) of cryoprecipitate raises the serum fibrinogen level by 6 to 7 mg/dL (37), so that 13 to 16 units of cryoprecipitate would be needed to raise the serum fibrinogen level by 100 mg/dL (17), in the event FFP is not used to correct the hypofibrinogenemia.

Invasive arterial blood pressure and central venous pressure monitoring is indicated in patients presenting with significant hemodynamic instability and class 3 to 4 hemorrhage to assess and guide fluid and blood management, to maintain urine output at 0.5 to 1 mL/kg/h, and to keep hemoglobin above 6 gm% (38) or 7 gm% (39) respectively.

Anesthetic care should be guided by the necessity for delivery of fetus and degree of placental abruption (12). Neuraxial anesthetic techniques such as continuous epidural analgesia and combined spinal–epidural analgesia may be used for labor and vaginal delivery provided there are no contraindications such as nonreassuring fetal status (NRFS), hypovolemia, or DIC (17). The appropriateness of regional anesthesia, the risk for further extension of abruption and further hemorrhage with an adverse impact on uteroplacental perfusion, is a major concern. Epidural anesthesia significantly worsened maternal hypotension, uterine blood flow, fetal PaO₂, and pH during untreated hemorrhage (20 mL/kg blood loss) in gravid ewes (40). However, with prompt recognition and adequate intravascular volume replacement, there were no differences between the cardiac output, mean arterial pressure, and fetal PaO₂ in the study and control groups. The authors concluded that epidural anesthesia and the associated sympathetic block may adversely affect the compensatory responses in untreated hemorrhage in pregnant patients.

Therefore, close supervision and observation is necessary since new onset hemorrhage or coagulopathy may set in after neuraxial analgesia is started requiring cessation of neuraxial technique; institution of appropriate hemodynamic and neurologic monitoring; and institution of appropriate hemodynamic and neurosurgical intervention.

Cesarean delivery for placental abruption is usually reserved for ongoing hemorrhage, DIC, or NRFS. General anesthesia, using rapid sequence induction/intubation technique and cricoid pressure, is favored. Ketamine, up to 1 mg/kg, is preferred if uterine tone is low or normal. Higher doses of ketamine may increase uterine tone in early pregnancy, but not at term (41). Etomidate, 0.3 mg/kg, should be used in situations such as increased uterine tone or hemodynamic instability (42). Propofol and sodium thiopental are relatively contraindicated in parturients with ongoing hemorrhage or hemodynamic instability because of the potential for exaggerating maternal hypotension and worsening fetal status. Maintenance of general anesthesia with low-dose inhalational agent is recommended to prevent awareness, but may worsen uterine atony, requiring uterotonics after delivery, and may worsen hypotension requiring vasopressor use to maintain hemodynamic stability.

Risk factors for placenta previa include conditions that prevent the upward migration of the placenta, within the uterus, such as previous uterine surgery (cesarean delivery, myomectomy, and dilation/curettage), previous history of placenta previa, advanced maternal age, and multiparity.

The incidence of placenta previa is 3.6/1,000 pregnancies (43), the distribution being 40% total previa, 30% partial placenta previa, and 30% marginal and low-lying placenta previa. Reported perinatal mortality rate is 2.3% (44).

The classic clinical hallmark of placenta previa is painless vaginal bleeding, that may be very subtle at times, and occurs especially during the second or third trimester. The absence of abdominal pain and abnormal uterine tone does not exclude placental abruption, because as many
as 10% of patients with placenta previa have coexisting placental abruption (45). The fetal presenting part is usually not palpable on cervical examination, since the placenta occupies the lower uterine segment, and consequently, a breech or transverse position is observed in 33% of parturients with placenta previa (46,47). The initial bleed usually stops spontaneously and seldom leads to maternal or fetal morbidity/mortality (12). Torrential hemorrhage may be precipitated on cervical examination in an undiagnosed placenta previa.

In contrast to placental abruption where diagnosis is largely clinical, placenta previa is diagnosed by ultrasonography, with 93% to 97% accuracy (48,49), in patients with a full urinary bladder. Transvaginal ultrasonography has 100% sensitivity and permits finer clarity of the placental–uterine border (50), but has the potential for trauma and hemorrhage provoked by vaginal probe placement. Magnetic resonance imaging provides an excellent resolution of the cervical–placental interface and is a useful and more accurate modality for diagnosing placenta previa (51); however, it can be cost prohibitive (17).

Obstetric management of placenta previa depends on the acuity of vaginal bleeding and degree of fetal lung maturity (12). However, if vaginal bleeding is minimal, fetal lungs are not mature, or patient is not in active labor, patients are hospitalized and managed conservatively (17). If vaginal bleeding has stopped for more than 48 hours and the patient has easy, quick access to a tertiary care hospital with facilities such as obstetrics, anesthesiology, neonatology, and blood banking the patients are sent home with clear instructions to return in the event of vaginal bleeding or onset of labor (17). Vaginal delivery may be chosen if the placenta is low-lying and more than 2 cm proximal to the internal cervical os (52) provided the fetal status is stable, maternal hemodynamics are stable, there is no ongoing vaginal hemorrhage, and facilities for cesarean delivery are readily available (53). However, cesarean delivery is indicated for a marginal or complete placenta previa (52,53). Cesarean delivery is also indicated if there is ongoing excessive hemorrhage, fetal lungs are mature, or the parturient is in active labor (17).

Tocolytic therapy is essential, especially before 32 weeks of gestation to allow fetal lung maturity, reduce neonatal morbidity and mortality (54), and provide fetal neuroprotection (55). However, most tocolytic agents have cardiovascular side effects that should be weighed against the benefit of improving fetal lung maturity (17). Similarly, blood transfusion therapy becomes essential for extending the pregnancy and for allowing fetal lungs to mature, but the risk of blood and blood product transfusion-related side effects must be constantly evaluated and compared (17).

Preanesthetic assessment is essential in all parturients presenting to labor and delivery with antepartum hemorrhage (56). Special emphasis should be placed on previous history of cesarean delivery, location of placenta in the current gestation, a thorough airway evaluation, assessment of intravascular volume status, and evaluation of any anticipated ongoing hemorrhage (12,17). Rapid placement of at least two short, but wide-bore peripheral intravenous catheters (16G), blood draw for blood type and screen and complete blood count, and assessment of fetal heart tones are essential (17). Intravascular volume may be replaced with a nondextrose crystalloid solution if hematocrit is acceptable and patient is hemodynamically stable, nonheme colloid solution if hematocrit is acceptable and patient is unstable, or packed erythrocytes if hematocrit is unacceptably low and patient is unstable. In the event of ongoing excessive hemorrhage in a hemodynamically stable patient or if the parturient is hemodynamically unstable, blood type and cross-match for 4 units of packed erythrocytes should be ordered and made available.

The choice of anesthetic management has to be individualized for each patient based on hemodynamic stability and preoperative airway assessment. Similar results, in terms of estimated blood loss, urine output, and neonatal Apgar scores have been observed in hemodynamically stable patients administered general anesthesia or epidural anesthesia for placenta previa requiring elective cesarean delivery (57). However, neuraxial anesthesia remains the preferred choice of anesthesia amongst anesthesiologists and anesthetists taking care of patients with placenta previa with no known placenta accreta, hemodynamic instability, or maternal hypovolemia (1,58). The choices within neuraxial anesthesia range from single-shot spinal anesthesia, continuous epidural anesthesia, and combined spinal–epidural anesthesia; and all three choices have been used successfully. However, the risk of excessive intraoperative hemorrhage in placenta previa patients is fairly high due to the direct surgical incision through an anteriorly located placenta previa, inability of the distended lower uterine segment to contract adequately after delivery, and the increased risk of placenta accreta in patients with previous uterine surgery including cesarean delivery (17). As a general rule, parturients with placenta previa undergoing cesarean delivery, under neuraxial anesthesia, should be made aware that intraoperative induction of general anesthesia, electively or emergently, may be necessary usually after delivery in the event of ongoing excessive hemorrhage requiring cesarean hysterectomy (12). Such ongoing hemorrhage is usually from placenta accreta. Securing the airway early allows the anesthesia care team to focus exclusively on maternal volume resuscitation.

General anesthesia should be chosen as the initial anesthetic in the bleeding placenta previa patient. Since the source of bleeding is the placenta itself, removal of the placenta following delivery of the fetus is essential. Typically, due to the emergent nature of these cases, adequate preoperative evaluation may not occur. However, one has to concurrently assess, resuscitate, and get the patient ready for cesarean delivery (12). Preoperative packed erythrocyte transfusion may be necessary emergently without a blood cross-match being available. In such situations, type specific blood or type O, Rh-negative blood should be administered. At Baylor College of Medicine (Ashutosh Wali), we have immediate access to 4 units of type O, Rh-negative erythrocytes, at all times in the labor and delivery refrigerator, for emergency use.

Invasive hemodynamic monitoring, including an intra-arterial catheter for beat to beat blood pressure recording and frequent blood sampling; and central venous catheter for intravascular volume status and volume replacement, is required for the patient with ongoing excessive hemorrhage (17). In addition, patient temperature should be monitored. Hypothermia should be avoided to prevent coagulopathy and shivering by using a rapid infuser, fluid warming device, warming mattress, and warming blanket.

If airway evaluation is not reassuring, one may either secure the airway awake or proceed with rapid sequence induction. However, in the event of rapid sequence induction, the difficult airway cart with advanced airway equipment must be available in the operating room, adequate backup personnel readily accessible, and an in-house surgeon informed and
available to provide surgical airway access, if necessary (see chapter on Difficult Airway Management for further details).

However, if the airway assessment is reassuring, one should proceed with rapid sequence induction of general anesthesia using appropriate gastrointestinal prophylaxis, adequate preoxygenation to allow effective denitrogenation of lungs, left uterine displacement, and efficacious cricoid pressure application to prevent regurgitation of gastric contents (17). The selection of the intravenous induction agent depends on the level of hemodynamic stability. Etomidate (0.3 mg/kg) has a good track record of safety in obstetric anesthesia (59) and is recommended if uterine tone is increased or the patient is hemodynamically unstable (42). Side effects of etomidate include pain at venous injection site, hiccups, nausea, vomiting, and myoclonus. Ketamine (0.75 to 1 mg/kg) is easy to administer and ideal for the bleeding parturient if uterine tone is normal or decreased (17). Ketamine stimulates the central sympathetic nervous system and inhibits the reuptake of norepinephrine resulting in indirect increase in heart rate, cardiac output, and arterial blood pressure. In patients with severe hemorrhagic shock where catecholamine stores may be exhausted, ketamine may cause direct myocardial depression, due to inhibition of calcium transients, and exaggerate the hypotension (60). Side effects include intraoperative increase in uterine tone compromising the already stressed fetus and postoperative nightmares/hallucinations in doses exceeding 2 mg/kg.

Choice of the maintenance anesthetic agent also depends on hemodynamic stability. Volatile halogenated agents result in uterine muscular relaxation and increased bleeding during cesarean delivery (61), but help to prevent maternal awareness. A combination of oxygen, nitrous oxide as tolerated to keep oxygen saturation within normal range, and low concentration volatile halogenated anesthetic are used until delivery of the fetus. After delivery, small doses of short-acting opioids and short-acting benzodiazepines are administered intravenously to supplement the anesthetic, thereby allowing a reduction in the concentration of the volatile agent and nitrous oxide as necessary (17).

After delivery of the fetus and placenta, because of the previous implantation of the placenta, the lower uterine segment may not contract and result in continued bleeding that may require discontinuing the volatile halogenated agent, administering intravenous oxytocin, intramuscular methylergonovine, intramuscular and/or intramyometrial 15-methyl prostaglandin F2£, and rectal misoprostol. Coagulopathy, in placenta previa, is unusual and may manifest as a dilutional thrombocytopenia from the use of crystalloids/colloids and packed erythrocytes (12,17).

Uterine rupture is essentially a problem leading to parting of the uterine muscle, either in the presence of a previous uterine scar or in the absence of one, and the commonest cause is due to the disruption of a previous cesarean hysterotomy scar (36).

The etiology of uterine rupture can be subdivided into two groups, pregestational and gestational. Pregestational causes include surgical (previous cesarean delivery, previous myomectomy scar (62), previous repair of uterine rupture, and dilation and curettage (63)), traumatic (blunt, penetrating, sharp trauma), and congenital anomalies (bicornuate uterus (64), and undeveloped uterine horn (36)). Gestational causes reflect causes in the current pregnancy and include antepartum (spontaneous and intense uterine hyperstimulation, augmented stimulation of labor with oxytocin or prostaglandins (64), external cephalic version, uterine overdistension from multiple gestation or polyhydramnios, intra-amniotic instillation of saline or prostaglandins), intrapartum (difficult forceps delivery, tumultuous breech extraction) (65), and acquired (placenta percreta, gestational trophoblastic neoplasia) (36). A recent study (2001) drew attention to the increased risk of uterine rupture associated with the use of prostaglandin induction and advised against its use in patients with previous cesarean delivery (66). The overall risk of real uterine rupture in an unscarred uterus is almost nonexistent (67) and in parturients with a scarred uterus, it is still low at 1% (64). However, the relative risk of uterine rupture during spontaneous labor compared to nonlaboring patients is 3.3 (95% C.I., 1.8 to 6), is considerably higher at 15.6 (95% C.I., 8.1 to 30) when prostaglandins are used for induction of labor, but is unclear for oxytocin use (68).

Most uterine rupture, during labor, occurs in the lower anterior uterine segment leading to increased maternal morbidity and mortality (7), because the anterior uterine wall is highly vascular and may include the site for placental implantation (12); whereas uterine rupture, before labor, occurs at the fundus (69). Fetal mortality rate of 35% has been reported in a review of 23 parturients with severe uterine rupture; no maternal mortality occurred in that series (65). Neonatal mortality rises 60 times in uterine rupture (67).

Risk factors include previous cesarean delivery, congenital uterine anomalies, fetal malpresentation, grand multiparity, labor induction with oxytocin or prostaglandins, and previous myomectomy (12).

Uterine rupture can be catastrophic to both, the mother and her fetus. Fortunately, it is very uncommon. However, when it occurs, maternal and fetal morbidity and mortality are dependent on its severity that in turn, relies on whether the rupture is complete or is merely a uterine scar dehiscence. Complete uterine rupture causes an extensive uterine wall deficiency, leading to fetal compromise and maternal hemorrhage, requiring surgical intervention (12). On the other hand, uterine scar dehiscence leads to a minimal uterine wall deficiency that may be asymptomatic or does not cause fetal compromise or maternal hemorrhage requiring surgical intervention (12).

The commonest and most reliable clinical sign of uterine rupture, in labor, is sudden onset of a nonreassuring fetal heart rate and is reported in 81% of patients (70). Other clinical findings include vaginal bleeding, hypotension, hematuria, and absence of uterine contraction (12). Abdominal pain may not be a consistent symptom of uterine rupture (71).

Obstetric management of uterine rupture has to be individualized and depends on the severity of signs and symptoms. If a uterine rent is noted during a postpartum examination following a vaginal birth after cesarean delivery, and the patient is hemodynamically stable without evidence of vaginal bleeding, parturients should be carefully monitored under close observation and concealed hemorrhage should be excluded (17). On the other hand, if there is ongoing excessive maternal hemorrhage and/or fetal distress, cesarean delivery with surgical repair of uterine rupture site may be undertaken, especially if future fertility is desired. If surgical repair is performed, elective cesarean delivery may be indicated in future pregnancies (24). However, surgical repair carries the risk of recurrence of uterine rupture, and may be fatal (24). Definitive management is proceeded with a hysterectomy, and subtotal hysterectomy has been shown to have decreased operating time, lower morbidity, lower mortality, and shorter hospital stay than surgical repair (72). Evidence shows that blood transfusion is required for patients with rupture of unscarred uterus as opposed to patients with scarred uterus. The fibrous and
scarred edges of a scar bleed less than the edges of a newly ruptured, unscarred uterus.

Anesthetic management includes caring for any bleeding parturient requiring a cesarean hysterectomy with particular emphasis on the airway, hemodynamics, hematologic system, and status of the fetus. Aggressive volume replacement with blood and blood products, general anesthesia, invasive hemodynamic monitoring, rapid infusion systems, warming devices should be employed for the hemodynamically unstable patient as has been addressed in the earlier section on placental abruption in this chapter. However, if the patient is hematologically and hemodynamically well compensated, a pre-existing labor epidural catheter may be activated for surgical anesthesia with the understanding that intraoperative induction of general anesthesia may be necessary, at any point during surgery to secure the airway and concentrate on volume resuscitation (73).

Fetal mortality is reported to be as high as 50% to 75% (12). Maternal hemodynamics and hematologic profile are usually not affected.

The only known risk factor is multiple gestation, so that the incidence of velamentous insertion of umbilical cord is directly proportional to the number of fetuses. However, the overall incidence is quite low at 0.0004% (52).

Diagnosis is commonly ultrasonographic (12), confirmed with color Doppler imaging (17), and made antenatally with good perinatal results (74). Sometimes, the diagnosis is based on the association between onset of vaginal bleeding and rupture of fetal membranes, followed by NRFS (12). At other times, diagnosis may be made by palpation of the pulsation in the fetal membranes during routine cervical examination of parturients (17). Chemical tests, such as the Apt test (resistance to denaturation of fetal hemoglobin under alkaline conditions) or the Wright stain (detection of nucleated erythrocytes in fetal blood), have been used to aid diagnosis in the setting of vaginal bleeding associated with fetal membrane rupture (17).

Obstetric management is focused toward optimizing fetal outcomes, especially in parturients with bleeding vasa previa where cesarean delivery is the norm. Elective cesarean delivery may have to be performed for preterm parturients at 36 weeks of gestation (52), and emergency cesarean delivery may have to be performed for a ruptured vasa previa. Emergency cesarean delivery has been associated with poor fetal outcomes (75), despite proceeding within minutes of vaginal bleeding (76) due to a small fetal blood volume reserve of 80 to 100 mL/kg (12), and commonly requires neonatal volume resuscitation with packed erythrocytes (12).

Anesthetic management should cater to the ongoing needs of both the mother and her fetus at risk, and has been addressed in the earlier section on placenta previa in this chapter.

Uterine atony is defined as inability of the uterine smooth muscle to contract satisfactorily after delivery of the fetus. PPH results from the dilated arterioles and veins in the placental bed (17) that would ordinarily be constricted by the contracting uterine smooth muscle and may be unresponsive to vasoconstrictors (82). Parturients with obstetric hemorrhage may have uterine arteries that are relatively unresponsive to vasoconstrictors (82). It is the commonest cause of PPH, accounting for almost 80% of the cases (1), and the commonest indication for postpartum blood transfusion (83,84). Uterine contraction and involution, mediated by endogenous oxytocin and prostaglandins, helps control PPH and acts as the primary hemostasis after delivery (12).

Risk factors for uterine atony are best divided into labor-related (arrested active phase of labor requiring oxytocin augmentation, precipitous labor, protracted labor); fetus-related (fetal macrosomia, multiple gestation, placental abruption, placenta previa, polyhydramnios); or mother-related (chorioamnionitis, family history, grand multiparity, laceration during cesarean delivery, use of tocolytics, high concentration of volatile anesthetic) causes (17).

Diagnosis is usually simple and is based on palpation of a soft postpartum uterus in the setting of vaginal bleeding (12). However, uterine atony may coexist with other causes of PPH and such causes should be excluded before initiating pharmacologic treatment. Inspection must be performed for placental fragmentation, uterine retained placental products, cervical laceration, and vaginal lacerations (17). A high index of suspicion for placenta accreta is warranted if the uterus feels gritty to palpation during manual exploration (17).

Obstetric management should consider early pharmacologic therapy (oxytocin, methylergonovine, 15-methyl prostaglandin F2 alpha, and misoprostol) (1); direct uterine manipulation (bimanual compression, uterine massage); or surgical intervention (B-Lynch procedure, hysterectomy) (17). Frequently, pharmacologic therapy and uterine manipulation are applied
concurrently and failure to respond to such treatment should be readily communicated between the anesthesiologist and the obstetrician before proceeding with surgical intervention (17). Early administration of oxytocin after delivery is essential in preventing uterine atony (1) and to prevent severe maternal morbidity/mortality (85,86). Evidence suggests that alternative uterotonics may not confer any benefit (87).

Anesthetic management is guided by the patient’s airway examination, hemodynamic stability, and hematologic status. Calcium chloride, administered intravenously, may augment uterine contractility in the setting of refractory uterine atony, especially when the patient has received magnesium sulfate. In addition to using uterotonic agents, essential principles are similar to any other case of PPH and are discussed, in detail, later in this chapter.