ESSENTIALS OF DIAGNOSIS
Severe Preeclampsia (one or more of below)
Blood pressure of 160 mm Hg or higher systolic or 110 mm Hg or higher diastolic.
Progressive renal insufficiency.
Hemolysis, elevated liver enzymes, low platelets (HELLP).
Vision changes or headache.
Preeclampsia is defined as the presence of newly elevated blood pressure and proteinuria during pregnancy. Eclampsia is diagnosed when seizures develop in a patient with evidence of preeclampsia. Historically, the presence of three elements was required for the diagnosis of preeclampsia: hypertension, proteinuria, and edema. Edema was difficult to objectively quantify and is no longer a required element.
Preeclampsia-eclampsia can occur any time after 20 weeks of gestation and up to 6 weeks postpartum. It is a disease unique to pregnancy, with the only cure being delivery of the fetus and placenta. Preeclampsia develops in approximately 7% of pregnant women in the United States; of those, eclampsia will develop in 5% (0.04% of pregnant women). Primiparas are most frequently affected; however, the incidence of preeclampsia-eclampsia is increased with multiple gestation pregnancies, chronic hypertension, diabetes mellitus, kidney disease, collagen-vascular and autoimmune disorders, and gestational trophoblastic disease. Uncontrolled eclampsia is a significant cause of maternal death. The cause of preeclampsia-eclampsia is not known, but it is likely a multifactorial, two-stage process. The first stage is thought to be a disturbance in placental implantation involving the spiral arteries very early in gestation. The abnormal placental perfusion that results leads to the formation of noxious free radicals. The second stage is characterized by excessive inflammation causing endothelial damage, vasospasm, and finally clinical signs and symptoms. An immunologic component to preeclampsia-eclampsia has been proposed, citing the increased incidence in primigravidas. This entire process is likely enhanced by environmental factors, genetic predisposition, and preexisting maternal disease.
Clinically, the severity of preeclampsia-eclampsia can be measured with reference to the six major sites in which it exerts its effects: the central nervous system, the kidneys, the liver, the hematologic system, the vascular system, and the fetal-placental unit. By evaluating each of these areas for the presence of mild to severe preeclampsia, the degree of involvement can be assessed, and an appropriate management plan can be formulated that balances the severity of disease and gestational age (Table 19–3).
Table 19–3.Indicators of mild to moderate versus severe preeclampsia-eclampsia. |Favorite Table|Download (.pdf) Table 19–3. Indicators of mild to moderate versus severe preeclampsia-eclampsia.
|Site ||Indicator ||Mild to Moderate ||Severe |
|Central nervous system ||Symptoms and signs ||Hyperreflexia ||Seizures |
| || || ||Blurred vision |
| || || ||Scotomas |
| || || ||Headache |
| || || ||Clonus |
| || || ||Irritability |
|Kidney ||Proteinuria ||0.3–5 g/24 h ||> 5 g/24 h or catheterized urine with 4+ protein |
| ||Urinary output ||> 30 mL/h ||< 30 mL/h |
|Liver ||AST, ALT, LD ||Normal liver enzymes ||Elevated liver enzymes |
| || || ||Epigastric pain |
| || || ||Ruptured liver |
|Hematologic ||Platelets || ||< 100,000/mcL |
| ||Hemoglobin ||Normal ||Elevated |
|Vascular ||Blood pressure ||< 160/110 mm Hg ||> 160/110 mm Hg |
| ||Retina ||Arteriolar spasm ||Retinal hemorrhages |
|Fetal-placental unit ||Growth restriction ||Absent ||Present |
| ||Oligohydramnios ||Absent ||Present |
| ||Fetal distress ||Absent ||Present |
Patients usually have few complaints, and the diastolic blood pressure is less than 110 mm Hg. Edema may be present. The platelet count is over 100,000/mcL, antepartum fetal testing is reassuring (see Tests & Procedures, above), central nervous system irritability is minimal, epigastric pain is not present, and liver enzymes are not elevated.
Symptoms are more dramatic and persistent. Patients may complain of headache and changes in vision. The blood pressure is often quite high, with readings at or above 160/110 mm Hg. Thrombocytopenia (platelet count less than 100,000/mcL) may be present and progress to disseminated intravascular coagulation. Severe epigastric pain may be present from hepatic subcapsular hemorrhage with significant stretch or rupture of the liver capsule. HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) is an advanced form of severe preeclampsia.
The occurrence of seizures defines eclampsia. It is a manifestation of severe central nervous system involvement. Other findings of preeclampsia are observed.
Preeclampsia-eclampsia can mimic and be confused with many other diseases, including chronic hypertension, chronic kidney disease, primary seizure disorders, gallbladder and pancreatic disease, immune thrombocytopenia, thrombotic thrombocytopenic purpura, and hemolytic-uremic syndrome. It must always be considered in any pregnant woman beyond 20 weeks of gestation with consistent signs and symptoms. Although it is most common in the third trimester, it can occur earlier, especially in women with comorbid conditions like hypertension, kidney disease, and systemic lupus erythematosus. It is particularly difficult to diagnose when a preexisting disease such as hypertension is present.
In clinical studies, diuretics, dietary restriction or enhancement, sodium restriction, and vitamin-mineral supplements (eg, calcium or vitamin C and E) have not been confirmed to be useful. The only cure is delivery of the fetus at a time as favorable as possible for its survival.
Early recognition is the key to treatment. This requires careful attention to the details of prenatal care—especially subtle changes in blood pressure and weight. The objectives are to prolong pregnancy if possible to allow fetal lung maturity while preventing progression to severe disease and eclampsia. The critical factors are the gestational age of the fetus, fetal pulmonary maturity, and the severity of maternal disease. Preeclampsia-eclampsia at term is managed by delivery. Prior to term, severe preeclampsia-eclampsia requires delivery with very few exceptions. Epigastric pain, seizures, severe range blood pressures, thrombocytopenia, and visual disturbances are strong indications for delivery of the fetus. Marked proteinuria alone can be managed more conservatively.
For mild preeclampsia, modified bed rest is the cornerstone of therapy. This increases central blood flow to the kidneys, heart, brain, liver, and placenta and may stabilize or even improve the degree of preeclampsia for a period of time.
Modified bed rest may be attempted at home or in the hospital. The goal is not to keep the woman in bed continuously but rather to limit her activity. Prior to making this decision, the clinician should evaluate the six sites of involvement listed in Table 19–3 and make an assessment about the severity of disease.
Home management with modified bed rest may be attempted for patients with mild preeclampsia and a stable home situation. This requires assistance at home, rapid access to the hospital, a reliable patient, and the ability to obtain frequent blood pressure readings. A home health nurse can often provide frequent home visits and assessments.
Hospitalization is required for women with severe preeclampsia or those with unreliable home situations. Regular assessments of blood pressure, urine protein, and fetal heart tones and activity are required. A CBC with platelet count, electrolyte panel, and liver enzymes should be checked regularly, with frequency dependent on severity. A 24-hour urine collection for total protein and creatinine clearance should be obtained on admission and repeated as indicated. Magnesium sulfate is not used until the diagnosis of severe preeclampsia is made and delivery planned (see Eclampsia, below).
Fetal evaluation should be obtained as part of the work-up. If the patient is being admitted to the hospital, fetal testing should be performed on the same day to assess fetal wellbeing. This may be done by fetal heart rate testing with nonstress testing or by biophysical profile. A regular schedule of fetal surveillance must then be followed. Daily fetal kick counts can be recorded by the patient herself. If the fetus is < 34 weeks gestation, corticosteroids (betamethasone 12 mg intramuscularly every 24 h for two doses, or dexamethasone 6 mg intramuscularly every 12 h for four doses) can be administered to the mother. However, when a woman is clearly suffering from unstable severe preeclampsia, delivery should not be delayed for fetal lung maturation or administration of corticosteroids.
The method of delivery is determined by the maternal and fetal status. A vaginal delivery is preferred because it has less blood loss than a cesarean section and requires less coagulation factors. Cesarean section is reserved for the usual fetal indications. For mild preeclampsia, delivery should take place at term.
If the patient is convulsing, she is turned on her side to prevent aspiration and to improve blood flow to the placenta. The seizure may be stopped by giving an intravenous bolus of either magnesium sulfate, 4–6 g, or lorazepam, 2–4 mg over 4 minutes or until the seizure stops. Magnesium sulfate is the preferred agent, and alternatives should only be used if magnesium sulfate is unavailable. A continuous intravenous infusion of magnesium sulfate is then started at a rate of 2–3 g/h unless the patient is known to have significantly reduced kidney function. Magnesium blood levels are then checked every 4–6 hours and the infusion rate adjusted to maintain a therapeutic blood level (4–6 mEq/L). Urinary output is checked hourly and the patient assessed for signs of possible magnesium toxicity such as loss of deep tendon reflexes or decrease in respiratory rate and depth, which can be reversed with calcium gluconate, 1 g intravenously over 2 minutes.
In patients with severe preeclampsia, magnesium sulfate should be given intravenously, 4- to 6-g load over 15–20 minutes followed by 2–3 g/h maintenance, for seizure prophylaxis. The occurrence of eclampsia necessitates delivery once the patient is stabilized. It is important, however, that assessment of the status of the patient and fetus take place first. Continuous fetal monitoring must be performed and maternal blood typed and cross-matched quickly. A urinary catheter is inserted to monitor urinary output, and a CBC with platelets, electrolytes, creatinine, and liver enzymes are obtained. If hypertension is present with systolic values of 160 mm Hg or higher or diastolic values 110 mm Hg or higher, antihypertensive medications should be administered to reduce the blood pressure to 140–150/90–100 mm Hg. Lower blood pressures than this may induce placental insufficiency through reduced perfusion. Hydralazine given in 5- to 10-mg increments intravenously every 20 minutes is frequently used to lower blood pressure. Labetalol, 10–20 mg intravenously, every 20 minutes as needed, can also be used.
Delivery is mandated once eclampsia has occurred. Vaginal delivery is preferred. The rapidity with which delivery must be achieved depends on the fetal and maternal status following the seizure and the availability of laboratory data on the patient. Oxytocin, given intravenously and titrated to a dose that results in adequate contractions, may be used to induce or augment labor. Oxytocin should only be administered by a clinician specifically trained in its use. Regional analgesia or general anesthesia is acceptable. Cesarean section is used for the usual obstetric indications.
Magnesium sulfate infusion (2–3 g/h) should be continued for 24 hours postpartum. Late-onset preeclampsia-eclampsia can occur during the postpartum period. It is usually manifested by either hypertension or seizures. Treatment is the same as prior to delivery—ie, with hydralazine and magnesium sulfate.
New onset of hypertension and proteinuria in a pregnant patient more than 20 weeks’ gestation.
New onset of seizure activity in a pregnant patient.
Symptoms of severe preeclampsia in a pregnant patient with elevated blood pressure above baseline.
Evidence of severe preeclampsia or eclampsia.
Evaluation for preeclampsia when severe disease is suspected.
Evaluation for preeclampsia in a patient with an unstable home environment.
et al.. Pathogenesis of the syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP): a review. Eur J Obstet Gynecol Reprod Biol. 2013 Feb;166(2):117–23.
American College of Obstetricians and Gynecologists
et al.. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013 Nov;122(5):1122–31.
JT. What is new in preeclampsia? Best articles from the past year. Obstet Gynecol. 2013 Mar;121(3):682–3.
ACUTE FATTY LIVER OF PREGNANCY
Acute fatty liver of pregnancy, a disorder limited to the gravid state, occurs in the third trimester of pregnancy and causes acute hepatic failure. With improved recognition and immediate delivery, the mortality rate is 10%. The disorder is usually seen after the 35th week of gestation and is more common in primigravidas and those with twins. The incidence is about 1:14,000 deliveries.
The etiology of acute fatty liver of pregnancy is likely poor placental mitochondrial function. Many cases may be due to a homozygous fetal deficiency of long-chain acyl coenzyme A dehydrogenase (LCHAD).
Pathologic findings are unique to the disorder, with fatty engorgement of hepatocytes. Clinical onset is gradual, with flu-like symptoms that progress to the development of abdominal pain, jaundice, encephalopathy, disseminated intravascular coagulation, and death. On examination, the patient shows signs of hepatic failure.
Laboratory findings include marked elevation of alkaline phosphatase but only moderate elevations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Prothrombin time and bilirubin are also elevated. The white blood cell count is elevated, and the platelet count is depressed. Hypoglycemia may be extreme.
The differential diagnosis is that of fulminant hepatitis. Liver aminotransferases for fulminant hepatitis are higher (greater than 1000 units/mL) than those for acute fatty liver of pregnancy (usually 500–1000 units/mL). Preeclampsia may involve the liver but typically does not cause jaundice; the elevations in liver function tests in patients with preeclampsia usually do not reach the levels seen in patients with acute fatty liver of pregnancy.
Diagnosis of acute fatty liver of pregnancy mandates immediate delivery. Supportive care during labor includes administration of glucose, platelets, and fresh frozen plasma as needed. Vaginal delivery is preferred. Resolution of encephalopathy occurs over days, and supportive care with a low-protein diet is needed.
Recurrence rates for this liver disorder are unclear but probably increased in families with proven LCHAD deficiency. Most authorities advise against subsequent pregnancy, but there have been reported cases of successful outcomes in later pregnancies.
et al.. Acute fatty liver of pregnancy: clinical outcomes and expected duration of recovery. Am J Obstet Gynecol. 2013 Nov;209(5):456.e1–7.
ESSENTIALS OF DIAGNOSIS
Preterm regular uterine contractions approximately 5 minutes apart.
Cervical dilatation, effacement, or both.
Preterm birth is defined as delivery prior to 37 weeks gestation, and spontaneous preterm labor with or without premature rupture of the fetal membranes is responsible for at least two-thirds of all preterm births. Prematurity is the largest single contributor to infant mortality, and survivors are at risk for a myriad of short- and long-term complications. Rates of infant death and long-term neurologic impairment are inversely related to gestational age at birth. Although infants born prior to 34 weeks are at greatest risk for adverse outcomes, infants born between 34 weeks and 36 weeks and 6 days (termed late preterm birth) are at significantly increased risk for both morbidity and mortality when compared to those infants born at term.
Major risk factors for spontaneous preterm labor include a past history of preterm birth and a short cervical length as measured by transvaginal ultrasound. Patients with one or both of these risk factors have largely been the focus of recent intervention trials aiming to prevent preterm birth (see below). Other known risk factors are many but include black race, multiple gestation, intrauterine infection, substance abuse, smoking, periodontal disease, and socioeconomic deprivation.
In women with regular uterine contractions and cervical change, the diagnosis of preterm labor is straightforward. However, symptoms such as pelvic pressure, cramping, or vaginal discharge may be the first complaints in high-risk patients who later develop preterm labor. Because these complaints may be vague and irregular uterine contractions are common, distinguishing which patients merit further evaluation can be problematic. In some cases, this distinction can be facilitated by the use of fetal fibronectin measurement in cervicovaginal specimens. This test is most useful when it is negative (less than 50 ng/mL), since the negative predictive value for delivery within 7–14 days is 93–97%. A negative test, therefore, usually means the patient can be reassured and discharged home. Because of its low sensitivity, however, fetal fibronectin is not recommended as a screening test in asymptomatic women.
Patients must be educated to identify symptoms associated with preterm labor to avoid unnecessary delay in their evaluation. In patients who are believed to be at increased risk for preterm delivery, conventional recommendations are for limited activity and bed rest. Randomized trials, however, have failed to demonstrate improved outcomes in women placed on activity restriction. Paradoxically, such recommendations may place a woman at an increased risk to deliver preterm.
In pregnancies between 24 and 34 weeks gestation where preterm birth is anticipated, a single short course of corticosteroids should be administered to promote fetal lung maturity. Such therapy has been demonstrated to reduce the frequency of respiratory distress syndrome, intracranial hemorrhage, and even death in preterm infants. Betamethasone, 12 mg intramuscularly repeated once 24 hours later, or dexamethasone, 6 mg intramuscularly repeated every 12 hours for four doses, both cross the placenta and are the preferred treatments in this setting. Repeat courses are not recommended. Although antibiotics have not been proven to forestall delivery, women in preterm labor should receive antimicrobial prophylaxis against group B streptococcus (see above).
Numerous pharmacologic agents—tocolytics—have been given in an attempt to forestall preterm birth, although none are completely effective, and there is no evidence that such therapy directly improves neonatal outcomes. Administering tocolytic agents, however, remains a reasonable approach to the initial management of preterm labor and may provide sufficient prolongation of pregnancy to administer a course of corticosteroids and (if appropriate) transport the patient to a facility better equipped to care for premature infants. Maintenance therapy (continuation of treatment beyond 48 hours) is not effective at preventing preterm birth and is not recommended. Likewise, despite the finding that preterm labor is associated with intrauterine infection in certain cases, there is no evidence that antibiotics forestall delivery in women with preterm labor and intact membranes.
Magnesium sulfate is commonly used, and there is evidence that it may also be protective against cerebral palsy in infants whose mothers were receiving magnesium infusions at time of birth. Magnesium sulfate is given intravenously as a 4- to 6-g bolus followed by a continuous infusion of 2 g/h. Magnesium levels are not typically checked but should be monitored if there is any concern for toxicity. Magnesium sulfate is entirely cleared by the kidney and must, therefore, be used with caution in women with any degree of renal insufficiency.
Beta-adrenergic drugs such as terbutaline can be given as an intravenous infusion starting at 2.5 mcg/min or as a subcutaneous injection starting at 250 mcg given every 30 minutes. Oral terbutaline is not recommended because of the lack of proven efficacy and concerns about maternal safety. Serious maternal side effects have been reported with the use of terbutaline and include tachycardia, pulmonary edema, arrhythmias, metabolic derangements (such as hyperglycemia and hypokalemia), and even death. Pulmonary edema occurs with increased frequency with concomitant administration of corticosteroids, large volume intravenous fluid infusion, maternal sepsis, or prolonged tocolysis. Because of these safety concerns, the US Food and Drug Administration warns that terbutaline be administered exclusively in a hospital setting and discontinued after 48–72 hours of treatment.
Nifedipine, 20 mg orally every 6 hours, and indomethacin, 50 mg orally once then 25 mg orally every 6 hours up to 48 hours, have also been used with limited success. Nifedipine should not be given in conjunction with magnesium sulfate.
Before attempts are made to prevent preterm delivery with tocolytic agents, the patient should be assessed for conditions in which delivery would be indicated. Severe preeclampsia, lethal fetal anomalies, placental abruption, and intrauterine infection are all examples of indications for preterm delivery. In such cases, attempts to forestall delivery would be inappropriate.
Strategies aimed at preventing preterm birth in high-risk women—principally those with a history of preterm birth or a shortened cervix (or both)—have focused on the administration of progesterone or progesterone compounds. Prospective randomized controlled trials have demonstrated reductions in rates of preterm birth in high-risk women with singleton pregnancies who received progesterone supplementation, although the optimal preparation, dose, and route of administration (intramuscular injection versus vaginal suppository) are unclear. Further, progesterone therapy has not been proven to be effective in nulliparous women who are noted to have a shortened cervix by transvaginal ultrasound, and universal screening of cervical length is controversial.
There is also evidence that women with a previous spontaneous preterm birth and a shortened cervix (less than 25 mm before 24 weeks gestation) may benefit from placement of a cervical cerclage. The use of cervical cerclage in conjunction with progesterone supplementation has not been adequately studied. In twin and triplet gestations, however, neither progesterone administration nor cervical cerclage placement has been effective at prolonging pregnancy, and these therapies are not recommended in women with multiple gestations.
American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 127: Management of preterm labor. Obstet Gynecol. 2012 Jun;119(6):1308–17.
American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 130: Prediction and prevention of preterm birth. Obstet Gynecol. 2012 Oct;120(4):964–73.
et al.. Cerclage for short cervix on ultrasonography in women with singleton gestations and previous preterm birth: a meta-analysis. Obstet Gynecol. 2011 Mar;117(3):663–71.
et al.. Activity restriction among women with a short cervix. Obstet Gynecol. 2013 Jun;121(6):1181–6.
et al.. 17 alpha-hydroxyprogesterone caproate to prevent prematurity in nulliparas with cervical length less than 30 mm. Am J Obstet Gynecol. 2012 Nov;207(5):390.e1–8.
JD. Clinical practice. Prevention of preterm parturition. N Engl J Med. 2014 Jan 16 ;370(3):254–61.
Five to 10 percent of women have vaginal bleeding in late pregnancy. The clinician must distinguish between placental causes (placenta previa, placental abruption, vasa previa) and nonplacental causes (labor, infection, disorders of the lower genital tract, systemic disease) (eFigures 19–10 and 19–11). The approach to bleeding in late pregnancy depends on the underlying cause, the gestational age at presentation, the degree of blood loss, and the overall status of the mother and her fetus.
Placenta previa. A: Partial. B: Complete. (Reproduced, with permission, from Benson RC. Handbook of Obstetrics & Gynecology, 8th ed. Originally published by Lange Medical Publications. Copyright © 1983 by The McGraw-Hill Companies, Inc.)
Spectrum of placental abruption. Sym, symphysis. (Redrawn and reproduced with permission from Beck and Rosenthal. Obstetrical Practice, 7th ed. Williams & Wilkins, 1957.)
The patient should initially be observed closely with continuous fetal monitoring to assess for fetal distress. A complete blood count with platelets, and a prothrombin time (INR) should be obtained and repeated serially if the bleeding continues. If hemorrhage is significant or if there is evidence of acute hypovolemia, the need for transfusion should be anticipated and an appropriate volume of red cells prepared with cross matching. Ultrasound examination should be performed to determine placental location (eFigure 19–12 and 19–13). Digital pelvic examinations are done only after ultrasound examination has ruled out placenta previa. Administration of anti-D immune globulin may be required for women who are Rh negative.
Total placenta previa. Sagittal midline sonogram in the last trimester shows the placenta (P) completely covering the internal cervical os (arrowhead). F, fetus. (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.)
Placenta previa. Sagittal sonogram of the lower uterine segment in a patient with vaginal bleeding. The placenta (P) is seen to encroach upon the cervix (arrows) consistent with a marginal placenta previa. (Courtesy of PW Callen.)
Placenta previa occurs when the placenta implants over the internal cervical os. Risk factors for this condition include previous cesarean delivery, increasing maternal age, multiparity, and smoking. If the diagnosis is initially made in the first or second trimester, the ultrasound should be repeated in the third trimester. Persistence of placenta previa at this point is an indication for cesarean as the route of delivery. Painless vaginal bleeding is the characteristic symptom in placenta previa and can range from light spotting to profuse hemorrhage. Hospitalization for extended evaluation is the appropriate initial management approach. For pregnancies that have reached 37 weeks gestation or beyond with continued bleeding, delivery is generally indicated. Pregnancies at 36 weeks or earlier are candidates for expectant management provided the bleeding is not prodigious, and a subset of these women can be discharged if the bleeding and contractions completely subside.
C. Morbidly Adherent Placenta
Morbidly adherent placenta is a general term describing an abnormally adherent placenta that has invaded into the uterus. The condition can be further classified depending on whether the depth of invasion is limited to the endometrium (accreta), extends into the myometrium (increta), or invades beyond the uterine serosa (percreta). The most important risk factor for a morbidly adherent placenta is a prior uterine scar—typically from one or more prior cesarean deliveries. The focus of invasion usually involves the scar itself, and placenta previa is commonly associated with morbid adherence. Of serious concern for the field of obstetrics, the incidence of these syndromes has increased dramatically over the last 50 years commensurate with the increasing cesarean delivery rate.
After delivery of the infant, the morbidly adherent placenta does not separate normally, and the bleeding that results can be torrential. Emergency hysterectomy is usually required to stop the hemorrhage, and transfusion requirements are often massive. Because of the considerable increase in both maternal morbidity and mortality associated with this condition, careful preoperative planning is imperative when the diagnosis is suspected antenatally. Ultrasound findings such as intraplacental lacunae, bridging vessels into the bladder, and loss of the retroplacental clear space suggest placental invasion in women who have placenta previa. Importantly, however, even if ultrasound findings are subtle, an abnormally adherent placenta should be suspected in any patient with one or more prior cesarean deliveries and an anterior placenta previa. Ideally, delivery planning should involve a multidisciplinary team, and the surgery should take place at an institution with appropriate personnel and a blood bank equipped to handle patients requiring massive transfusion. It has been demonstrated that a systematic approach to management with a multidisciplinary team improves patient outcomes.
Placental abruption is the premature separation of the placenta from its implantation site before delivery. Hypertension is a known risk factor for abruption. Other risk factors include multiparity, cocaine use, smoking, previous abruption, and thrombophilias. Classic symptoms are vaginal bleeding, uterine tenderness, and frequent contractions, but the clinical presentation is highly variable. Profound coagulopathy and acute hypovolemia from blood loss can occur and are more likely with an abruption severe enough to kill the fetus. Ultrasound may be helpful to exclude placenta previa, but failure to identify a retroplacental clot does not exclude abruption. In most cases, abruption is an indication for immediate delivery because of the high risk of fetal death.
A. Morbidly adherent placenta. Semin Perinatol. 2013 Oct;37(5):359–64.
American College of Obstetricians and Gynecologists. Committee Opinion No. 529: Placenta accreta. Obstet Gynecol. 2012 Jul;120(1):207–11.
et al.. Maternal morbidity in patients with morbidly adherent placenta treated with and without a standardized multidisciplinary approach. Am J Obstet Gynecol. 2015 Feb;212(2):218.e1–9.