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Obstetric Complications During Pregnancy

  • Jeffrey D. QuinlanEmail author
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Abstract

There are a wide range of obstetric complications that may occur during pregnancy. This chapter will focus on six of the most common complications including spontaneous abortion, ectopic pregnancy, hypertensive disorders of pregnancy, placenta previa, and preterm labor.

There are a wide range of obstetric complications that may occur during pregnancy. This chapter will focus on six of the most common complications including spontaneous abortion, ectopic pregnancy, hypertensive disorders of pregnancy, placenta previa, and preterm labor.

Spontaneous Abortion

Spontaneous abortion is defined as the involuntary loss of pregnancy prior to 20 weeks of gestation.

Vaginal bleeding in the first trimester of pregnancy is common. It may occur as a result of spontaneous abortion, ectopic pregnancy, gestational trophoblastic disease, or cervical causes. Approximately half the pregnancies complicated by first trimester bleeding result in viable pregnancies.

Epidemiology

Spontaneous abortion or miscarriage occurs in about 15% of clinically identified pregnancies and may occur in up to 50% of pregnancies prior to clinical identification [1].

Etiology

The cause of spontaneous abortion is rarely identified in the individual patient. Research has demonstrated, however, that approximately half of miscarriages occur as a result of trisomy, triploidy, monosomy, or another significant genetic abnormality [2]. Additionally, several environmental factors have been associated with miscarriage including both internal and external factors. Internal factors include advanced maternal age, uterine anomalies, leiomyomata, incompetent cervix, and luteal phase defects that lead to progesterone deficiency. External factors include substance use such as tobacco, alcohol, and cocaine, radiation exposure, infections, and occupational chemical exposure to substances such as arsenic, benzene, ethylene oxide, formaldehyde, or lead.

Diagnosis

Women experiencing a spontaneous abortion typically present with vaginal bleeding and cramping. They may also report a diminution or reversal of early pregnancy symptoms (fatigue, nausea, breast tenderness).

The first steps in evaluation of a patient with suspected miscarriage are to obtain vital signs and establish an estimated gestational age based on last menstrual period. If the estimated gestational age is greater than 9 weeks, an attempt should be made to auscultate fetal heart tones. Examination should then include abdominal, speculum, and pelvic examinations. If adnexal tenderness is identified, ectopic pregnancy should be considered. Non-uterine causes of bleeding can be identified during the speculum examination as can the presence or absence of cervical dilation. The diagnosis of spontaneous abortion can be assisted by use of transvaginal ultrasound. A completed spontaneous abortion will present with an empty uterus with an echogenic endometrial stripe. In a viable gestation, a gestational sac should be visualized between 4 and 5 weeks gestation and must be present with a beta-HCG greater than 1500–2000 mIU/mL. The yolk sac should be visualized between 5 and 6 weeks gestation and must be present with a gestational sac >10 mm, the embryo should be visualized between 5 and 6 weeks gestation and must be present with a gestational sac >18 mm, and cardiac activity should be visualized between 5 and 6 weeks gestation and must be present if the crown-rump length is greater than 5 mm [3]. The presence of a gestational sac with a diameter greater than 20 mm without an identifiable embryo or presence of an embryo with a crown-rump length greater than 5 mm without a heartbeat is diagnostic of a pregnancy demise [4].

In patients with unclear course, serial quantitative beta-HCGs and ultrasounds may be beneficial. Between the 4th and 8th week of gestation, beta-HCG levels should double every 48–72 h. Likewise, both the diameter of the gestational sac and the crown-rump length should increase by 1 mm/day. Therefore, repeating labs and an ultrasound in 7–10 days should demonstrate a measurable change in both.

Prevention

Several interventions can lower the risk of spontaneous abortion. These include avoiding smoking, drinking alcohol, and using recreational drugs. Additionally, avoiding exposure to certain viral infections such as rubella can lower the risk. Finally, obesity increases the risk of miscarriage; therefore, patients should be encouraged to achieve a healthy weight prior to pregnancy.

Management

Miscarriage can be managed expectantly, medically, or surgically. Frequently, spontaneous abortions complete without intervention. In women with significant bleeding, pain, or infection, either medical or surgical intervention should be considered [5]. Other women may desire to avoid the watchful waiting that is often required with expectant management. Misoprostol administered either 600 micrograms orally or 600–800 micrograms vaginally can be utilized for medical management of miscarriage. The initial dose can be repeated in 24–48 h if the initial dose is unsuccessful [6]. Surgical management can be performed using either sharp curettage or vacuum aspiration. While complication rates are comparable between the two, vacuum aspiration is faster and causes less pain and bleeding [7].

Ectopic Pregnancy

Ectopic pregnancy is the implantation of an embryo outside of the uterine cavity. The vast majority are located in the fallopian tubes; however, they may rarely occur in the broad ligament, cervix, ovary, or abdominal cavity. Ectopic pregnancy is the second most common cause of maternal mortality.

Epidemiology

Between 2002 and 2007, a study of women enrolled in health plans demonstrated the ectopic pregnancy rate in the United States to be 0.64% [8]. Previous data, which included patients enrolled in Medicaid, demonstrated a rate of 1.9% in 1992 [9]. Both data sets demonstrate an increasing rate of ectopic pregnancy with age. Mortality rates have declined from 1.15 deaths in 100,000 live births to 0.50 deaths per 100,000 live births between 1980–1984 and 2003–2007 [10]. This is a result of increased awareness and improvements in early diagnosis.

Etiology

Any factor that interferes with the fallopian tube’s function and ciliary motility increases the risk of ectopic pregnancy. Risk factors can be divided into anatomic and functional. Anatomic risk factors include a history of tubal ectopic pregnancy, infection (e.g., pelvic inflammatory disease), ligation, or surgery. Functional risk factors include hormonal stimulation of ovulation, use of progestin-containing contraceptives, and tobacco use. Risk factors can also be divided based on the strength of their risk for ectopic pregnancy. Factors strongly associated with ectopic pregnancy include previous ectopic pregnancy, history of tubal surgery, and history of DES exposure. Factors moderately associated with ectopic pregnancy include history of sexually transmitted infection, having more than one sexual partner, and cigarette smoking. Finally, factors slightly associated with ectopic pregnancy include prior abdominal or pelvic surgery, douching, and sexual intercourse prior to age 18 [11].

Diagnosis

Most patients presenting with an ectopic pregnancy will have abdominal pain, typically lower abdominal and unilateral, and bleeding. Physical examination may help identify a tender adnexal mass, as well as signs of shock (hypotension, tachycardia, altered mental state) or hemoperitoneum (distended abdomen with decreased bowel sounds, referred shoulder pain, and a posterior cul-de-sac which bulges into the vaginal fornix). Serum hCG and progesterone can both contribute to making the diagnosis of anectopic pregnancy. Serum hCG will typically increase early in pregnancy then plateau and possibly fall. If the initial hCG is <1500 mIU/mL, a rise of at least 53% over 48 h is indicative of a viable pregnancy [12].

A recent meta-analysis reviewing 26 cohort studies, including over 9400 women in the first trimester of pregnancy, found that in women with abdominal pain and/or bleeding and an inconclusive ultrasound, a single progesterone test (cutoff between 3.2 and 6 ng/mL) predicts a nonviable pregnancy with pooled sensitivity of 74.6% (95% confidence interval 50.6–89.4%) and specificity of 98.4% (90.9–99.7%) [13].

The gold standard for diagnosis of ectopic pregnancy is the transvaginal ultrasound. At an hCG level between 1500 and 2000 mIU/mL or higher, a gestational sac should be seen in the uterus using transvaginal ultrasound. Identification of an intrauterine pregnancy essentially rules out ectopic pregnancy (heterotopic pregnancy is exceedingly rare). Ectopic pregnancy is very likely if any adnexal mass or significant free pelvic fluid is identified. Finally, ectopic pregnancy is confirmed if a gestational sac with embryo and heartbeat is identified outside of the uterus [14].

Prevention

While there is no specific prevention strategy for ectopic pregnancy, the risk can be minimized by avoiding modifiable risk factors that increase the risk of an ectopic. These include not smoking, avoiding pregnancy before age 18, and taking precautions to prevent sexually transmitted infections.

Management

The management of ectopic pregnancy can be expectant, medical, or surgical. In reliable patients with an hCG <1000 mIU/mL that is declining, expectant management can be considered if there is minimal pain and bleeding and no evidence of rupture, and if a mass is detected, it is <3 cm in diameter, and no fetal heartbeat is detected [15]. Close follow-up is required, and hCG levels should be followed until they are <5 mIU/mL.

Medical management of ectopic pregnancy has utilized the folic acid antagonist, methotrexate. Single-dose methotrexate is administered at 1 mg/kg or 50 mg/m2. It should be considered in patients with stable vital signs, an hCG of <2000 mIU/mL, a mass < = 3.5 cm in diameter without fetal heartbeat, and no evidence of rupture. Additionally, patients should not have a contraindication to methotrexate administration such as elevated liver enzymes, immunodeficiency, or blood dyscrasias. Serum hCG levels should be checked at days 4 and 7 and then weekly until it is <5 mIU/mL. If the hCG level does not fall between days 4 and 7, a second dose of methotrexate or surgical intervention should be considered [16, 17].

Surgical management of ectopic pregnancy should be considered when the patient is unreliable for follow-up, is unstable, has signs of hemoperitoneum, or has a more advanced ectopic pregnancy. Additionally, surgical intervention should be considered when the diagnosis is unclear or there is a contraindication to either expectant or medical management. Surgical interventions include linear salpingostomy (opening the fallopian tube and removing the ectopic pregnancy) or salpingectomy (removing the fallopian tube) via laparoscopy or laparotomy. Salpingostomy is preferred in patients who wish to maintain fertility [18]. Laparotomy should be limited to patients in whom visualization is compromised or hemostasis cannot be achieved utilizing laparoscopy [19].

Hypertensive Disorders of Pregnancy

Hypertensive disorders of pregnancy can be classified into chronic hypertension, gestational hypertension, preeclampsia, and chronic hypertension with superimposed preeclampsia. The term “gestational hypertension” replaces “pregnancy-induced hypertension.” The nomenclature of “mild” and “severe” preeclampsia has been abandoned, and preeclampsia is now characterized as being with or without severe features [20]. This distinction helps to emphasize that severe features may develop at any time and that ongoing evaluation is essential in identifying patients with more severe disease.

Epidemiology

Hypertensive disorders of pregnancy affect between 6% and 8% of pregnancies in the United States making them the most common medical complication of pregnancy [21]. The majority of women that develop preeclampsia are nulliparous. In multiparous women, those with multiple gestations, age > 40, history of preeclampsia in prior pregnancy, chronic disease (hypertension, diabetes, and renal disease), elevated BMI, and the presence of the antiphospholipid syndrome increase the risk of developing preeclampsia [22]. Approximately 20% of women with chronic hypertension will develop preeclampsia [20]. Additionally, a family history of preeclampsia, African-American and Latina race, lower socioeconomic class, and women who do not seek or do not have access to prenatal care are at increased risk for developing preeclampsia [20].

Etiology

It has been hypothesized that the pathophysiology of preeclampsia may be the result of a genetic predisposition, an immunologic condition, abnormal implantation of the placenta, endothelial injury to the vascular system, activation of platelets, placental growth factor deficiency, or vasoconstriction as a result of maladaptation of the cardiovascular system. Despite these theories, the exact etiology remains unknown [23].

Diagnosis

Hypertension during pregnancy is defined as a blood pressure of > = 140/90 on two separate occasions 4 h apart or > = 160/110 on a single occasion. Chronic hypertension is defined as hypertension that presents before 20 weeks of gestation or that persists after 6 weeks postpartum. Gestational hypertension is ultimately a provisional diagnosis. It is defined as the presence of hypertension after 20 weeks gestation without the features of preeclampsia defined below. Of those women initially diagnosed with gestational hypertension, approximately 50% will go on to develop preeclampsia [24]. Another proportion will have persistent hypertension after 6 weeks postpartum and be diagnosed with chronic hypertension.

In preeclampsia, hypertension (blood pressure > = 140.90) develops after 20 weeks of gestation and is accompanied by proteinuria. Proteinuria can be identified through a 24 h protein demonstrating > = 300 mg of protein, a protein/creatinine ratio of >0.3 on a random voided urine, or a dipstick of +1 protein on a random voided urine. It is important to note that the presence of edema is no longer a criterion for preeclampsia [20].

Severe features of preeclampsia include two blood pressures of > = 160/110 obtained 4 h apart while the patient is on bed rest, a platelet count <100,000/mL, doubling of AST or ALT, severe right upper quadrant pain without other etiology, creatinine >1.1 mg/dL, doubling of baseline creatinine without evidence of other renal disease, development of pulmonary edema, and cerebral/visual disturbances that did not preexist. Intrauterine growth restriction and proteinuria >5 g in a 24 h urine collection are no longer considered criteria for severe features [20].

Prevention

A Cochrane review of prophylactically treating women with increased risk of developing preeclampsia with low-dose aspirin demonstrated that the numbers needed to treat to prevent one case of preeclampsia and one fetal death were 69 and 227, respectively [25]. Among women with the highest risk of developing preeclampsia, the number needed to treat to prevent one case of preeclampsia was 18 [25]. Similarly, a Cochrane review of calcium supplementation demonstrated reduced risk of preeclampsia among women at high risk for this condition with low calcium intake [26]. However, routine prophylaxis/supplementation with calcium, magnesium, omega 3 fatty acids, vitamin C, and vitamin E in low-risk patients has not been demonstrated to be effective in lowering the risk of preeclampsia.

Management

For both gestational hypertension and preeclampsia without severe features, patients should be instructed to do daily kick counts to assess for fetal well-being and to self-assess for severe signs or symptoms such as development of a new headache, visual disturbances, chest pain, shortness of breath, persistent nausea and vomiting, or right upper quadrant pain. Patients should be evaluated in the office weekly with blood pressure measurement, platelet count, and liver enzymes. For patients with gestational hypertension, urine should be collected weekly to assess for protein. There is low-quality evidence to support weekly antenatal testing. Additionally, serial ultrasounds should be obtained to assess for growth restriction. Bed rest is no longer recommended [20]. In both gestational hypertension and preeclampsia without severe features, delivery is recommended at 37 weeks gestation [20]. Neither magnesium sulfate during labor nor antihypertensives are recommended.

Once a patient develops preeclampsia with severe features > = 34 weeks gestation, the goal is to stabilize the patient and move toward delivery. If the patient is <= 34 weeks gestation, they should be cared for at a facility that has the required resources to provide care to both the mother and premature fetus. For women who develop preeclampsia with severe features before fetal viability is attained (22–24 weeks depending on location and available resources), once the patient is stabilized delivery should be planned. In women with preeclampsia and severe features <= 34 weeks gestation who are stable, expectant management with close monitoring and appropriate hypertensive control is recommended until the patient is >34 weeks gestation, and then delivery should be planned. In women with preeclampsia with severe features who have reached viability but are <34 weeks gestation and also present with preterm premature rupture of membranes, labor, platelet count <100,000/mL, AST or ALT elevated > twice the upper limit of normal, growth restriction, severe oligohydramnios, new onset or worsening renal dysfunction, or reversed end-flow umbilical Doppler readings, steroids should be administered to promote fetal lung maturity, and an attempt should be made to delay delivery for 48 h to maximize their effectiveness. For patients <34 weeks who present with preeclampsia with severe features and uncontrollable severe hypertension, eclampsia, pulmonary edema, placenta abruption, disseminated intravascular coagulopathy, or Category III fetal heart rate tracing (defined as a sinusoidal pattern or a tracing with absent variability and recurrent late decelerations, variable decelerations, or bradycardia, replaces “non-reassuring” terminology), steroids should be administered to promote fetal lung maturity, but delivery should not be delayed to maximize effectiveness of the steroids. Finally, in women with intrauterine fetal demise, steroid administration is unnecessary, and delivery should be planned [20].

Magnesium sulfate is recommended for patients who present with either preeclampsia with severe features to prevent a seizure or eclampsia to prevent further seizures. The Magpie Trial determined that in women with severe preeclampsia (old nomenclature), 63 women needed to be treated with magnesium sulfate to prevent one seizure [27]. Magnesium sulfate should typically be continued until 24 h postpartum or until the patient has demonstrated significant diuresis indicating resolution of vasoconstriction.

Antihypertensive medications are indicated in patients that have blood pressures > = 160/110, although the optimal blood pressure goal is unclear. In acute management, intravenous medications offer a rapid onset and the ability to titrate therapy. Both labetalol and hydralazine have been commonly used. For chronic management of patients with preeclampsia with severe features being expectantly managed, oral medications are preferred. Both oral nifedipine and labetalol have been used in these patients [21].

Placenta Previa

Normal placental implantation occurs at the uterine fundus. Placenta previa, however, occurs when the site of implantation is the lower uterine segment and the placenta overlies or approaches the cervical os. Marginal previa is defined as placenta located within 2 centimeters of the os, whereas complete previa indicates that the placenta covers the os. Morbidity related to placenta previa occurs with maternal hemorrhage, need for cesarean delivery, and risk of abnormal placental implantation (accreta, increta, percreta) which may result in hysterectomy.

Epidemiology

Placenta previa affects approximately 0.4% of pregnancies at term [28]. It typically presents as painless vaginal bleeding in the second or third trimesters which are often triggered by sexual intercourse. Risk factors include chronic hypertension, history of uterine curettage or cesarean delivery (incidence increases to 2.3% after just two cesarean deliveries [29]), cocaine or tobacco use, increasing maternal age, multiparity, and male fetuses [28].

Etiology

The exact etiology of placenta previa is unknown. It has been hypothesized that atrophy or scarring of the endometrium related to prior trauma, surgery (uterine curettage or cesarean), or infection may lead to inadequate or abnormal vascularization of the endometrium in the fundus to allow for implantation [30]. Further research is required to evaluate this hypothesis.

Diagnosis

The diagnosis of placenta previa should be suspected in women who present in either the second or third trimester with painless vaginal bleeding. Additionally, persistent breech or malpresentation at term should raise suspicion. Diagnosis is confirmed with ultrasonography to locate the site of placental implantation. Transvaginal ultrasound is more sensitive and specific than transabdominal ultrasound and has been demonstrated to be safe to perform [31]. In patients in whom abnormal insertion is suspected (accreta, increta, percreta), MRI may be useful in differentiating the level of invasion into the uterine wall.

Prevention

While there is no specific prevention strategy for placenta previa, the risk can be minimized by avoiding modifiable risk factors that increase risk for previa. These include not smoking or using cocaine when considering and during pregnancy and careful consideration of first cesarean in patients who desire additional children.

Management

The management of placenta previa remains somewhat controversial. Most authors recommend expectant management between the time of identification of previa and the first (sentinel) bleed as long as they have ready access to a hospital that provides maternity care services [32]. A similar strategy is reasonable for patients after a sentinel bleed following a period of inpatient hospitalization, stabilization, and observation. Patients should be advised to avoid placing any object in the vagina, including intercourse and tampons. In patients with recurrent bleeding, delivery should be considered at 36 weeks gestational age; and in patients without vaginal bleeding, delivery should be considered at 38 weeks gestational age [32].

In women with marginal previa, the mode of delivery should be determined following ultrasound at 36 weeks. If the placental edge is > = 2 cm from the cervical os, an attempt of vaginal delivery should be made. In cases where the placental edge is 1–2 cm from the cervical os, vaginal delivery can be considered; however, facilities should be prepared for the need for emergent cesarean delivery [33].

In women with complete previa, cesarean delivery should be planned for between 36 and 38 weeks gestation, as noted above. Because of the increased risk of placenta accreta, increta, or percreta, the delivery team should be prepared to perform a cesarean hysterectomy [32].

In women with recurrent episodes of bleeding prior to delivery, transfusion should be considered for signs or symptoms of symptomatic anemia. Additionally, because of the risk of severe postpartum hemorrhage and disseminated intravascular coagulopathy during or following delivery, patients should be evaluated for transfusion and the blood bank notified of the potential need to activate massive transfusion protocols.

Preterm Labor and Delivery

Preterm labor is defined as the development of regular uterine contractions that result in cervical change, effacement, and dilation, occurring before 37 weeks of gestation. The greatest risk of preterm labor is resultant preterm delivery.

Epidemiology

In the United States, 11.39% of deliveries in 2013 occurred prior to 37 weeks [34], 40–45% of which are the result of preterm labor without premature rupture of membranes [35]. Between 1990 and 2006, the incidence of preterm delivery increased 20%, largely as a result of an increase in multiple gestations (resulting from increased use of assistive reproductive technology) and late preterm deliveries. Since that time, with an increased focus on decreasing the number of near-term inductions and cesarean deliveries, that rate has fallen to a 15-year low [34, 35]. While efforts persist to decrease the number of preterm deliveries, it will be difficult to eliminate them completely as 30–35% of preterm deliveries are secondary to medically indicated inductions or cesarean deliveries (preeclampsia with severe features, placental abruption, etc.) [35].

Etiology

Common pathways resulting in preterm labor and delivery include immune mediation, inflammation, stress, overdistension of the uterus, uteroplacental hemorrhage, and uteroplacental ischemia [36]. Many risk factors for preterm labor and delivery, which activate these pathways, have been identified and can be divided into preconception, maternal, and fetal factors. These are summarized in Table 1. Unfortunately, nearly 50% of preterm deliveries occur in women without known risk factors for preterm labor or delivery [37]. Of the known risk factors, history of both spontaneous and medically indicated preterm delivery is the most significant distinguishable risk factor for recurrence, increasing the risk by 2.5-fold [38].
Table 1

Risk factors for preterm delivery

Preconception

Maternal

Fetal

Body mass index <20 or poor nutrition

Abdominal surgery

Assisted reproductive technology (both singleton and multiple

Gestations)

History of LEEP or cone biopsy of the cervix

African-American race

Congenital anomalies

Interpregnancy interval

<6 months

Chronic medical conditions (diabetes,

Hypertension)

Intrauterine fetal demise

Psychological stress and emotional or

Physical abuse

History of preterm delivery

Intrauterine growth restriction

Sexually transmitted illnesses

Infection (bacterial vaginosis, chlamydia,

Trichomonas)

Multiple gestation

Smoking

Lack of prenatal care

 

Substance abuse (cocaine, amphetamines)

Oligohydramnios

 

Uterine anomaly

Periodontal disease

 
 

Placenta abruption

 
 

Placenta previa

 
 

Polyhydramnios

 
 

Poor social support

 
 

Short cervix

 
 

Smoking

 
 

Strenuous work

 
 

Uterine contractions

 

Infection is an important cause of preterm labor and delivery and may be responsible for 25–40% of all preterm births. Bacterial vaginosis increases the risk of preterm delivery between 1.5 and 3 times. In women with the TNF-alpha allele 2 gene, the presence of bacterial vaginosis doubles the risk of preterm delivery [36]. Asymptomatic bacteriuria and pyelonephritis have both been associated with preterm delivery. Periodontal disease increases the risk by twofold. Sexually transmitted infections including chlamydia, gonorrhea, and syphilis likewise increase the risk of preterm birth. While group B Streptococcus, M. hominis, and U. urealyticum are commonly identified in women with preterm labor, they are not felt to be causal of the preterm labor [35].

Diagnosis

Patients presenting with complaint of preterm contractions should be placed on a tocodynamometer to assess for frequency of uterine contractions. Fetal well-being should be assessed by continuous Doppler and position determined by ultrasound.

In a patient presenting with preterm contractions, assessment should evaluate for status of amniotic membranes (intact or ruptured), presence of infection, and likelihood that contractions will lead to delivery. Evaluation for rupture of membranes is discussed below in the section entitled “Premature Rupture of Membranes.” Patients should be evaluated for bacterial vaginosis, gonorrhea and chlamydia, urinary tract infection, and group B Streptococcus.

Likelihood of delivery can be assessed via digital cervical examination, terbutaline challenge, fetal fibronectin collection, and measurement of cervical length. Digital cervical examination, while subjective in nature, may be useful if advanced dilation or effacement is noted on examination. A single dose of terbutaline 0.25 mg administered subcutaneously may result in resolution of contractions in patients not in preterm labor. Fetal fibronectin, a placental glycoprotein, is typically absent from vaginal secretions prior to term, and its presence between 24 and 34 weeks has been associated with preterm delivery. The presence of fetal fibronectin in vaginal secretions collected in the posterior fornix between 24 and 34 weeks has a positive predictive value of 13–30% for delivery in the next 7–10 days. Its absence has a negative predictive value of 99% for delivery in the following 2 weeks [39]. False-positive results may occur if the patient has had intercourse, a digital cervical exam, or transvaginal ultrasound in the past 24 h or is having active bleeding from the cervix or vagina. Transvaginal measurement of cervical length can also be useful in stratifying risk for preterm delivery. In symptomatic women, an initial cervical length of >30 mm excludes the diagnosis of preterm labor, whereas women with a cervical length < 15 mm are at high risk for preterm delivery [40].

Prevention

In women with a history of preterm delivery (spontaneous and not medically indicated), 17-alpha-hydroxyprogesterone caproate (17P) has been demonstrated to reduce the recurrence rate of preterm delivery. It is indicated in women between 16 and 36 weeks gestation who have a history of preterm delivery, who have not demonstrated signs of preterm labor in the current pregnancy, and who are not allergic to the compound. Beginning at 16 weeks, patients should receive 250 mg intramuscularly weekly through 36 weeks or delivery. Studies have demonstrated a decrease in preterm deliveries in women meeting the above criteria who are treated with 17P versus controls (37% vice 55%) as well as an improvement in the health of their infants [41]. Vaginal progesterone has not been shown to be beneficial in this population.

Women with a history of preterm delivery should have their cervical length evaluated by transvaginal ultrasound between 16 and 24 weeks gestation [42]. If the cervical length is found to be <25 mm, cervical cerclage should be offered. Studies have demonstrated a decrease in preterm birth and perinatal morbidity and mortality when cerclage is used in this population [42]. Additionally, in women with history of preterm delivery and a cervical length of <20 mm, vaginal progesterone 100–200 mg administered vaginally on a daily basis has shown to decrease rates of preterm delivery and perinatal morbidity and mortality [43]. Intramuscular progesterone has not been demonstrated to improve outcome in this population.

It is important to note that while published meta-analyses have reported the benefits above with the use of either intramuscular or vaginal progesterone, three recent trials (OPPTIMUM, PROGRESS, and PROLONG) failed to demonstrate similar decreases in preterm labor rates and/or fetal death [44, 45, 46]. As a result, while progesterone remains widely utilized, there is some controversy, in particular for the use of intramuscular progesterone.

Although several studies have examined the treatment of asymptomatic bacterial vaginosis in the prevention of preterm labor and delivery, data remains conflicted. The US Preventive Services Task Force recommends against screening in low-risk women and states that there is insufficient evidence to recommend for or against screening and treatment of women at high risk for preterm labor [47].

Management

Women diagnosed with preterm labor should, when feasible, be transferred to a facility that has the capability to manage a preterm infant. Antenatal corticosteroids should be administered to women between 24 and 34 weeks gestation who present in preterm labor. Either betamethasone 12 mg administered intramuscularly for two doses 12 h apart or dexamethasone 6 mg administered intramuscularly for four doses 6 h apart has been shown to be effective in decreasing perinatal morbidity and mortality [48]. Magnesium sulfate administered intravenously as a 4–6 g bolus followed by a maintenance dose of 1–2 g/h for 24 h in women with preterm labor has been shown to decrease the rate of cerebral palsy in their infants [49]. It should be noted that magnesium sulfate is no longer recommended for use as a tocolytic in these patients.

Short-term tocolysis may be considered in women presenting with preterm labor to allow time to transfer to a facility with a higher level of.

care, to allow administration of corticosteroids and magnesium sulfate, and to provide for group B Streptococcus prophylaxis. Nifedipine has been shown to decrease the risk of delivery within 48 h and has the advantage of increased latency till birth, improved neonatal outcomes, and decreased maternal side effects compared to other tocolytics [48]. Beta mimetics, such as terbutaline, may also be used to delay delivery. Magnesium sulfate, on the other hand, has not been shown to prolong pregnancy or to improve perinatal morbidity [50].

Group B Streptococcus is the leading cause of death secondary to infection in newborns despite widespread implementation of CDC guidelines for its prevention. In women presenting with preterm labor, either ampicillin 2 g intravenously on admission then 1 g every 4 h through delivery or penicillin G 5 million units intravenously on admission then 2.5–3 million units every 4 h through delivery should be administered [51]. Dosing may be discontinued if preterm labor is ruled out or if a negative group B Streptococcus culture is obtained. Cefazolin should be used in women with a non-anaphylactic allergy to penicillin. In women with a history of anaphylaxis, clindamycin or vancomycin should be utilized.

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Copyright information

© This is a U.S. Government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020

Authors and Affiliations

  1. 1.Department of Family MedicineUniformed Services University of the Health SciencesBethesdaUSA

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