Preterm Premature Rupture of Membranes (PPROM) and Intra-Amniotic Infection Case File
Eugene C. Toy, MD, Patti Jayne Ross, MD, Benton Baker III, MD, John C. Jennings, MD
CASE 18
A 24-year-old G2P1 woman at 30 weeks’ gestation was admitted to the hospital 2 days ago for premature rupture of membranes. Her antenatal history has been unremarkable. Today, she states that her baby is moving normally, and she denies any fever or chills. Her past medical and surgical histories are unremarkable. On examination, her temperature is 100.8°F (38.2°C), blood pressure (BP) is 100/60 mm Hg, and heart rate (HR) is 90 beats per minute (bpm). Her lungs are clear to auscultation. No costovertebral angle tenderness is found. The uterine fundal height is 30 cm, and the uterus is slightly tender to palpation. No lower extremity cords are palpated. The fetal heart tones are persistently in the range of 170 to 175 bpm without decelerations. There are no uterine contractions.
» What is the most likely diagnosis?
» What is the best management for this patient?
» What is the most likely etiology of this condition?
ANSWER TO CASE 18:
Preterm Premature Rupture of Membranes (PPROM)
and Intra-Amniotic Infection
Summary: A 24-year-old G2P1 woman at 30 weeks’ gestation was admitted 2 days ago for premature rupture of membranes. Her temperature is 100.8°F (38.2°C). The uterine fundus is slightly tender. There is persistent fetal tachycardia in the range of 170 to 175 bpm.
- Most likely diagnosis: Intra-amniotic infection (chorioamnionitis).
- Best management for this patient: Intravenous (IV) antibiotics (ampicillin and gentamicin) and induction of labor.
- Etiology of this condition: Ascending infection from vaginal organisms.
ANALYSIS
Objectives
- Know that infection and labor are the two most common acute complications of preterm premature rupture of membranes.
- Know the clinical presentation of intra-amniotic infection, and that fetal tachycardia is an early sign of this infection.
- Understand that broad-spectrum antibiotic therapy and delivery are the appropriate treatment of intra-amniotic infection.
Considerations
This 24-year-old woman at 30 weeks’ gestation has preterm premature rupture of membranes. Upon presentation to the hospital, the practitioner should assess for infection; in the absence of signs of overt systemic infection, corticosteroid therapy should be administered to reduce the risk of respiratory distress syndrome in the infant if delivery occurs. Additionally, broad-spectrum antibiotic therapy is given to help reduce the incidence of intra-amniotic infection, delay delivery, and reduce the risk of maternal uterine infection. The scenario does not indicate whether antibiotics were initiated upon admission to the hospital. At a gestational age of < 34 weeks, the risks of prematurity outweigh the risks of infection, so expectant management was chosen. After 2 days in the hospital, the patient develops fever, uterine tenderness, and fetal tachycardia, which are all signs consistent with intraamniotic infection. Upon recognition of this diagnosis, the patient should be given intravenous antibiotic therapy, such as ampicillin and gentamicin. Neonates are most commonly affected by group B streptococci and gram-negative enteric organisms such as Escherichia coli. Since delivery is also an important aspect of therapy for both neonatal and maternal well-being, induction of labor and vaginal delivery is the best course of action in this case. See Figure 18– 1 for a management scheme.
Figure 18–1. Algorithm for the management of PPROM.
APPROACH TO:
Preterm PR
DEFINITIONS
PREMATURE RUPTURE OF MEMBRANES: Rupture of membranes prior to the onset of labor.
PRETERM PREMATURE RUPTURE OF MEMBRANES: Rupture of membranes in a gestation <37 weeks, prior to the onset of labor.
LATENCY PERIOD: The duration of time from rupture of membranes to onset of labor.
CLINICAL APPROACH
Preterm premature rupture of membrane is defined as rupture of membranes prior to the onset of labor and at < 37 weeks of pregnancy. This complication occurs in about 1% of all pregnancies. Approximately one-third of preterm births are associated with PPROM. Risk factors are noted in Table 18– 1.
Clinical Evaluation
The history consistent with PPROM is that of a loss or “gush” of fluid per vagina followed by a constant leakage of fluid, which is very accurate and should be taken seriously. The diagnosis is confirmed with a speculum examination showing the pooling of amniotic fluid in the posterior vaginal vault, positive nitrazine test showing alkaline changes of the vaginal fluid, and a ferning pattern of the fluid when seen on microscopy. Occasionally, the speculum examination may be negative, but clinical suspicion is high; in these cases, an ultrasound examination revealing oligohydramnios is consistent with PPROM. AmniSure is an immunoassay test recently approved by the Food Drug Administration to assess for ROM; it tests for placental alpha macroglobulin-1, a protein which is 10,000 times more concentrated in amniotic fluid than cervical or vaginal secretions. The sensitivity is noted to be 96% and specificity of nearly 100%. The swab should be placed in the posterior vaginal prior to any vaginal examination. Etiologies for PPROM should be undertaken such as: urine culture, genital assay for chlamydia and gonorrhea. Ultrasound examination for fetal weight, presentation, and amniotic fluid volume is performed. GBS cultures are usually performed.
Outcome
The outcome is dependent on the gestational age. Approximately half of patients with PPROM will go into labor within 48 hours, and 90% within 1 week. Complications of preterm delivery, such as respiratory distress syndrome, are common. Other complications include chorioamnionitis (intra-amniotic infection), placental abruption, and necrotizing enterocolitis.
Chorioamnionitis affects about 1% of all pregnancies, and 7% to 10% of those with PPROM with prolonged rupture of membranes. Maternal fever, maternal tachycardia, uterine tenderness, and malodorous vaginal discharge are some clinical indicators. An early sign is fetal tachycardia, a baseline heart rate of > 160 bpm.
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Table 18–1 • RISK FACTORS
FOR PPROM
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Lower socioeconomic status Sexually transmitted diseases Cigarette smoking Cervical conization Emergency cerclage Multiple gestations Hydramnios Placental abruption |
Treatment
The treatment of PPROM is controversial. Prior to 34 weeks’ gestation, antenatal steroids are given to enhance fetal lung maturity in the absence of overt infection. Broad-spectrum antibiotic therapy (usually ampicillin and erythromycin, initially IV for 48 hours and then orally for 5 days to complete a 7-day course) has been shown to delay delivery and decrease the incidence of chorioamnionitis. Patients are placed on bed rest and expectantly managed when the risk of infection is thought to be less than the risk of prematurity, which is usually at 34 weeks’ gestation. Occasionally (<10%) of patients with PPROM will have resealing of membranes and may be discharged home; to confirm that the membrane has resealed, there should be absence of leakage of fluid, several negative speculum examinations, and normal amniotic fluid volume.
With previable PPROM, particularly at <22 weeks’ gestation, the patient and family should be given informed consent about the risks of pulmonary hypoplasia and outcomes. Corticosteroids and antibiotics are not recommended at this gestational age.
After a gestational age of 34 to 35 weeks, the treatment is usually delivery. Some of the risks of expectant management include stillbirth, cord accident, infection, and abruption. When infection is apparent, broad-spectrum antibiotics, such as intravenous ampicillin and gentamicin, should be initiated and labor should be induced. Also, the infant should be delivered when there is evidence of fetal lung maturity, such as by the presence of phosphatidyl glycerol (PG) in the vaginal pool amniotic fluid.
Controversies
Some practitioners will use tocolytic agents with PPROM to delay delivery for 48 hours, allowing the corticosteroids to have its effect. Others argue that preterm labor likely indicates subclinical infection and tocolysis causes harm. There is no clear consensus on this issue. Progesterone may be proven to be useful in women who have had PPROM in a prior pregnancy or who currently have PPROM; studies are ongoing at the writing of this chapter.
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CASE CORRELATION
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COMPREHENSION QUESTIONS
18.1 A 31-year-old G1P0 at 33 weeks’ gestation is admitted for preterm premature rupture of membranes. Which of the following statements is correct?
A. Magnesium sulfate should be given for neuroprotection.B. Broad-spectrum antibiotic therapy is indicated only with maternal fever.C. Labor is the most common acute complication to be expected.D. Vaginal candidiasis is a risk factor for preterm premature rupture of membranes.
18.2 A 30-year-old G2P1 woman at 28 weeks’ gestation with preterm premature rupture of membranes is suspected of having intra-amniotic infection based on fetal tachycardia. The maternal temperature is 98.8°F. Which of the following is the most accurate method to confirm the intra-amniotic infection?
A. Serum maternal leukocyte countB. Speculum examination of the vaginal dischargeC. Amniotic fluid Gram stain by amniocentesisD. Palpation of the maternal uterusE. Height of oral temperature
18.3 An 18-year-old Hispanic G1P0 woman has a clinical presentation of intraamniotic infection. She denies any leakage of fluid per vagina, and repeated speculum examinations fail to identify rupture of membranes. Which of the following organisms is most likely to be the underlying etiology?
A. Group B streptococciB. Listeria monocytogenesC. Clostridia difficileD. Chlamydia trachomatisE. Escherichia coli
18.4 A 32-year-old woman at 33 weeks’ gestation notes leakage of clear vaginal fluid. She denies uterine contractions. The estimated fetal weight on sonography is 2000 g. Vaginal fluid shows the presence of phosphatidyl glycerol. Which of the following is the next step?
A. Expectant managementB. Intramuscular corticosteroidsC. Induction of laborD. Ultrasound-guided amniocentesis
18.5 A 30-year-old woman G2P1001 is at 32 weeks’ gestation and is diagnosed with PPROM. She is placed on bed rest and reports continued leakage of clear fluid each day. There are no signs of infection. A fetal heart rate tracing is performed twice weekly. Today, there is an abnormality of the fetal heart rate tracing. Which of the following is most likely to be seen?
A. Early decelerationsB. Late decelerationsC. Variable decelerationsD. Sinusoidal heart rate pattern
ANSWERS
18.1 C. Labor is the most common complication associated with PROM. Antibiotics should be given to prolong the pregnancy and decrease the risk of infection. The gestational age is <34 weeks, so antenatal steroids should be given. Magnesium sulfate is given for neuroprotection for pregnancies <32 weeks. Vaginal candidiasis is not a risk factor for PPROM; however, a lower socioeconomic status, STDs, cigarette smoking, cervical conization, emergency cerclage, multiple gestation, hydramnios, and placental abruption are risk factors.
18.2 C. Amniocentesis-revealing organisms on Gram stain are diagnostic of infection. A high serum maternal leukocyte count may be suggestive of infection, but it would not be specific for an intra-amniotic infection. Similarly, a speculum examination may reveal an infectious-appearing vaginal discharge; however, this would neither confirm that an infection is present or that a specific type of infection is present, especially since increased vaginal discharge is common in pregnancy. Palpation of the maternal uterus and height of an oral temperature would also not be diagnostic.
18.3 B. Listeria may induce chorioamnionitis without rupture of membranes; the mechanism is transplacental spread. A history of ingesting unpasteurized milk products (eg, some varieties of goat cheese) should raise clinical suspicion of Listeria. Group B streptococci and gram-negative enteric organisms such as E. coli are the most common organisms to affect neonates.
18.4 C. When fetal lung maturity is demonstrated on vaginal amniotic fluid by the presence of PG, delivery is the best next step when there is leakage of fluid. Expectant management and intramuscular corticosteroids place the mother at an increased risk of developing an intra-amniotic infection. Corticosteroids suppress the immune system, and expectant management prolongs the time frame that an ascending infection from the vagina can cause an intra-amniotic infection. Expectant management is undertaken when the risk of infection is thought to be less than the risk of prematurity, but this is not the case for this scenario with a fetus that shows signs of lung maturity. There is no indication for an ultrasound-guided amniocentesis.
18.5 C. The most common finding with PPROM would be variable decelerations likely due to oligohydramnios from the rupture of membranes. With ROM, there is insufficient fluid to “buffer the cord” from compression, and variable decelerations are common. A change of the patient’s position often alleviates the decelerations.
CLINICAL PEARLS
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» Pregnancies complicated by premature rupture of membranes after 34 to 35 weeks’ gestation are usually managed by induction of labor. » Pregnancies with PPROM <34 weeks’ gestation are usually managed expectantly. » The earliest sign of chorioamnionitis (intra-amniotic infection) is usually fetal tachycardia. » Pregnancies complicated by PPROM and chorioamnionitis should be treated with broad-spectrum antibiotics (like ampicillin and gentamicin) and delivery. » Antenatal corticosteroids should be given to patients with PPROM up to 34 weeks’ gestation, unless there is overt infection. |
REFERENCES
American College of Obstetricians and Gynecologists. Premature rupture of membranes. ACOG Practice Bulletin 139. Washington, DC; 2013.
Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Rouse DJ, Spong CY. Preterm birth. In: Williams Obstetrics. 24th ed. New York, NY: McGraw-Hill; 2014:804-831.
Hobel CJ. Obstetrical complications: preterm labor, PROM, IUGR, postterm pregnancy, and IUFD. In: Hacker NF, Gambone JC, Hobel CJ, eds. Essentials of Obstetrics and Gynecology. 5th ed. Philadelphia, PA: Saunders; 2009:146-159.
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