Management of Premature Rupture of

Membranes: What Should Childbirth Educators

Be Teaching?
McKeon, Valerie A . International Journal of Childbirth Education ; Minneapolis  Vol. 6, Iss. 1,  (Feb 28,
1991): 14-16.

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ABSTRACT (ABSTRACT)
 
Conventional techniques for diagnosing ruptured membranes include: visualizing pooled amniotic fluid in the
vagina via sterile speculum examination; determining the vaginal pH with nitrazine paper (which turns blue in the
presence of amniotic fluid) and observing amniotic fluid crystallization or ferning ([Rudd] 1985). Microscopic
examination of dried amniotic fluid shows a fernlike pattern due to the fluid's elevated protein and electrolyte
levels (Rudd 1985; [Kappy] 1986; [Gilbert] and Harmon 1986). Sonography may prove helpful in making the
diagnosis by demonstrating oligohydramnios, although diminished fluid may result from conditions other than
PROM.

External electronic fetal heart monitoring is done on all patients with PROM as part of the evaluation process.
Tracings that reveal a fetal tachycardia or variable decelerations may indicate fetal distress resulting from cord
compression, decreased amniotic fluid or infection. Efforts are also made to rule out chorioamnionitis. Recent
studies suggest that a positive Gram stain and culture of amniotic fluid obtained by amniocentesis; a biophysical
profile score of <7 (Table 1) or a rise in C-reactive protein (> 40 mg/liter) are accurate predictors of infection in
preterm PROM (Fisk 1988). C-reactive protein (CRP) is an abnormal specific protein produced in increased
quantities in the serum when inflammation or infection is present (Hollander 1986). Other indicators of
chorioamnionitis include maternal fever, maternal or fetal tachycardia, uterine tenderness, uterine contractions,
foul, purulent vaginal discharge and changes in the white blood count (elevated with a shift in the differential)
(Kappy 1986; Gilbert and Harmon 1986; Hollander 1986).

Every case of PROM involves a risk-benefit analysis in which the complications of prematurity are balanced
against the risks of expectant management for both mother and fetus (Schwartz 1986). Because of conflicting
scientific data, managing PROM remains a significant problem area in obstetrics and one of the most controversial
issues (Rudd 1985; Gilbert and Harmon 1986). In general there is agreement that when fetal lung maturity is
expected or documented, lengthy delay in delivery should be avoided. Because of the risk of chorioamnionitis,
most women whose membranes rupture after thirty-four to thirty-six weeks of gestation are delivered within twelve
to twenty-four hours by induction if labor has not begun spontaneously. Some obstetricians take a more
conservative approach when the cervix is unfavorable for induction and there is no evidence of chorioamnionitis.
They wait for labor to begin spontaneously while observing for signs of infection. This approach has been found to
decrease the occurrence of cesarean deliveries without increasing the risk of infection (Kappy et al 1982).

FULL TEXT
 
Management of Premature Rupture of Membranes: What Should Childbirth Educators Be Teaching?

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Premature rupture of membranes (PROM) is the spontaneous rupture of the chorioamnion and leakage of amniotic
fluid prior to the onset of labor. Latency, or the latent phase, is the time interval between membrane rupture and
the onset of uterine contractions (Crenshaw 1986). The incidence of PROM is 3% at term and 18.5% with a preterm
pregnancy (Creasy and Resnik 1984). One out of five subsequent pregnancies is similarly affected (Naeye 1982).

The major risk to the mother in PROM is sepsis as a result of intraamniotic infection (chorioamnionitis) or
postpartum endometritis (Rudd 1985). Prolonged bedrest, which may be advised when the fetus is preterm, can
lead to muscle wasting and deep vein thrombosis. In addition, anxiety and concern about the implications of
PROM result in increased maternal stress.

Fetal risks of PROM include: prematurity, sepsis and physiologic or physical anomalies caused by the chronic
absence of amniotic fluid (Rudd 1985). Pulmonary hypoplasia has been reported with prolonged PROM and
skeletal deformities due to compression have also been observed (Nimrod, et al 1984). Further there is a greater
risk of cord compression and fetal hypoxia or death when amniotic fluid is diminished; iatrogenic harm is also a
possibility.

Etiology of PROM

Although there has been considerable research on this topic, the exact etiology of premature rupture of
membranes remains unknown (Alger and Pupkin 1986). Possible predisposing factors include advanced maternal
age, non-white race, multiparity, instrumentation of the cervix prior to pregnancy, cigarette smoking, cervical
incompetence, low pregnancy weight gain and recent coitus (Flood and Naeye 1984). In addition, inherent
weakness of the membranes, placenta previa, abruptio placenta, fetal malpresentation, trauma and nutritional
deficiencies have been implicated as possible etiologies (Alger and Pupkin 1986; Kappy 1986). The risk of PROM is
also increased in women from lower socioeconomic groups, sexually promiscuous teenagers and individuals with
decreased immunity (Gilbert and Harmon 1986; Gazaway and Mullins 1986).

Current evidence strongly suggests that maternal genital tract infection, such as vaginitis or endocervicitis, often
precedes and may possibly be the cause of PROM in a large percentage of cases (Crenshaw 1986; Rudd 1985;
Alger and Pupkin 1986; Kappy 1986; Gilbert and Harmon 1986; Miller and Pastorek 1986). Perhaps the proteolytic
enzymes produced by bacteria and the inflammatory response they elicit in the host so weaken the membranes
that PROM occurs. Whatever the initiating factor(s), the end result is a thinning out and disintegration of the
membranes that results in a local defect unable to withstand the stresses of pregnancy (Alger and Pupkin 1986).

Diagnosing PROM

Rupture of the membranes may be signaled by a sudden gush or a slight trickle of clear fluid from the vagina.
Although it would seem that ruptured membranes could be easily diagnosed, scanty residual fluid, blood in the
vagina, leaking rather than ruptured membranes and maternal urinary incontinence can all make it difficult to
reach a definitive diagnosis (Nagay and Saller 1986). Nevertheless it is very important that the diagnosis be made
as quickly and as accurately as possible. A false-positive determination may lead to unnecessary intervention that
results in the birth of a preterm infant and/or cesarean delivery. A false-negative diagnosis places the mother and
infant at increased risk for infection, which is potentially a life-threatening complication (Kappy 1986).

Conventional techniques for diagnosing ruptured membranes include: visualizing pooled amniotic fluid in the
vagina via sterile speculum examination; determining the vaginal pH with nitrazine paper (which turns blue in the

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presence of amniotic fluid) and observing amniotic fluid crystallization or ferning (Rudd 1985). Microscopic
examination of dried amniotic fluid shows a fernlike pattern due to the fluid's elevated protein and electrolyte
levels (Rudd 1985; Kappy 1986; Gilbert and Harmon 1986). Sonography may prove helpful in making the diagnosis
by demonstrating oligohydramnios, although diminished fluid may result from conditions other than PROM.

During the sterile speculum examination, the cervix is inspected in an attempt to evaluate effacement and
dilatation and estimate inductibility. A culture of the cervix is also taken when PROM is diagnosed or even
suspected. This allows for early identification of potentially serious pathogens. Digital vaginal examination is
avoided in women with PROM who are not in labor since the finger can transport organisms from the vagina into
the cervical canal, thereby increasing the risk of chorioamnionitis (Kappy 1986; Gilbert and Harmon 1986; Nagay
and Saller 1986).

Once the diagnosis of PROM is made, it is very important that gestational age be determined before therapy is
started. The menstrual history, corroborating evidence (such as an early pregnancy test, date of quickening, date
fetal heart tones were first heard via fetoscope and fundal growth), and the results of sonography are all taken into
consideration in making this determination (Kappy 1986; Nagay and Saller 1986). Since gestational age alone can
be an unreliable indicator of fetal maturity, amniotic fluid may be used to determine maturity of the lungs. Fluid
from the vaginal pool can be tested for phosphatidylglycerol (PG) and if present, fetal lung maturity is indicated.
Pulmonary maturity can also be determined by collecting fluid via amniocentesis and evaluating it for L/S ratio and
the presence of PG. An L/S ratio of 1.8:1 and 2:1 and/or the presence of PG indicate lung maturity (Gilbert and
Harmon 1986).

External electronic fetal heart monitoring is done on all patients with PROM as part of the evaluation process.
Tracings that reveal a fetal tachycardia or variable decelerations may indicate fetal distress resulting from cord
compression, decreased amniotic fluid or infection. Efforts are also made to rule out chorioamnionitis. Recent
studies suggest that a positive Gram stain and culture of amniotic fluid obtained by amniocentesis; a biophysical
profile score of <7 (Table 1) or a rise in C-reactive protein (> 40 mg/liter) are accurate predictors of infection in
preterm PROM (Fisk 1988). C-reactive protein (CRP) is an abnormal specific protein produced in increased
quantities in the serum when inflammation or infection is present (Hollander 1986). Other indicators of
chorioamnionitis include maternal fever, maternal or fetal tachycardia, uterine tenderness, uterine contractions,
foul, purulent vaginal discharge and changes in the white blood count (elevated with a shift in the differential)
(Kappy 1986; Gilbert and Harmon 1986; Hollander 1986).

Usual medical management

Every case of PROM involves a risk-benefit analysis in which the complications of prematurity are balanced
against the risks of expectant management for both mother and fetus (Schwartz 1986). Because of conflicting
scientific data, managing PROM remains a significant problem area in obstetrics and one of the most controversial
issues (Rudd 1985; Gilbert and Harmon 1986). In general there is agreement that when fetal lung maturity is
expected or documented, lengthy delay in delivery should be avoided. Because of the risk of chorioamnionitis,
most women whose membranes rupture after thirty-four to thirty-six weeks of gestation are delivered within twelve
to twenty-four hours by induction if labor has not begun spontaneously. Some obstetricians take a more
conservative approach when the cervix is unfavorable for induction and there is no evidence of chorioamnionitis.
They wait for labor to begin spontaneously while observing for signs of infection. This approach has been found to
decrease the occurrence of cesarean deliveries without increasing the risk of infection (Kappy et al 1982).

When gestational age is under twenty-eight weeks and no signs of infection are present, expectant management

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without amniocentesis is the usual treatment plan (Gilbert and Harmon 1986). These women are kept on bedrest
and followed closely for as long as they continue to leak fluid (Kappy 1986). The risk of prematurity is far greater
than the risk of chorioamnionitis in such cases.

When the gestational age is over twenty-eight weeks but under thirty-four to thirty-six weeks, care must be
individualized with the risk of interference weighed against the risk of infection. In deciding between expectant
management and delivery, assessments for fetal maturity, chorioamnionitis and fetal distress have to be made.
Delivery is the choice when fetal maturity is documented, chorioamnionitis is suspected or fetal distress is
present. Induction is usually attempted unless there are obstetrical contraindications in which case a cesarean
delivery is performed. Immediate delivery is required when fetal distress is present since hypoxia or a traumatic
delivery increases the risk of perinatal mortality and morbidity associated with prematurity.

The value of prophylactic antibiotics, the potential benefits and/or dangers of using steroids for induction of fetal
pulmonary maturity, the use of tocolytic agents to delay labor and the method and route of delivery are all
controversial issues. In a published review of PROM, Rudd reported that therapeutic agents to accelerate lung
maturity, stop labor or prevent infections must be considered investigational when used during the latency phase
of premature rupture of the membranes (Rudd 1985), Because of these uncertainties and the risk of
chorioamnionitis, some physicians deliver every fetus following PROM without delay. Regardless of the
management plan decided upon, 95% of women deliver within two weeks following PROM (Gilbert and Harmon
1986).

What should childbirth educators be teaching?

All pregnant women should be taught the danger signs of pregnancy including PROM. The signs of membrane
rupture and the importance of promptly notifying the health care provider should be explained in early pregnancy,
with subsequent reinforcement. Since the etiology of PROM is unknown, preventing this complication is difficult.
However, it may be helpful to consider risk factors and ways to modify them. Since poor nutrition probably
increases the risk of PROM, it is important that pregnant women receive instructions early in pregnancy regarding
a healthful diet and the importance of adhering to it (Alger and Pupkin 1986; Kappy 1986; Gilbert and Harmon
1986). Referral to financial assistance programs and instruction in food preparation may also be necessary.

Good personal hygiene and cleanliness may help to decrease the risk of PROM by keeping potentially harmful
bacteria to a minimum. Pregnant women should be made aware of the importance of daily bathing and wiping the
perineum from front to back to avoid contaminating the vagina with bacteria from the rectum. Women should also
be cautioned to avoid multiple sexual partners and coital practices which increase the risk of genital infection and
PROM. Measures which promote health and may guard against PROM include drinking six to eight glasses of fluid
per day, regular exercise with adequate rest to avoid fatigue and avoidance of smoking. Pregnant women who do
smoke should be supported in their attempts to stop.

Once the membranes have ruptured, women may have varied ideas about what caused this to happen. They are
also concerned about the implications for themselves and their unborn child. In addition, they may feel anxious,
fearful and/or guilty, thinking they did something to cause the membranes to rupture. By being an active listener,
the childbirth educator can allow for ventilation of emotions and provide an opportunity for questions and
clarification. Informing women that the reason for PROM is usually unknown and reassuring them that their
actions did not cause the membranes to rupture may help to correct misconceptions and allay feelings of guilt.
Working with the health care team to help women understand the goals and objectives of various management
strategies for PROM may be effective in reducing anxiety and promoting cooperation with the plan of care.

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References

Alger, L. and J. Pupkin. 1986. Etiology of preterm premature rupture of the membranes. Clin Obstet Gynecol
29:758-78.

Creasy, R. and R. Resnik. 1984. Maternal fetal medicine: principles and practice. Philadelphia: W.B. Saunders Co.

Crenshaw, C. 1986. Preterm premature rupture of the membranes. Clin Obstet Gynecol 29:735-8.

Fisk, N. 1988. Modifications to selective conservative management in preterm premature rupture of the
membranes. Obstet Gynecol Surv 43:328-34.

Flood, B. and R. Naeye. 1984. Factors that predispose to premature rupture of the fetal membranes. JOGN Nursing
13:119-22.

Gazaway, P. and C. Mullins. 1986. Prevention of preterm labor and premature rupture of the membranes. Clin
Obstet Gynecol 29:739-57.

Gilbert, E. and J. Harmon. 1986. High-risk pregnancy and delivery. St. Louis: C.V. Mosby Co.

Hollander, D. 1986. Diagnosis of chorionamnionitis. Clin Obstet Gynecol 29:816-25.

Kappy, K., C. Cetrulo, R. Knuppel, C. Ingardia, A. Sbarra, J. Scerbo, G. Mitchell. 1982. Premature rupture of the
membranes at term: a comparison on induced and spontaneous labors. J Reprod Med 27:29-33.

Kappy, K. 1986. Premature rupture of the membranes, in Knuppel R. and J. Drukker (eds). High-risk pregnancy.
Philadelphia: W.B. Saunders Co.

Manning, F., I. Morrison, I. Lange, C. Harman and P. Chamberlain. 1985. Fetal assessment based on fetal
biophysical profile scoring: experience in 12,620 referred high-risk pregnancies. Am J Obstet Gynecol 151:343-9.

Miller, J. and J. Pastorek. 1986. The microbiology of premature rupture of the membranes. Clin Obstet Gynecol
29:739-57.

Naeye, R. 1982. Factors that predispose to premature rupture of the fetal membranes. Obstet Gynecol 60:93-8.

Nagay, D. and D. Saller. 1986. An analysis of the decisions in the management of premature rupture of the
membranes. Clin Obstet Gynecol 29:826-34.

Nimrod, C., F. Varela-Gittings, G. Machin, D. Cambell, R. Wesenberg. 1984. The effect of very prolonged membrane
rupture on fetal development. Am J Obstet Gynecol 148:540-3.

Rudd, E. 1985. Premature rupture of the membranes: a review. J Reprod Med 30:841-8.

Schwartz, M. 1986. Genetic aspects of premature rupture of membranes. Clin Obstet Gynecol 29:771-8.

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DETAILS

Subject: Births; Health; Health care; Obstetrics; Preventive medicine; Women

Publication title: International Journal of Childbirth Education; Minneapolis

Volume: 6

Issue: 1

Pages: 14-16

Number of pages: 0

Publication year: 1991

Publication date: Feb 28, 1991

Publisher: INTERNATIONAL CHILDBIRTH EDUCATION ASSOCIATION

Place of publication: Minneapolis

Country of publication: United States, Minneapolis

Publication subject: Medical Sciences--Obstetrics And Gynecology, Medical Sciences--Pediatrics

ISSN: 08878625

Source type: Scholarly Journals

Language of publication: English

Document type: Feature

Accession number: SFLNSNCBE0997IJLR869000313

ProQuest document ID: 212866920

Document URL: https://search.proquest.com/docview/212866920?accountid=188397

Copyright: Copyright INTERNATIONAL CHILDBIRTH EDUCATION ASSOCIATION Feb 28, 1991

Last updated: 2017-11-10

Database: Research Library

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