Premature rupture of membranes: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
Membrane strength is dependant on extracellular proteins including but not limited to collagen, fibronectin and laminin. Matrix metalloproteases (MMPs) degrade collagen which reduces membrane strength. It is thought that PROM and pPROM can be caused by a combination of events that lead to membrane weakening via direct damage or reduction of supporting elements. Up to a third of PROM are linked to amniotic fluid positive for bacteria. These infections may be asymptomatic until presentation. In case of an altered flora of the vaginal canal, some invasive species of bacteria produce collagenases, proteases, which directly degrade the amniotic membranes, in addition to the inflammatory effect and subsequent damage to the membranes by the host immune system.  
Membrane strength is dependent on extracellular proteins including but not limited to collagen, fibronectin and laminin. Matrix metalloproteases (MMPs) degrade collagen which reduces membrane strength. These are inhibited by metalloproteinase inhibitors. The balance between these proteins maintains membrane integrity. It is thought that PROM and pPROM can be caused by a combination of events that lead to membrane weakening via direct damage or reduction of supporting elements. Up to a third of PROM cases are linked to amniotic fluid positive for bacteria. These infections may be asymptomatic until presentation. In case of an altered flora of the vaginal canal, some invasive species of bacteria produce collagenases, proteases, which directly degrade the amniotic membranes, in addition to the inflammatory effect and subsequent damage to the membranes by the host immune system.  


Hypoxic stress to the fetus and placenta are linked to a three to seven times likelihood of PROM. This stress can be due to maternal hypertension, preeclampsia/eclampsia and problems with the umbilical cord. This stress causes release of fetal corticotropin releasing hormone (CRH), leading to inhibition of transcription in decidual cells (via the glucocorticoid and progesterone receptor ligand), leading to a state of progesterone resistance and consequent weakening of membranes.   
Hypoxic stress to the fetus and placenta are linked to a three to seven times likelihood of PROM. This stress can be due to maternal hypertension, preeclampsia/eclampsia and problems with the umbilical cord. This stress causes release of fetal corticotropin releasing hormone (CRH), leading to inhibition of transcription in decidual cells (via the glucocorticoid and progesterone receptor ligand), leading to a state of progesterone resistance and consequent weakening of membranes.   


Fetal ACTH release also results in a downstream increase of androgens, which are converted by the placenta into estrones. These estrones act on the myometrium to increase gap junctions and receptors for pro-contractile hormones. Coupled with the anti-progesterone effects of fetal CRH, this pathway results in an excitable and activated myometrium. <br />  
Fetal ACTH release also results in a downstream increase of androgens, which are converted by the placenta into estrones. These estrones act on the myometrium to increase gap junctions and receptors for pro-contractile hormones. Coupled with the anti-progesterone effects of fetal CRH, this pathway results in an excitable and procontractile myometrium. <br />  


==Differentiating PROM from other Diseases==
==Differentiating PROM from other Diseases==
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Common risk factors in the development of PROM include  
Common risk factors in the development of PROM include  


*Important maternal risk factors include [[chorioamnionitis]], [[sepsis]], previous history of PROM. Additional factors are similar to those for preterm birth such as abnormal bleeding during the second trimester or late in the pregnancy, low BMI, reduced cervical length, smoking and drug abuse.
*Important maternal risk factors include [[chorioamnionitis]], [[sepsis]], previous history of PROM. Additional factors are similar to those for preterm birth such as abnormal bleeding during the second trimester or late in the pregnancy, low BMI, reduced cervical length, smoking and drug abuse. Low socioeconomic status and deficiency of copper or vitamin C, along with connective tissue disorders are also linked to increased risk of PROM. Fetal factors include prematurity, [[infection]], [[cord prolapse]], or [[malpresentation]].
*Fetal factors include prematurity, [[infection]], [[cord prolapse]], or [[malpresentation]].


==Screening==
==Screening==
Line 90: Line 89:


==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
the majority of pregnancies progress to delivery within one week of membrane rupture, the common cause of induced or spontaneous labor is chorioamnionitis, which complicates up to 60% of PROM cases. In usual cases of PROM, labor is induced as soon as possible if pregnancy is viable. If expectant management is practiced, the patient is at increased risk of infection, abruptio placentae, and umbilical cord accident as well as complications linked to residual oligohydramnios. The risk of long term neurodevelopmental problems however, is not affected. PROM and PPROM are the most common cause of premature delivery, neonatal respiratory distress syndrome and neonatal death.
The majority of pregnancies progress to delivery within one week of membrane rupture, the common cause of induced or spontaneous labor is chorioamnionitis, which complicates up to 60% of PROM cases. In usual cases of PROM, labor is induced as soon as possible if pregnancy is viable. If expectant management is practiced, the patient is at increased risk of infection, abruptio placentae, and umbilical cord accident as well as complications linked to residual oligohydramnios. The risk of long term neurodevelopmental problems however, is not affected. PROM and PPROM are the most common cause of premature delivery, neonatal respiratory distress syndrome and neonatal death.


==Diagnosis==
==Diagnosis==
Assessment of a rupture of membranes involves taking a proper [[medical history]], a [[gynecological exam]] using a [[speculum]], [[nitrazine]], [[cytologic]] (ferning) tests, and [[ultrasound]].
Assessment of PROM involves taking a focused [[medical history]], a physical examination with a sterile speculum, ultrasound and other commercial tests if a diagnosis is not reached prior.


===Diagnostic Study of Choice===
===Diagnostic Study of Choice===

Revision as of 06:26, 1 October 2020

Premature rupture of membranes
ICD-10 O42
ICD-9 658.1
DiseasesDB 10600

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Treatment

  • In a term pregnany where premature rupture of membranes has occurred, spontaneous labour should be permitted. Current obstetrical management includes an induction of labour at approximately 6 hours if it has not already begun, and Group B Streptococcal prophylaxis at 18 hours. Some hospitals, birth centers and private midwives do not induce labor at any point after PROM, but rather watch carefully for any signs of infection and ensure that nothing is introduced into the vagina after the PROM, including sterile vaginal exams.

Ampicillin or erythromycin should be administered for 7 days, and antenatal steroids if the gestational age is less than 30 weeks. Tocolysis is also used, though its use in this context is controversial. The mother should be admitted to hospital and put under careful surveillance for preterm labour and chorioamnionitis. Induction of labour should happen at around 36 weeks. de:Blasensprung

Overview

Premature rupture of membranes (PROM) (referred to as pre-labor rupture of membranes for simplicity in this article) is a condition which occurs in pregnancy when the amniotic sac ruptures before the onset of labor. A related term is pPROM which stands for preterm premature rupture of the membranes which occurs when the rupture happens before 37 weeks gestation. Risk factors include maternal vaginal infections which ascend to the amniotic membrane, vaginal bleeding during pregnancy and maternal stature, among others.

PPROM

Preterm prelabor rupture of membranes (PPROM) is a condition where the amniotic sac leaks fluid before 37 weeks of gestation.[1] This can be caused by a bacterial infection or by a defect in the structure of the amniotic sac, uterus, or cervix. In some cases, the leak can spontaneously heal, but in most cases of PPROM, labor begins within 48 hours of membrane rupture. When this occurs, it is necessary that the mother receive treatment to avoid possible infection in the newborn.


Historical Perspective

[Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].

The association between [important risk factor/cause] and [disease name] was made in/during [year/event].

In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].

In [year], [gene] mutations were first implicated in the pathogenesis of [disease name].

There have been several outbreaks of [disease name], including -----.

In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].

Classification

Prelabor rupture of membranes may be classified according to gestational age at which the rupture occurs. If more than 18 hours have passed after the rupture of membranes without the onset of labor it is termed as prolonged PROM. If rupture occurs before age of viability (37 weeks) it is termed as preterm prelabor rupture of membranes (pPROM). If the gestational age is between 20 0/7 weeks to 25 6/7 it is considered as "periviable PROM". Other types of rupture of membranes are artificial rupture of membranes (AROM), spontaneous rupture of membranes (SROM).

Pathophysiology

Membrane strength is dependent on extracellular proteins including but not limited to collagen, fibronectin and laminin. Matrix metalloproteases (MMPs) degrade collagen which reduces membrane strength. These are inhibited by metalloproteinase inhibitors. The balance between these proteins maintains membrane integrity. It is thought that PROM and pPROM can be caused by a combination of events that lead to membrane weakening via direct damage or reduction of supporting elements. Up to a third of PROM cases are linked to amniotic fluid positive for bacteria. These infections may be asymptomatic until presentation. In case of an altered flora of the vaginal canal, some invasive species of bacteria produce collagenases, proteases, which directly degrade the amniotic membranes, in addition to the inflammatory effect and subsequent damage to the membranes by the host immune system.

Hypoxic stress to the fetus and placenta are linked to a three to seven times likelihood of PROM. This stress can be due to maternal hypertension, preeclampsia/eclampsia and problems with the umbilical cord. This stress causes release of fetal corticotropin releasing hormone (CRH), leading to inhibition of transcription in decidual cells (via the glucocorticoid and progesterone receptor ligand), leading to a state of progesterone resistance and consequent weakening of membranes.

Fetal ACTH release also results in a downstream increase of androgens, which are converted by the placenta into estrones. These estrones act on the myometrium to increase gap junctions and receptors for pro-contractile hormones. Coupled with the anti-progesterone effects of fetal CRH, this pathway results in an excitable and procontractile myometrium.

Differentiating PROM from other Diseases

Other disorders causing abnormal vaginal wetness are:


The diagnosis of PROM is done via careful history and physical examination, ultrasound is employed to confirm oligohydramnios. These tests can also be done to rule out the differentials listed.

Epidemiology and Demographics

PROM complicates 3% of preterm pregnancies and occurs in 5% to 10% of term pregnancies. 60% to 80% cases of PROM occur in term pregnancies."Support Epidemiology and Prognosis of Premature Rupture of Membranes in Pikine National Hospital Center". Open Journal of Obstetrics and Gynecology. 9.

Pregnant females of all age groups may develop PROM, however there is a higher chance of adolescent pregnancies progressing towards PROM and pPROM. "Premature and preterm premature rupture of membranes in adolescent compared to adult pregnancy". Medicinski glasnik.

African american females are more likely to experience PROM.

Risk Factors

Common risk factors in the development of PROM include

  • Important maternal risk factors include chorioamnionitis, sepsis, previous history of PROM. Additional factors are similar to those for preterm birth such as abnormal bleeding during the second trimester or late in the pregnancy, low BMI, reduced cervical length, smoking and drug abuse. Low socioeconomic status and deficiency of copper or vitamin C, along with connective tissue disorders are also linked to increased risk of PROM. Fetal factors include prematurity, infection, cord prolapse, or malpresentation.

Screening

There is insufficient evidence to recommend routine screening for PROM. In women with positive vaginal-rectal group B strep (GBS) cultures within the past 5 weeks, antibiotic prophylaxis is recommended intrapartum by the CDC. If the patient is not in labour, antibiotics are to be continued for 48 hours and cultures to be repeated. If repeat cultures are positive, intrapartum antibiotics are recommened.

Natural History, Complications, and Prognosis

The majority of pregnancies progress to delivery within one week of membrane rupture, the common cause of induced or spontaneous labor is chorioamnionitis, which complicates up to 60% of PROM cases. In usual cases of PROM, labor is induced as soon as possible if pregnancy is viable. If expectant management is practiced, the patient is at increased risk of infection, abruptio placentae, and umbilical cord accident as well as complications linked to residual oligohydramnios. The risk of long term neurodevelopmental problems however, is not affected. PROM and PPROM are the most common cause of premature delivery, neonatal respiratory distress syndrome and neonatal death.

Diagnosis

Assessment of PROM involves taking a focused medical history, a physical examination with a sterile speculum, ultrasound and other commercial tests if a diagnosis is not reached prior.

Diagnostic Study of Choice

The diagnosis of PROM is made according to characteristic findings on history and physical examination. Usual cases present as a woman in late trimester pregnancy complaining of leakage of fluid. The gold standard for diagnosis per speculum is pooling of fluid in the posterior vaginal vault. If there is no pooling observed, the patient is told to bear down or apply fundal pressure in order to increase the outflow of amniotic fluid and get visual confirmation of leakage. There may still be no pooling observed, in which case diagnostic testing is employed in the form of ultrasound to gauge the amniotic fluid volume. Ultrasound is also useful to assess fetal wellbeing. If oligohydramnios is detected, the diagnosis of PROM is confirmed. In cases of low-normal or normal amniotic fluid volume, other tests can be done to confirm PROM/PPROM.

History and Symptoms

The hallmark of PROM is pooling of fluid. A history of leakage of clear fluid from the vagina is suggestive of PROM.

Physical Examination

Patients with PROM usually appear well, some may be in active labor. Physical examination of patients is usually remarkable for leakage of clear or yellow fluid from the vagina, which may be a sudden gush or a slow leak that is evident by wetting of clothes. For women in active labor, sterile speculum examination is recommended to confirm pooling of amniotic fluid, as digital examination has been shown to increase the risk of infection and early labor.

Laboratory Findings

Bedside dipstick or strip based testing for specific amniotic fluid proteins has shown to be highly sensitive and specific for detecting PROM. An elevated concentration of vaginal fluid placental alpha microglobulin-1 protein is highly suggestive of PROM (Amnisure Test). IGFBP-1, or placental protein 12 (PP12) is another protein found in high concentrations in amniotic fluid and is the target of dipstick tests to detect PROM.

Less sensitive tests include the nitrazine and fern tests. A nitrazine paper test strip is used to test the pH of vaginal fluid. normal vaginal pH is from 3.8 to 4.2, the pH of urine, which is typically <6.0 but may be higher, amniotic fluid usually has a pH range of 7.0 to 7.3. False negatives can occur if the leaking sporadic or if the amniotic fluid is diluted by other vaginal fluids. False positives can be attributed to alkaline fluids in the vagina, like blood, seminal fluid, or soap. Urinary tract infections can also raise the urine pH.

Amniotic fluid forms a "ferning" pattern when allowed to dry on a slide. Fluid collected from the posterior fornix is dried on a glass slide for 10 minutes. Amniotic fluid produces a delicate ferning pattern, while dried cervival mucus forms a thicker, wider pattern. Well-estrogenized cervical mucus or a fingerprint on the microscope slide may cause a false positive fern test. False negatives may be because of the slide being prepared with inadequate amniotic fluid or contamination with vaginal discharge or blood.

Electrocardiogram

There are no ECG findings associated with PROM.

X-ray

There are no x-ray findings associated with PROM.

Ultrasound

Echocardiography/ultrasound may be helpful in the diagnosis of PROM/pPROM. Findings on an ultrasound diagnostic of PROM include .

CT scan

There are no CT scan findings associated with [disease name].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

There are no other diagnostic studies associated with [disease name].

OR

[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

There is no treatment for [disease name]; the mainstay of therapy is supportive care.

OR

Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].

OR

The majority of cases of [disease name] are self-limited and require only supportive care.

OR

[Disease name] is a medical emergency and requires prompt treatment.

OR

The mainstay of treatment for [disease name] is [therapy].

OR   The optimal therapy for [malignancy name] depends on the stage at diagnosis.

OR

[Therapy] is recommended among all patients who develop [disease name].

OR

Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].

OR

Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].

OR

Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].

OR

Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].

Surgery

Surgical intervention is not recommended for the management of [disease name].

OR

Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]

OR

The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].

OR

The feasibility of surgery depends on the stage of [malignancy] at diagnosis.

OR

Surgery is the mainstay of treatment for [disease or malignancy].

Primary Prevention

There are no established measures for the primary prevention of [disease name].

OR

There are no available vaccines against [disease name].

OR

Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].

OR

[Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].

Secondary Prevention

There are no established measures for the secondary prevention of [disease name].

OR

Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3]. Template:WH Template:WS

References

  1. Deering SH, Patel N, Spong CY, Pezzullo JC, Ghidini A (2007). "Fetal growth after preterm premature rupture of membranes: is it related to amniotic fluid volume?". J. Matern. Fetal. Neonatal. Med. 20 (5): 397–400. doi:10.1080/14767050701280249. PMID 17674244.

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