PATHOPHYSIOLOGY OF

PREMATURE RUPTURE OF
THE FETAL MEMBRANE
Novi Vicahyani Utami

PRESENTATION FLOW

INTRODUCTION
STRUCTURE OF THE FETAL MEMBRANES
MECHANISMS OF PREMATURE RUPTURE
OF THE MEMBRANES (PROM)
CLINICAL FACTORS ASSOCIATED WITH
COLLAGEN DEGRADATION AND PROM

INTRODUCTION

PROM: rupture of the fetal membrane

before the onset of labor
PPROM: PROM that occurring before
37 weeks gestation
10% of all pregnancies: PROM
PPROM : in 2-4% gestations
responsible for 30-40% of all preterm
deliveriesneonatal morbidity&mortality

STRUCTURE OF THE FETAL MEMBRANES

The fetal membranes are: amnion&chorion

MECHANISMS OF PREMATURE RUPTURE OF

THE MEMBRANES (PROM)

Intrapartum rupture:
generalized weakening due to uterine
contractions&repeated stretching
Membranes that rupture prematurely: focally
defective rather than generally weakened
The area near the rupture site:
restricted zone of extreme altered
morphologyswelling and disruption of the
fibrillar collagen network within the compact,
fibroblast, and spongy layers

Despite the divergent characteristics of

PROM and intrapartum rupture of the
membranes, there is little evidence to
suggest that the mechanisms that
predispose women to the former are not
identical to those that normally precede
labor.
This has led to the view that premature
rupture of the membranes represents an
acceleration or exaggeration of the
processes precipitating spontaneous
rupture of the membranes during labor.

CLINICAL FACTORS ASSOCIATED WITH

PREMATURE RUPTURE OF THE MEMBRANE

Infection
Hormones
Programmed Cell Death
Membrane Stretch and
Premature Rupture of the
Membranes

The maintenance of the tensile strength of

fetal membranes: equilibrium between
the synthesis and the degradation of the
components of the extracellular matrix
It has been proposed that changes in the
membranes, including:
-decreased collagen content
-altered collagen structure
-increased collagenolytic activity
=are associated with premature rupture
of the membranes.

Infection

Support the concept that bacterial

infection may have a role in the
pathogenesis of PROM: Pathologic
Microorganisms in human vaginal flora
soon after membrane rupture
Intrauterine infection predispose
women to PROM through any of several
mechanisms
each of which induces degradation of
the extracellular matrix

Several Organisms: Secrete PROTEASE

degrade collagen and weaken
the fetal membranes
The host inflammatory response to
bacterial infection: (mediated by
polymorphonuclear neutrophils and
macrophages) produce cytokines,
matrix metalloproteinases, and
prostaglandins.
another host response to infection:
production of glucocorticoids
(stimulate PG production)

Hormones

Low concentrations of progesterone

and estradiol production of
collagenase (collagen degradation)
RELAXIN: reverses
increasing MMP activities in fetal membranes
Expression of the relaxin gene is
increased before labor in human fetal
membranes at term

Programmed Cell Death

Human amnion and chorion obtained at

term after premature rupture of the
membranes contain many apoptotic
cells in areas adjacent to the rupture
site and fewer apoptotic cells in other
areas of the membranes.
Infection: host immune response
accelerate cell death in fetal
membranes

Membrane Stretch and

Premature Rupture of the
Membranes

Uterine overdistention
(polyhydramnios and multifetal):
induces membrane stretch and
increases the risk of PROM
Mechanical stretching of the fetal
membranes up-regulates the
production of several amniotic factors,
including prostaglandin E2 and
interleukin-8.

Mechanical stretching of the fetal

membranes up-regulates the
production of several amniotic
factors, including prostaglandin E2
and interleukin-8.
PGE2:
- MMP production
- uterine irritability
- collagen synthesis
IL-8:
- stimulate collagenase activity
( collagen degradation)

VARIOUS MECHANISMS THAT HAVE BEEN PROPOSED TO RESULT IN PROM

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