What goes wrong in most
cases of preterm labour? Why PTL at all
occurs??
The most common pathology
in cases of PTL is maternal T-cell infiltration of the chorion laeve with
trophoblast apoptosis, resembles allograft rejection. Spontaneous preterm labor and birth is the
leading cause of neonatal morbidity and mortality. It is obvious that preterm
labor is much more than labor occurring early. There are a number of possible
reasons that the quiescent
myometrium gets activated to contract before term, immune mechanisms may be
looked upon as contributors from the point of view that the maternal tolerance
of the fetal/placental allograft is exhausted, leading to its
expulsion. Anatomical defect may be
one of cause of PTL where Cx encerclage may be beneficial but most PTL are due
to Chronic chorioamnionitis of many
etiology. The most common placental
lesion in late spontaneous preterm birth, which is characterized by maternal
T-cell infiltration of the chorion laeve with trophoblast apoptosis, resembles
allograft rejection.
Prediction of PTL?? How best to know that
mother is prone to have PTL, well ahead?? How to know that fetal systemic
inflammation is there? Ans:-Maternal
sensitization to fetal human leukocyte antigens (HLAs) is frequently found in
patients with chronic chorioamnionitis and is accompanied by complement
deposition in umbilical vein endothelium. A novel form of fetal systemic
inflammation characterized by over-expression of T-cell chemokines (e.g.,
CXCL-10) has been observed in chronic chorioamnionitis.
Breakdown of
maternal-fetal tolerance may be particularly relevant to preterm labor
occurring after fetal surgery or stem cell transplantation—interventions in
which there is an increase in the number of maternal T cells in the fetal
circulation. The mechanisms linking disorders in tolerance and spontaneous
preterm labor remain to be defined.
How does myometrial
activation occurs??
Ans: The immune response is also of importance in the
pathway leading to myometrial activation from other causes such as infection.
The current understanding of this process is that the switch of the myometrium
from a quiescent to a contractile state is accompanied by a shift in signaling
between anti-inflammatory and proinflammatory pathways, including chemokines
(interleukin-8), cytokines (interleukin-1 and -6) and contraction-associated
proteins (oxytocin receptor, connexin 43, prostaglandin receptors). Increased
expression of inflammatory cytokines (TNF-a and IL-1) and chemokines, increased
activity of proteases [matrix metalloproteinase (MMP)-8 and MMP-9, dissolution
of cellular cements such as fibronectin and apoptosis have been implicated in
the process of membrane rupture.
Unfortunately there are
no ideal drug to control inflammation
& release of cytokines which finally cause activation of so long quiescent
myometrium!!!! no These mechanisms
are relevant because we need to look for new interventions to reduce preterm
births. The mainstay of current clinical practice is tocolysis. This has been
of limited value in preventing preterm birth. New approaches addressing the
root cause rather than the symptom of uterine contractions need to be evaluated
to tackle this problem.
\
A primigravida woman at 32 weeks gestation presents to the birth suite with painful regular contractions. She has presented twice previously with the same complaint and each time been determined to have a closed, non-effacing cervix, a normal CTG and has been discharged home after 24 hours of observation. At her first presentation at 28 weeks she was given two doses of betamethasone. How should her pregnancy be managed?
A primigravida woman at 32 weeks gestation presents to the birth suite with painful regular contractions. She has presented twice previously with the same complaint and each time been determined to have a closed, non-effacing cervix, a normal CTG and has been discharged home after 24 hours of observation. At her first presentation at 28 weeks she was given two doses of betamethasone. How should her pregnancy be managed?
Threatened
preterm Labour:: For women experiencing ongoing uterine irritability without any labour
(TPL) is a serious and should be treated according to best practice guidelines.
1 While some women who experience preterm
contractions will settle spontaneously, some will continue to experience
painful contractions, without cervical changes, for the remainder of their
pregnancy. The management of the ‘irritable uterus’ represents a dilemma in
management for clinicians.Any woman presenting with painful regular
contractions should be offered adequate analgesia and assessed for imminent
delivery. Physical assessment of the mother, including abdominal palpation
/.and cervical assessment via a speculum examination, vaginal examination or a
transvaginal ultrasound scan for cervical length
(TVCL)
2 should be undertaken, as well as tests such as fetal fibronectin (fFN)
detection to establish the likelihood of delivery.
Depending
on gestation and local facility guidelines, it may be
appropriate
to consider tocolysis and steroid cover. A number of
women
will not demonstrate any of the features of labour and a
diagnosis
of irritable uterus may be entertained.
Irritable
uterine activity may commence at any stage during a
pregnancy
and persist for its entirety or be only a transient experience Inflammatory
conditions, such as subclinical horioamnionitis, upper genital tract infection
and urinary tract infections or pyelonephritis,
may
be associated with irritable contractions.
Likewise,
gastrointestinal
problems, such as gastroenteritis with vomiting and
diarrhoea
or even significant constipation, may also trigger uterine
irritability.
Assessment should include investigations for inflammatory
causes,
genital and cervical culture swabs. Other causes for uterine
irritability
include subchorionic placental bleeding. ultrasound scan
for
fetal growth and well-being and examination of the placenta for evidence
of concealed bleeding may be performed in conjunction with
TVCL assessment.
Identification
and, where possible, treatment of underlying causes
of
uterine irritability may allow for complete resolution. Admission to
the
antenatal ward for ongoing observation and assessment is often
warranted.
Occasionally, contractions thought to be associated
with
TPL or uterine irritability may be the result of pseudo-labour, a
poorly
understood variant of conversion disorder, often associated
with
anxiety and emotional disturbance
obvious
cause, antenatal care can usually proceed in the normal
manner.
Maintenance tocolysis is not recommended for uterine
irritability.
8,9,10,11,12 Not only have studies demonstrated that they are
of
questionable value in terms of prolonging the pregnancy, but it is
also
suggested that women with uterine irritability may demonstrate
resistance
to commonly used tocolytics. 13 Vaginal progesterone may
play
a role in prolonging pregnancy to 34 weeks. 14,15,16,17 Further
analysis
is still required to determine if improvement in neonatal
outcomes
warrants this intervention for women with irritable uterus.
uterine
irritability is associated with a higher rate of preterm delivery
than
the general population (although lower than for women with
other
preterm labour risk factors). 13 It is possible that a woman with
ongoing
irritable uterine contractions may develop preterm labour,
but
fail to recognise it until ‘too late’. Thus the question facing
clinicians
revolves around how to mitigate these risks.
Administering
corticosteroids for fetal lung maturity is a routine
part
of managing preterm labour. It has been demonstrated that a
single
course of corticosteroids administered after 27 weeks is as
efficacious
as multiple ‘rescue’ doses. 18 It could be proposed that
all
women presenting with contractions after 27 weeks gestation
be
given corticosteroids at their initial presentation, regardless of
cervical
assessment or likelihood of imminent delivery, in order to
ensure
optimal fetal lung maturity.
Infants
delivered prior to 37 weeks gestation are at increased
risk
from group B streptococcal infection and women in preterm
labour
should receive antibiotic prophylaxis. 1,19 Antibiotic cover
needs
to be initiated at least hours hours prior to delivery in order
to
have the full protective effect. The key to management remains
careful
surveillance.
Many
women will self-refer for assessment due to concerns
regarding
the changing nature of their ‘regular’ uterine irritability,
suspected
ruptured membranes, bleeding or altered fetal movement
patterns.
For women with other risk factors for preterm labour,
regular
TVCL measurement may be necessary and repeat fFN
assessment
may be warranted.
Our
primigravida is almost certainly experiencing an irritable uterus.
She
was given corticosteroids at her first admission at 28 weeks,
and
evidence suggests her baby will not benefit from any further 
Women’s
health
doses.
Management at this presentation should consist of analgesia
and
routine assessment, including CTG monitoring. She should
have
cervical assessment incorporating swabs for fFN, vaginal and
endocervical
cultures. Cervical dilatation should be checked and
urine
analysis performed.
If
it is determined she is in labour, she will require antibiotics and
possibly
transfer to an appropriate facility. If the assessment does
not
suggest imminent delivery, she should have an ultrasound scan
arranged,
including TVCL. Admission to the antenatal ward may be
appropriate
and any possible underlying causes of uterine irritability
should
be identified and treated.
Her
ongoing antenatal care should involve careful assessment
of
uterine activity and causes of uterine irritation should
continue
to be explored. There is no indication for prophylactic
tocolysis;
however, vaginal progesterone may be of benefit. Her
management
should include assessment of any contributing
psycho-social
factors, in addition to providing reassurance that her
concerns
are being taken seriously.
Encouragingly,
many women with this presentation will continue
their
pregnancy to term and deliver without complications.
References
Goldenberg
RL. (2002). The management of preterm labor. Obstetrics 1
and
Gynecology, 31(5 Pt 1), 354–358.
2
kagan kO, To M, Tsoi E & Nicolaides kH. Preterm birth: the value
of
sonographic measurement of cervical length. BJOG, 113 Suppl,
52–6.
3
Goldenberg RL, Mercer BM, Meis PJ, Copper RL, Das A & McNellis
D.
The Preterm Prediction Study: Fetal Fibronectin Testing and
Spontaneous
Preterm Birth. Obstetrics Gynecology, 87(1), 643–648.
4
Tsoi E, Akmal S, Geerts L, Jeffery B, & Nicolaides, kH. Sonographic
measurement
of cervical length and fetal fibronectin testing in
threatened
preterm labor. ultrasound in Obstetrics Gynecology, 27(4),
368–372.
5
Goldenberg RL, Thom E, Moawad AH, Johnson F, Roberts J &
Caritis
SN. The Preterm Prediction Study: Fetal Fibronectin, Bacterial
Vaginosis,
and Peripartum Infection. Obstetrics Gynecology, 87(1),
656–660.
6
7
8
9
10
11
12
13
14
15
16
17
18
19
Romero
R, Espinoza J, Gonçalves LF, kusanovic JP Friel LA & Nien Jk. ,
Inflammation
in preterm and term labour and delivery. Seminars in
Fetal
Neonatal Medicine, 11(5), 317–26.
Lyman
D. Pseudolabor: A New Conversion Disorder Subtype? A Case
Presentation
and Literature Review. Primary Care Companion to the
Journal
of Clinical Psychiatry, 6(2), 61–64.
Dodd
JM, Crowther CA, Dare MR & Middleton P Oral betamimetics .
for
maintenance therapy after threatened preterm labour. Cochrane
database
of systematic reviews Online, (1), CD003927.
Gaunekar
NN & Crowther CA. Maintenance therapy with calcium
channel
blockers for preventing preterm birth after threatened preterm
labour.
Cochrane Database of Systematic Reviews, (3), CD004071.
Han
S, Crowther CA & Moore V. Magnesium maintenance therapy for
preventing
preterm birth after threatened preterm labour. Cochrane
database
of systematic reviews Online, (7), CD000940.
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