Discussion
Though, it was suspected preoperatively, the diagnosis of clinical
chorioamnionitis was made at surgery as the liquor was very foul
smelling. The risk factors were preterm pre-labour rupture of membranes
(PROM) and gestational diabetes. There was initially no maternal fever
which is present in most cases. This confirmed that knowing the risk
factors can add to the diagnostic accuracy, as in all situation
treatment needs to be initiated based on clinical diagnosis. Hence the
definition of chorioamnionitis varies according to the key diagnostic
criteria which can be clinical based on the presence of typical findings
like maternal fever and tachycardia and foul-smelling liquor or vaginal
discharge; microbiologic based on the culture of microbes from properly
collected amniotic fluid or chorioamnion histo-pathologic based on
microscopic evidence of infection or inflammation on examination of
placenta or chorioamnionic specimen. Histologic chorioamnionitis is a
more common diagnosis as it includes both subclinical and clinical
chorioamnionitis. Funisitis occurs when infection/inflammation extends
to the umbilical cord1,2-4.
When chorioamnionitis is suspected in the absence typical clinical
signs, biochemical, serum or amniotic fluid tests may be used to
diagnose subclinical chorioamnionitis. Amniocentesis for amniotic fluid
culture is the best method for diagnosis of subclinical chorioamnionitis
in preterm gestations. Other tests that can be obtained rapidly include
white cell count, c-Reactive Protein (CRP) level, leukocyte esterase
level, gram stain and glucose concentration and cytokine level
(IL-6)1,5-7. Blood culture was not done in our patient
as she initially did not have fever. Ideally this should be done prior
to administration of antibiotics which should be done within an hour of
recognition of severe sepsis and sepsis bundle protocol should be
implemented. Critical care outreach team should be contacted if
indicated8.
The maternal complications of chorioamnionitis are postpartum
haemorhage, endometritis, wound infection, sepsis and death. The
neonatal complications include premature birth, stillbirth, neonatal
sepsis, chronic lung disease and brain injury causing cerebral palsy and
other neuro-developmental disabilities1,5-6.
Route of infection is ascending infection in 96% of cases. The
remainder are from haematogenous spread due to maternal septiaemia,
iatrogenic from procedures like amniocentensis and CVS. Infection from
the peritoneum via the fallopian tubes have been
postulated1,2.
The most common organisms identified in pregnant women dying from sepsis
are genital mycoplasmas, Lancefield group A beta haemolytic
streptococcus and Escherichia Coli9. E. Coli belongs
to the family of Enterobacteriaceae - a large order of different types
of bacteria that commonly cause infections both in healthcare settings
and in communities. To survive the effects of antibiotics, some
Enterobacteriaceae produce extended-spectrum beta-lactamase (ESBL)
enzyme that destroy and render ineffective commonly used antibiotics
like penicillins and 1st, 2nd and
3rd generation cephalosporins, but not cephamycin and
carbapenems. This resistance means fewer antibiotic options available to
treat ESBL producing bacterial infection and even more common infection
caused by such organism may require more complex treatment requiring
prolonged hospitalization and intravenous carbapenem antibiotics - a
class of highly effective antibiotic agents commonly used for the
treatment of severe or high-risk bacterial
infections9-11. This class of antibiotics is usually
reserved for known or suspected multidrug-resistant bacterial
infections. Resistance that render these antibiotics ineffective are on
the rise too. Therefore, appropriate and justified use of this important
class of antibiotics is necessary to decrease the risk of emergence of
resistance. Our patient’s specimen from placental tissue and wound pus
culture was resistant to commonly used antibiotics and was sensitive
only to Meropenem, Ertapenem and Gentamicin. Resistance that destroys
these antibiotics are on the rise
too. The more we rely on this
important class of antibiotics, the greater the risk of spreading
resistance to them. This mandates the practice of sending appropriate
specimens for culture before initiating antimicrobials as well as
implementation of stewardship programs to regulate the appropriate use
of antimicrobials to reduce emergence of resistance. As well as, robust
infection control practices that help to prevent cross transmission of
infection11.
ESBL- producing organisms were first found in Europe and the earliest
cases were identified in the USA in 198810. A pooled
prevalence of faecal colonization of 14% globally was estimated by a
systematic review9 and Villa HE10 et
al in Argentina quoted 5.4% of pregnant women in their study had
ESBL-producing E coli vaginal colonization revealing that colonization
with resistant Enterobacteriaceae is significant in pregnancy. A higher
prevalence of 22% was reported in South-Asia9 where
our patient came from.
According to CDC, ESBL-producing Enterobacteriaceae pose challenging
infection control issues and are a serious global threat that requires
prompt and sustained action12. Appropriate use of
antibiotic therapy under the guidance of infectious disease team is
imperative. Prophylactic use of antibiotics during conservative
management of PROM and prompt delivery after 34 weeks will help reduce
the risk of infection. Screening strategies designed to monitor for
ESBL-producing E. coli could be useful in women from endemic areas to
prevent perinatal transmission and the introduction of multi-resistant
strains to the maternity ward.