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Jurnal Pubmed Endo
Jurnal Pubmed Endo
Jurnal Pubmed Endo
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Introduction
Endometritis is inflammation of the uterine lining. It can affect all layers of the
uterus. The uterus is typically aseptic. However, the travel of microbes from the
cervix and vagina can lead to inflammation and infection. This condition usually
occurs as a result of the rupture of membranes during childbirth. Endometritis is the
most common postpartum infection. Puerperal endometritis is 25 times more
common in patients that underwent cesarean sections. Most cases of postpartum
endometritis are polymicrobial, involving aerobic and anaerobic bacteria.
Etiology
Endometritis results from the travel of normal bacterial flora from the cervix and
vagina. The uterus is sterile until the amniotic sac ruptures during childbirth.
Bacteria is more likely to colonize uterine tissue that has been devitalized, bleeding,
or otherwise damaged (such as during a cesarean section).[1]
Between 60% and 70% of infections are due to both aerobes and
anaerobes. Examples of anaerobic
species are Peptostreptococcus, Peptococcus, Bacteroides, Prevotella,
and Clostridium. Examples of aerobic species are
primarily groups A and B Streptococci, Enterococcus, Staphylococcus, Klebsiella
pneumoniae, Proteus species, and Escherichia coli. Uterine tissue damaged by
cesarean section is particularly susceptible to Streptococcus
pyogenes and Staphylococcus aureus. Chlamydia endometritis often presents at a
later date, seven or more days postpartum.[2][3]
Epidemiology
Puerperal endometritis is the most common postpartum infection.[4] In patients
without risk factors, following normal spontaneous vaginal delivery, there is an
incidence of 1% to 2%. Risk factors, however, can increase this rate to a 5% to 6%
risk of infection following vaginal delivery. Risk factors include chorioamnionitis,
low socioeconomic status, prolonged labor, membrane rupture, multiple cervical
examinations, internal fetal monitoring, young maternal age, nulliparity, obesity,
meconium-stained amniotic fluid, and bacterial colonization of the lower genital
tract with bacteria such as Group B streptococcus (GBS), Chlamydia
trachomatis, Mycoplasma hominis, Ureaplasma urealyticum, or Gardnerella
vaginalis. The route of delivery is the most significant risk factor for endometritis,
with cesarean deliveries (especially for multifetal gestation) having a much higher
likelihood of leading to endometritis and a 25-fold increase in infection-related
mortality.[5][6]
Pathophysiology
Most cases of endometritis result from childbirth. Specifically, the rupture of the
amniotic sac allows the translocation of normal bacterial flora from the cervix and
vagina to the usually aseptic uterus. This bacteria is more likely to colonize uterine
tissue that has been devitalized, bleeding, or otherwise damaged (such as during a
cesarean section). This bacteria can invade the endometrium-, myometrium-, and
perimetrium, causing inflammation and infection.
Treatment / Management
The threshold for obstetrics should be low in any provider considering a diagnosis
of endometritis. Oral antibiotic regimens are an option for mild disease. The options
are similar to those used for pelvic inflammatory disease:
For patients with moderate to severe endometritis and/or patients with endometritis
s/p cesarean section, intravenous antibiotics and admission are recommended.
Options are as follows:
Differential Diagnosis
In the patient with postpartum fever and abdominal pain, diagnoses other than
endometritis that merit consideration include urinary tract infections (including
pyelonephritis), pneumonia, septic pelvic thrombophlebitis. The clinician should
keep an open mind to these diagnoses, especially if antibiotic and/or surgical
management for endometritis is not leading to clinical improvement.
Prognosis
If untreated, the fatality rate of endometritis is approximately 17%. Thankfully this
is reduced to 2% with proper recognition and treatment. Cesarean deliveries
(especially for multifetal gestation) have a 25-fold increase in infection-related
mortality.[11]
Complications
Approximately 1% to 4% of patients will have complications such as sepsis,
abscesses, hematomas, septic pelvic thrombophlebitis, and necrotizing
fasciitis. Such complications can then lead to uterine necrosis, requiring a
hysterectomy for infection resolution. Surgical intervention may also be necessary
if the infection has produced a drainable fluid collection.[6]
Review Questions
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References
1.
Sherman D, Lurie S, Betzer M, Pinhasi Y, Arieli S, Boldur I. Uterine flora at
cesarean and its relationship to postpartum endometritis. Obstet
Gynecol. 1999 Nov;94(5 Pt 1):787-91. [PubMed]
2.
Morgan J, Roberts S. Maternal sepsis. Obstet Gynecol Clin North Am. 2013
Mar;40(1):69-87. [PubMed]
3.
Dalton E, Castillo E. Post partum infections: A review for the non-
OBGYN. Obstet Med. 2014 Sep;7(3):98-102. [PMC free article] [PubMed]
4.
Chaim W, Bashiri A, Bar-David J, Shoham-Vardi I, Mazor M. Prevalence
and clinical significance of postpartum endometritis and wound
infection. Infect Dis Obstet Gynecol. 2000;8(2):77-82. [PMC free article]
[PubMed]
5.
Boggess KA, Tita A, Jauk V, Saade G, Longo S, Clark EAS, Esplin S, Cleary
K, Wapner R, Letson K, Owens M, Blackwell S, Beamon C, Szychowski JM,
Andrews W., Cesarean Section Optimal Antibiotic Prophylaxis Trial
Consortium. Risk Factors for Postcesarean Maternal Infection in a Trial of
Extended-Spectrum Antibiotic Prophylaxis. Obstet Gynecol. 2017
Mar;129(3):481-485. [PMC free article] [PubMed]
6.
Karsnitz DB. Puerperal infections of the genital tract: a clinical review. J
Midwifery Womens Health. 2013 Nov-Dec;58(6):632-42. [PubMed]