Introduction
Chorioamnionitis is a distinctive complication of the pregnancy associated with the inflammation of the amniotic membrane and is the primary cause of neonatal and maternal morbidity. Chorioamnionitis infection results from acute inflammation of the chorion and placental membranes, commonly because of the polymicrobial bacterial infection in the initiation of membrane rupture (Peng, Chang, Lin, Cheng, & Su, 2018). Chorioamnionitis is often caused by infection and typically results from the untimely rapture of the protective membranes. The condition is characteristically caused by the polymicrobial infection resulting from the Mycoplasma hominis, Ureaplasma urealyticum, Gram-negative anaerobes. The primary treatment includes antipyretics, antimicrobial agents, supportive care, and expedition of delivery. Further research is necessary for the identification of early biomarkers and mechanistic pathways that accurately predict patients at higher risk of adverse neonatal and maternal outcomes for the development of more effective prevention and treatment interventions.
Etiology
Chorioamnionitis is an aftereffect of the ascending bacteria from the cervix and vagina and commonly perceived as a secondary complication of a delayed rupture of the membranes. The less common transmission mode is the hematogenous transmission as a result of an invasive procedure. Various viral, bacteria and often fungal agents are associated with the underlying pathogenesis of the condition and preterm birth. The commonly cited pathogenesis includes Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, Neisseria gonorrhea, Trichomonas vaginalis, and group B streptococcus. Other bacterial agents are gram-negative anaerobes, such as Bacteroides species and Gardnerella vaginalis. Cultured specimens with clinical chorioamnionitis tend to reveal polymicrobial infection with most patients having at least two visible pathogens. The rate of isolation of some pathogens varies with tissue and study analyzed. The most common isolates ate G. vaginalis and U. urealyticum. Equivalent microbiological isolates were identified within the amniotic fluid of the infected women with U. urealyticum being the highly detected pathogen.
Viruses also assume a critical role in the condition, and they include adenovirus, cytomegalovirus, Epstein-Barr virus, enterovirus, and respiratory syncytial virus. According to Czikk, McCarthy, and Murphy (2011), recent studies have revealed a strongly linked placental adenovirus with histological chorioamnionitis. Despite the isolation and implication of these viruses in cases of chorioamnionitis, there is limited supportive evidence. Fungal organisms have similarly been associated with the condition. Such cases are associated with in vitro fertilization pregnancies, prolonged membrane, and intrauterine contraceptive devices. Despite their rarity, fungal associated complications can be extremely severe.
Risk Factors
There are a number of risk factors for the condition apart from the colonization of viruses and bacteria. Risk factors, at term, include the rapture of membranes, prolonged labor, and nulliparity. In addition, patients with prolonged labor, premature membrane raptures at term with are exposed to multiple vaginal examinations and meconium-stained liquor are at an increased risk of developing chorioamnionitis.
Diagnosis
The diagnosis of chorioamnionitis is through clinical or histological criteria. The clinical diagnosis is premised on symptoms and signs of systemic or local infection. The typical definition comprises maternal pyrexia and either of the following: uterine tenderness, maternal tachycardia, high maternal white-blood-cell count, foul vaginal discharge, fetal tachycardia, and abdominal pain. For maternal pyrexia, the cut-off varies widely, although a value of >38.0C is commonly quoted for purposes of definition and to exclude patients with low-grade fever not associated with an infectious process. Histologically, chorioamnionitis is possible and is staged based on specific measures, with the development of necrosis and increasing neutrophil infiltration and the thickening of amnion basement membrane and chorionic microabscesses, as well as the advancement of fetal inflammatory response from chorionic/umbilical vasculitis to necrotizing funisitis. Clinically, the diagnosis of chorioamnionitis is conversely not confirmed by microbiological or histological examinations.
Amniotic fluid culture is considered ideal for the isolation of bacteria, and amniocentesis is the reference standard for the diagnosis. However, the test is associated with forty-eight-hour delay of cultures without evidence of predictive value for possible neonatal and maternal outcomes. Furthermore, the number of trials is insufficient to demonstrate the efficacy of the approach to the reduction of neonatal and maternal morbidity. There is a strong correlation between clinical early-onset sepsis and inflected amniotic cultures, although there is still insufficient evidence to support the application of amniocentesis for diagnosis purposes. Evidence backing the application of blood cultures for the purpose of diagnosis is similarly limited, as it appears that maternal blood cultures do not provide relevant information to warrant changes in clinical management. In addition, there is limited evidence to demonstrate the benefit of the application of vaginal swabs for the management and diagnosis of chorioamnionitis.
Multiple laboratory tests have been examined for the possible value in the timely prediction and diagnosis of the condition. A low glucose measurement in the amniotic fluid has been proved as a predictive but insensitive marker for the infection. At the same time, Erdemir et al (2013) list placental alkaline phosphatase, matrix metalloproteinase-8, interleukin-8, interleukin-6, ferritin and C-reactive protein as potential biomarkers of chorioamnionitis. The effectiveness and reliability of these biomarkers are yet to be confirmed through clinical trials. Other biomarkers, including thrombin-antithrombin complex, salivary proteases, relaxin, and fetal fibronectin have been examined but tend to be more specific in the prediction of the preterm births as opposed to chorioamnionitis. Protein biomarkers, such as neutrophil defensin-1 and 2 and calgranulin-A and B have been linked to the inflammation of the placenta and the amniotic membrane. These have been biomarkers have been associated with histological chorioamnionitis, as well as neonatal sepsis. Further technological development in diagnosis will be critical in the determination of the risk of adverse outcomes from the supposed intra-amniotic infection and ultimately chorioamnionitis.
Treatment and Prevention
The treatment of acute cases of chorioamnionitis included antipyretics, antimicrobial agents, management of symptoms and expedition delivery. A specific antibiotic regimen is not known despite the prevalence of the infection. Intravenous ampicillin is used for coverage of gram-positive agents whereas clindamycin is used to address anaerobes for cesarean cases. The treatment regimen varies widely across the literature (Peng, Chang, Lin, Cheng, & Su, 2018). Trials have concentrated on variations in the timing and dosage of drug administration and changes in the coverage spectrum. Preventive strategies to mitigate chorioamnionitis and related neonatal outcomes have concentrated on the coverage of risk factors. PPROM is among the key risk factors for the disease, and its subsequent coverage will lower the risk of infection and adverse neonatal outcomes.
Conclusion
Chorioamnionitis is an obstetric problem that can result in significant neonatal and maternal mortality and morbidity. The infection is diagnosed based on histological and clinical outcomes. prompt treatment is recommended following the identification of chorioamnionitis using broad-spectrum antipyretics, antibiotics, expedition delivery, and supportive care. Further research is necessary for the characterization of microbial communities located within the female genital tract. In addition, further research is necessary for the identification of predictive and screening tests, with effective prospective validation of possible tests before widespread adoption.
References
Czikk, M. J., McCarthy, F. P., & Murphy, K. E. (2011). Chorioamnionitis: from pathogenesis to treatment. Clinical Microbiology and Infection, 17, 9.)Erdemir, G., Kultursay, N., Calkavur, S., Zekio??lu, O., Koroglu, O. A., Cakmak, B., Yalaz, M.,
Sagol, S. (2013). Histological Chorioamnionitis: Effects on Premature Delivery and
Neonatal Prognosis. Pediatrics & Neonatology, 54, 4, 267-274.
Peng, C., Chang, J., Lin, H., Cheng, P., & Su, B. (2018). Intrauterine inflammation, infection, or both (Triple I): A new concept for chorioamnionitis. Pediatrics & Neonatology, 59(3), 231-237. doi:10.1016/j.pedneo.2017.09.001
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