What is the clinical history of chorioamnionitis?

Updated: May 08, 2018
  • Author: Fayez M Bany-Mohammed, MD; Chief Editor: Ted Rosenkrantz, MD  more...
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Of these criteria, intrapartum maternal fever appears to be the most frequent and necessary to make the diagnosis of intrauterine infection according to the workshop conducted by NICHD [2] and later endorsed by the American College of Obstetricians and Gynecologists (ACOG). [30] According to this report, women who have fever without other chorioamnionitis symptoms or signs are regarded as having “isolated fever” and should not be diagnosed as having chorioamnionitis or “triple I.” Additionally, the NICHD report deemphasized nonspecific signs like uterine tenderness, maternal tachycardia, and vaginal discharge because some of these signs occur during the normal course of physiologic labor or can be masked by neuraxial anesthesia. Of note, for treatment purposes, ACOG further suggests that patients with isolated fever of at least 39.0°C (102.2°F) should be managed as having suspected intraamniotic infection. [30]

When at least two of the aforementioned criteria are present, the risk of neonatal sepsis is increased. Each clinical sign and symptom of chorioamnionitis, however, is by itself of low predictive value. The signs and symptoms of maternal chorioamnionitis are so subjective and the term “chorioamnionitis,” which should be reserved to describe histologic changes in the placenta and membranes, has been used widely by clinicians, sometimes to describe isolated intrapartum low-grade fever. This has led to too many asymptomatic newborns being evaluated for early-onset sepsis (EOS) and being unnecessarily exposed to antibiotics, with significant variations in practice among neonatal intensive care unitis (NICUs). [121] The NICHD workshop expert panel report, even though not considered a formal consensus recommendation by the NICHD, is a step in the right direction to define the problem and recommend a unified approach for diagnosis and management of chorioamnionitis, both for obstetric and neonatal care providers.

The NICHD workshop recommended using the term “triple I” to address the heterogeneity of this disorder. The term "triple I" refers to intrauterine infection or inflammation or both, and it is defined by strict diagnostic criteria (see Diagnostic Considerations); however, this terminology has not been universally accepted. [3] It is important to differentiate between clinical and histologic chorioamnionitis; the latter tend to be “silent” and present only with preterm labor or preterm premature rupture of membranes (PPROM). The risk of neonatal sepsis is increased when chorioamnionitis is diagnosed in the laboring mother; however, the risk is much lower than anticipated based on historical figures when widespread use of intrapartum antibiotics was not a common practice. [4]

An increasing or decreasing total leukocyte count may be more important than a single determination. Abnormalities in either umbilical vein interleukin (IL)-6 levels or an increasing neonatal immature-to-total neutrophil ratio, along with clinical criteria associated with chorioamnionitis, improve the sensitivity and predictive accuracy of identifying the septic neonate.

Although many cytokines and inflammatory markers have been proposed as diagnostic tests for EOS in the newborn, none has been of sufficient predictive value to gain wide acceptance. [10, 122, 123] Some cytokines are only secreted over a limited time frame during the start of infection, and inflammatory markers may be more sustained in their presence. Levels of C-reactive proteins (CRPs) are useful to exclude infection and discontinue antibiotics. Some investigators suggest that using a combination of markers like CRP, procalcitonin, IL-6, presepsin (soluble CD14 subtype), in conjunction with other cell-surface antigens such as CD11b, CD64, and human leukocyte antigen-antigen D related (HLA-DR) may enhance the laboratory diagnosis of EOS. [124, 125, 126]


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