Introduction: Birth Asphyxia is a severe condition that includes many potential pathways of occurrence both in utero and during childbirth. We aimed to identify and describe specific macroscopic and microscopic placental injuries in birth asphyxia to serve as a quick tool to stratify a newborn’s potential further evolution, as hypoxic-ischemic encephalopathy can be responsible for neonatal death or severe neurologic sequelae further compromising the affected persons’ quality of life. Materials and methods: We conducted an observational prospective study over 3 years. 62 patients diagnosed with birth asphyxia which had placental histopathological examination performed were enrolled. The control group consisted of 69 term newborns that required neonatal intensive care for at least three days, in the same period, for any other reason and that also had available placental exams. In our study, placental histopathological lesions identified in birth asphyxia have been classified according to Amsterdam Criteria. Results: We analysed data gathered from both groups by applying specific statistical tests for each type of variable and hypothesis. Thus, umbilical cord abnormalities were associated with hypoxic-ischemic encephalopathy in a statistically significant manner when comparing the birth asphyxia group of newborns with the control group. Also, we identified a high statistical level of significance for maternal and fetal vascular malperfusion and the occurrence of hypoxic-ischemic syndrome when comparing the two groups (p = .00). Conclusion: The macroscopic and microscopic placental examination can provide important information on the evolution of the disease in selected newborns according to the identified lesions.

Ureaplasma urealyticum and Ureaplasma parvum occupy an odd place in perinatal medicine: dismissed for decades as harmless residents of the female genital tract, they are now recognized as pathogens with real consequences for preterm newborns. This review traces that paradigm shift, from organisms once dismissed as harmless colonizers to pathogens now implicated in chorioamnionitis, preterm birth, and a range of serious neonatal morbidities, and describes the molecular mechanisms that underlie their pathogenicity: Toll-like receptor (TLR1/2/6/9)-mediated NF-κB and MyD88/IRAK4/TRAF6 signaling, NLRP3 inflammasome activation and pyroptosis, and blood–brain barrier disruption via claudin-5/occludin downregulation and MMP-mediated tight junction cleavage. We also review the evidence for biofilm-conferred antibiotic tolerance and the clinical associations between Ureaplasma colonization and intraventricular hemorrhage (pooled OR 1.62, 95% CI 1.23–2.13), bronchopulmonary dysplasia (pooled OR 2.30, 95% CI 1.65–3.20), late-onset sepsis, and neurodevelopmental impairment. Diagnosis remains a weak point: culture sensitivity is below 10% compared with polymerase chain reaction (PCR) testing, and no randomized trial has yet shown that microbiological eradication translates into better clinical outcomes—a gap we examine critically. Whether these organisms cause disease seems to depend on gestational age, bacterial load, serovar-specific virulence, and host immune competence. We argue that this conditionality calls for risk stratification rather than dismissal whenever Ureaplasma is identified in clinical specimens, and that the field needs a paradigm shift toward Ureaplasma screening in high-risk pregnancies and targeted neonatal PCR testing, backed by adequately powered interventional trials.