Placental correlates in categories of preterm births based on gestational age.

ABSTRACT

Placental abnormalities can precipitate preterm birth (PTB), a principal contributor to neonatal morbidity and mortality. This study targets understanding placental variations among different gestational age-based categories of PTB. METHODS: A three-year retrospective study conducted a detailed clinicopathological analysis of PTB placentas categorized by gestational age extremely preterm (EPTB,<28 weeks), very preterm (VPTB, 28 to 31 + 6 weeks), moderate preterm (MPTB, 32 to 33 + 6 weeks), and late preterm (LPTB, 34 to 36 + 6 weeks). Macroscopic parameters sourced from pathology records and microscopic examination assessed for maternal and fetal stromal-vascular lesions, inflammatory and hypoxic lesions and others. Stillbirths/intrauterine demise and multifetal gestation were excluded. Clinical data were gathered from medical records. RESULTS: A total of 645 preterm placentas were received and 538 were included. The majority were LPTB(46.3 %), while EPTB, VPTB and MPTB accounted for 5.8 %, 28.4 % and 19.5 % respectively. Low birth weight and low Apgar were prevalent in EPTB(p < 0.001), while obstetric complications were higher in other PTB categories. Placental infarction was higher in VPTB and MPTB(p = 0.006). On microscopy, maternal (48.4 %), fetal (29 %) inflammatory response and villous edema (48.4 %) was higher in EPTB(p = 0.04 & p < 0.001 respectively), while maternal stromal-vascular lesions were higher in VPTB and MPTB(67.3 % & 64.8 %, p < 0.001). Delayed villous maturation (17.7 %,p = 0.02), chronic chorioamnionitis (11.3 %,p = 0.02), membrane hypoxia (38.6 %,p = 0.007), and massive fibrin deposition (10.8 %,p < 0.001) featured higher in LPTB. DISCUSSION: Acute inflammatory pathology was common in EPTB, strongly suggesting inflammation in triggering parturition. Frequent obstetric complications and maternal stromal-vascular lesions in VPTB and MPTB may underscore maternal vascular compromise in this group. Villous maturation defects, chronic chorioamnionitis, massive fibrin deposition and membrane hypoxia in LPTB, likely contribute to long-term neonatal morbidity.