# Placenta Percreta in the Absence of a Previous Uterine Scar

## TL;DR

Two rare cases of placenta percreta occurred in women without prior uterine surgery, suggesting non-surgical factors like beta-thalassemia may contribute to this dangerous condition.

## Contribution

Reports two rare cases of placenta percreta without prior uterine scars and suggests beta-thalassemia as a possible contributing factor.

## Key findings

- Placenta percreta occurred in a woman with beta-thalassemia and a prior cesarean section, leading to maternal death.
- Another case of placenta percreta was found in a multiparous woman with no surgical history and resulted in a favorable outcome after hysterectomy.
- Systemic conditions like beta-thalassemia, chronic hypoxia, and oxidative stress may contribute to abnormal placental invasion.

## Abstract

Placenta accreta spectrum (PAS) encompasses abnormal placental adherence to the myometrium, ranging from accreta to percreta, and is a major cause of life-threatening hemorrhage. While prior cesarean section and placenta previa are the main risk factors, PAS in the absence of uterine scarring is rare. We report two cases of PAS without prior uterine surgery. The first involved a 42-year-old woman with beta-thalassemia major and a history of cesarean section, who conceived via in vitro fertilization (IVF). She presented at 30 weeks with acute abdominal pain, hypovolemic shock, and fetal demise. Emergency laparotomy revealed posterior uterine rupture and placenta percreta. Despite a hysterectomy and repeated interventions, the patient died due to uncontrolled hemorrhage and coagulopathy. The second case involved a multiparous woman with no surgical history, who presented at 32 weeks with severe bleeding and fetal distress. Intraoperatively, an anterior placenta percreta invading through the uterine serosa was found. A hysterectomy was performed with a favorable maternal outcome. These cases highlight PAS occurrence in women without prior uterine scars, suggesting that additional factors such as beta-thalassemia, chronic hypoxia, oxidative stress, and altered angiogenesis may contribute to abnormal placental invasion. The first case strongly suggests a possible association between beta-thalassemia and PAS. Spontaneous uterine rupture due to unrecognized PAS underscores the need for vigilance even in low-risk women. PAS can occur without classic risk factors and may be linked to systemic conditions such as beta-thalassemia. Early recognition, multidisciplinary management, and timely hysterectomy are crucial to improving maternal outcomes. Further studies are warranted to clarify the role of beta-thalassemia and other non-surgical risk factors in PAS pathogenesis.