MRI findings associated with placenta accreta include dark T2 bands, bulging of the uterus, and loss of the dark T2 interface.Although there are isolated case reports of placenta accreta being diagnosed in the first trimester or at the time of abortion <20 weeks gestational age, the predictive value of first-trimester ultrasound for this diagnosis remains unknown. Women with a placenta previa or "low-lying placenta" overlying a uterine scar early in pregnancy should undergo follow-up imaging in the third trimester with attention to the potential presence of placenta accreta. Complications
Damage to local organs (e.g., bowel, bladder, uterus and neurovascular structures in the retroperitoneum and lateral pelvic sidewalls from placental implantation and its removal;
Postoperative bleeding requiring repeated surgery;
Amniotic fluid embolism;
Complications (such as dilutional coagulopathy, consumptive coagulopathy, acute transfusion reactions, transfusion-associated lung injury, acute respiratory distress syndrome, and electrolyte abnormalities) caused by transfusion of large volumes of blood products, crystalloids, and other volume expanders;
Postoperative thromboembolism, infection, multisystem organ failure, and maternal death.The exact incidence of maternal mortality related to placenta accreta and its complications is unknown, but it is significant, especially if the urinary bladder is involved

Treatment
Treatment may be delivery by caesarean section and abdominal hysterectomy if placenta accreta is diagnosed before birth. Oxytocin and antibiotics are used for post-surgical management. When there is partially separated placenta with focal accreta, best option is removal of placenta. If it is important to save the womans uterus (for future pregnancies) then resection around the placenta may be successful.
These three compounds are formed by means of similar chemical processes, and oil that contains one of the three substances is likely to contain the other two. Oil samples that are suspected to have been ingested by people who later developed TOS often contain all three of these contaminants (among other substances), but are most likely to contain OOPAP. However, when these three substances were given to laboratory animals, OOPAP was not acutely toxic, PAP was toxic only after injection, but not after oral administration, and OPAP was toxic only after injection of high doses. Therefore, none of these three substances is thought to cause TOS. Similar results were obtained after administration of fatty acid anilides.Data discrepancies combined with both a high level of secrecy surrounding the huge investigation and the fact that the first cases of the syndrome were located in Madrid (near the U.S. military base in Torrejón de Ardoz) spread the idea of a conspiracy. Several of those affected by TOS claim they never consumed any of the tainted oil products. Furthermore, the tainted oil was primarily sold in low-cost street markets; yet, a considerable percentage of the patients were wealthy. Another theory suggests the toxic reaction was triggered by organophosphate poisoning (e. g., from pesticide residues in tomatoes) and covered up by the Spanish government and the WHO. See also
Eosinophilia-myalgia syndrome
Ginger Jake
Health crisis
The Jungle
List of food contamination incidents

References
External links
WHO Report: Toxic Oil Syndrome - Ten years of progress