Severe fetal hemorrhage and maternal coagulopathy following intentional bromadiolone ingestion in late pregnancy: a case report
- 1Department of Obstetrics and Gynecology, Hangzhou Xiaoshan Second People’s Hospital, Hangzhou, Zhejiang, China
- 2Department of Science and Education, Hangzhou Xiaoshan Second People’s Hospital, Hangzhou, Zhejiang, China
- 3Department of Pediatrics, Hangzhou Xiaoshan Second People’s Hospital, Hangzhou, Zhejiang, China
Abstract
Introduction and importance:: Long-acting anticoagulant rodenticide poisoning during pregnancy is extremely rare but potentially catastrophic. Bromadiolone, a highly lipophilic superwarfarin, crosses the placenta and can cause fetal coagulopathy.
Case presentation:: A 19-year-old primigravida at 37 weeks of gestation presented with abdominal pain and fetal distress. Ultrasound showed mild fetal ventriculomegaly and pleural and pericardial effusions. An emergency cesarean delivery was performed for a Category III fetal heart rate tracing. The neonate died shortly after birth, with copious bright red blood observed in the airway during intubation. Postoperatively, the mother developed profound coagulopathy (PT >150 s, unmeasurable INR, prolonged aPTT) with preserved platelet count and fibrinogen. Repeated history-taking revealed intentional ingestion of bromadiolone bait 12 days earlier. She was treated successfully with fresh frozen plasma and prolonged vitamin K1 therapy.
Clinical discussion:: Marked PT/aPTT prolongation with normal platelet count and fibrinogen supported acquired vitamin K-dependent factor deficiency rather than obstetric DIC. Although toxicological confirmation and autopsy were unavailable, the exposure history, coagulation pattern, neonatal airway bleeding, and response to vitamin K1 strongly supported bromadiolone-associated coagulopathy with suspected severe perinatal hemorrhage.
Conclusion:: LAAR poisoning should be considered in pregnant patients with unexplained severe coagulopathy and a preserved platelet count and fibrinogen levels. Delayed fetal compromise may occur even when maternal symptoms are minimal. Early multidisciplinary management, prolonged vitamin K1 therapy, and psychosocial support are important.
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BibTeX
@article{chen2026severe,
title = {{Severe fetal hemorrhage and maternal coagulopathy following intentional bromadiolone ingestion in late pregnancy: a case report}},
author = {Zhiyan Chen and Meifeng Shen and Chenyang Ma and Huifei Kong},
journal = {International Journal of Surgery Case Reports},
year = {2026},
month = oct,
doi = {10.1097/rc9.0000000000001043},
url = {https://doi.org/10.1097/rc9.0000000000001043},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Severe fetal hemorrhage and maternal coagulopathy following intentional bromadiolone ingestion in late pregnancy: a case report
AU - Zhiyan Chen
AU - Meifeng Shen
AU - Chenyang Ma
AU - Huifei Kong
PY - 2026
DA - 2026/10/07
JO - International Journal of Surgery Case Reports
DO - 10.1097/rc9.0000000000001043
UR - https://doi.org/10.1097/rc9.0000000000001043
AB - Introduction and importance:: Long-acting anticoagulant rodenticide poisoning during pregnancy is extremely rare but potentially catastrophic. Bromadiolone, a highly lipophilic superwarfarin, crosses the placenta and can cause fetal coagulopathy. Case presentation:: A 19-year-old primigravida at 37 weeks of gestation presented with abdominal pain and fetal distress. Ultrasound showed mild fetal ventriculomegaly and pleural and pericardial effusions. An emergency cesarean delivery was performed for a Category III fetal heart rate tracing. The neonate died shortly after birth, with copious bright red blood observed in the airway during intubation. Postoperatively, the mother developed profound coagulopathy (PT >150 s, unmeasurable INR, prolonged aPTT) with preserved platelet count and fibrinogen. Repeated history-taking revealed intentional ingestion of bromadiolone bait 12 days earlier. She was treated successfully with fresh frozen plasma and prolonged vitamin K1 therapy. Clinical discussion:: Marked PT/aPTT prolongation with normal platelet count and fibrinogen supported acquired vitamin K-dependent factor deficiency rather than obstetric DIC. Although toxicological confirmation and autopsy were unavailable, the exposure history, coagulation pattern, neonatal airway bleeding, and response to vitamin K1 strongly supported bromadiolone-associated coagulopathy with suspected severe perinatal hemorrhage. Conclusion:: LAAR poisoning should be considered in pregnant patients with unexplained severe coagulopathy and a preserved platelet count and fibrinogen levels. Delayed fetal compromise may occur even when maternal symptoms are minimal. Early multidisciplinary management, prolonged vitamin K1 therapy, and psychosocial support are important.
SN - 2210-2612
ER -