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A COMPLEX CASE OF PORTAL VEIN THROMBOSIS IN THE POSTPARTUM PERIOD
Karlee Mott
*1, Ross M. Dies
1, Brendan Chou
1, Mohammad Al Efishat
1,21LSU Health New Orleans, New Orleans, LA; 2Our Lady of the Lake Regional Medical Center, Baton Rouge, LA
Introduction: Hypercoagulability in pregnancy is a protective physiological adaptation that reduces the risk of postpartum hemorrhage. Hormonal shifts increase clotting factors, decrease fibrinolysis, and increase resistance to protein C
1,2. The resulting prothrombotic state most commonly presents as deep vein thrombosis or pulmonary embolism
1. We aim to describe the case of a multiparous woman with a rare presentation of portal vein thrombosis (PVT).
Case: A 27-year-old woman, G2P0202, with no prior history of thrombosis or hypercoagulability presented to the emergency department 26 days postpartum with severe abdominal pain. Her obstetric course had been complicated by iron deficiency anemia and preeclampsia. However, she had an uncomplicated spontaneous vaginal delivery at 36 weeks gestational age. On examination, she was febrile, tachycardic, tachypneic, and peritonitic. Contrast enhanced computed tomography revealed a Yerdel Grade III portal vein thrombus extending into the proximal splenic vein and diffusely involving the superior mesenteric vein and its branches. Emergent laparotomy identified 45cm of necrotic small bowel, which was resected. Postoperative therapeutic anticoagulation with continuous heparin was initiated. Overnight, the patient experienced severe hematemesis. Endoscopy suggested the bleeding originated from the anastomotic site. Anticoagulation was held, and blood products were transfused. Suction thrombectomy was performed to restore patency of the portal vein. The patient’s postoperative course was further complicated by a symptomatic abdominal hematoma, acute kidney injury, pleural effusion, and decompensated heart failure. Thrombophilia workup was negative for anticardiolipin antibodies, beta-2-glycoprotein I antibodies, factor II DNA mutations, factor V activation, dilute Russell's Viper Venom time, and JAK2 mutations. Her PVT was attributed to physiological changes of pregnancy. The patient was discharged on rivaroxaban and advised that future pregnancies would pose significant, life-threatening risks.
Discussion: Portal vein thrombosis is an uncommon manifestation of postpartum hypercoagulability. Risk factors associated with thrombosis include advanced maternal age, obesity, operative delivery, decreased mobility, inherited or acquired thrombophilia, a personal or family history of thrombosis, and smoking
1,3. In this case, the patient’s history was significant only for preeclampsia. Anticoagulation is the mainstay of treatment for PVT, rather than surgical or percutaneous thrombectomy, due to the heightened risk of recurrence from intimal trauma
2. However, in this patient with postoperative bleeding, a procedural approach was warranted. This case underscores the importance of thoroughly evaluating postpartum abdominal pain and performing a comprehensive assessment of thrombotic risk to prevent life-altering sequelae.
Axial contrast enhanced computed tomography
Coronal contrast enhanced computed tomography
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