2025 FSA Podium and Poster Abstracts

Mirror syndrome is a rare second- and third-trimester complication characterized by placental, maternal, and fetal edema (1). First described by John William Ballantyne in 1892, its exact cause remains unclear (1). Maternal symptoms resemble preeclampsia, including generalized edema, anemia, elevated liver enzymes, proteinuria, hypertension, and visual disturbances (2), but are distinguished by the concurrent presence of fetal hydrops and maternal edema (1). The condition carries significant maternal morbidity and fetal mortality, with rates as high as 67.3% (5). Management focuses on treating fetal hydrops, but severe cases often necessitate delivery or pregnancy termination (1). 

Figure 1: Proposed pathophysiology of preeclampsia and mirror syndrome. sFlt-1 levels disrupt VEGF signaling and reduce activation of the Flt-1 and Flk-1/KDR receptors. This results in altered mitochondrial oxygen consumption (OCR) and endothelial cells that shift toward a glycolytic phenotype (ECAR). The subsequent loss of mitochondrial bioenergetics increases oxidative stress (mtROS), which ultimately causes mitochondrial dysfunction with vascular changes and preeclampsia onset. 

This is a 38-year-old G5P0130 woman at 32w4d gestation with a history of obesity (BMI 32), GERD, hypertension, stillbirth, and right salpingectomy for ectopic pregnancy. Fetal hydrops was diagnosed 1/8/2025 requiring fetal transfusion on 1/9/2025. She received steroids on 1/11 and presented on 1/16 with sudden-onset dyspnea, dry cough, generalized edema, and worsening contractions over two days. Oxygen saturation remained normal without tachypnea. Exam revealed 1 cm cervical dilation, normal blood pressure, platelets (158), but evidence of hemolysis (LDH 431), elevated LFTs (ALT 216, AST 240), and low fibrinogen (143). Chest X-ray showed mild cardiomegaly and pulmonary congestion, while bedside TTE confirmed preserved ventricular function. She was diagnosed with Mirror syndrome and early atypical HELLP, prompting emergent C-section. 

Intraoperatively, she underwent C-section with magnesium for seizure prophylaxis and cryoprecipitate for hypofibrinogenemia. Precedex was used for anxiolysis, along with standard nausea prophylaxis and analgesia. Epidural supplementation was required for pain control, and a phenylephrine infusion for pressure support. Significant hemorrhage from the hysterotomy prompted intubation and initiation of a massive transfusion protocol (4 FFP, 2 platelets, 4 pRBCs, and cell saver blood). An infant was delivered atraumatically with 1- and 5-minute APGAR scores of 3 and 7. An enlarged, edematous, and fragmented placenta was removed. Uterine atony was managed with misoprostol, carboprost, oxytocin, and TXA, achieving hemostasis with an EBL of 3,596 mL. 

Her postpartum course was complicated by post-hemorrhagic anemia, acute CHF requiring pressors, and kidney injury requiring dialysis. She was extubated on 2/7 with stable hemodynamics and renal function and discharged on 2/10 in stable condition with outpatient follow-up. The neonate continues to receive NICU care. 

This case highlights the complex peripartum management of mirror syndrome. The absence of clear predisposing factors underscores the condition’s poorly understood etiology. While treatment primarily targets the underlying fetal hydrops, this case reinforces the necessity of immediate delivery when such measures fail. Further research is essential to clarify the pathogenesis, improve diagnostic strategies, and optimize patient outcomes.