Septic shock in a woman with a hydatidiform mole: A case report.

Hydatidiform moles can be fatal because of the risk of massive bleeding or thyroid storm; however, they rarely occur concomitantly with sepsis. We present herein the case of a woman with a hydatidiform mole with septic shock. A 30-year-old multiparous woman with Basedow's disease presented with fever, amenorrhea, and vaginal bleeding. Transvaginal ultrasonography revealed an enlarged uterus with an intrauterine vesicular mass (74.3 × 93.0 mm). Human chorionic gonadotropin level was 994,000 mIU/mL. C-reactive protein was elevated, and blood cultures were positive (gram-negative rods), indicating infection. After administering antibiotics (tazobactam and piperacillin), blood pressure suddenly decreased (69/45 mmHg), requiring stabilization with noradrenaline and albumin. The uterine contents were naturally expelled, followed by dilatation and curettage after her vital signs and general condition gradually improved. The pathological diagnosis was a complete hydatidiform mole. Culture of the intrauterine contents revealed Escherichia coli, leading to the potentially fatal diagnosis of septic shock associated with a hydatidiform mole.

Potential critical risks of pulmonary thromboembolism from an asymptomatic postpartum ovarian vein thrombosis: a case report.

BACKGROUND: Ovarian vein thrombosis (OVT) may cause maternal mortality by inducing pulmonary thromboembolism (PTE). However, the prevalence, etiology, risk factors, prognosis, and optimal treatments for asymptomatic OVT during and after pregnancies are unclear, which therefore requires a high clinical index of suspicion for certain diagnoses due to its vague presentation. We herein present a case of asymptomatic postpartum OVT that extended toward the inferior vena cava (IVC), resulting in a potential risk of PTE. CASE PRESENTATION: A 30-year-old postpartum woman presented with slight dyspnea after an uneventful vaginal delivery at 40 weeks of gestation. We checked her laboratory data to exclude lethal thrombosis; D-dimer levels were 85.6 µg/mL. We performed computed tomography (CT) to search the presence of PTE and deep vein thrombosis (DVT); although no signs of PTE and DVT in her legs were detected, CT and trans-abdominal ultrasonography (TAUS) revealed a right OVT. Heparin was administered, and D-dimer levels decreased; warfarin at a dose of 2 mg/day was subsequently administered to control anti-coagulopathy. However, D-dimer was re-elevated despite adequate anticoagulation treatment, and extension of the right OVT to the IVC was detected by CT and TAUS. With warfarin administration, CT and TAUS showed the disappearance of right OVT. The patient was discharged from the hospital 17 days after delivery. CONCLUSIONS: Even asymptomatic postpartum OVT may lead to PTE. Universal screening guidelines and optimal treatment strategies for asymptomatic OVT in pregnant and postpartum women should be established through future studies.

Gallbladder wall thickening in a woman with postpartum preeclampsia: A case report.

BACKGROUND: Preeclampsia (PE) is hallmarked by dysfunction of various organs; therefore, its diagnosis can be challenging, especially when patients present with right upper abdominal pain. Herein, we present a case of postpartum gallbladder wall thickening (GBWT) that led to a diagnosis of PE, rather than hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome or gallbladder and biliary disease. CASE PRESENTATION: A 31-year-old postpartum woman presented with a fever, hypertension, headache, and right upper abdominal pain. HELLP syndrome and intracranial hemorrhage were initially suspected, due to the combination of symptoms and elevated levels of aspartate transaminase, alanine transaminase, and lactate dehydrogenase. However, hemolysis and thrombocytopenia were absent, and a computed tomography (CT) scan of the head did not indicate the presence of intracranial hemorrhage. Further, transabdominal ultrasound and CT revealed GBWT (edematous gallbladder); CT also revealed an enlarged heart, lung edema, pleural effusion, and ascites. Thus, PE, rather than HELLP syndrome or gallbladder or biliary disease, was diagnosed based on gestational hypertension and proteinuria, new-onset headache, liver dysfunction, and edema in several organs, including the lung. Nicardipine treatment quickly improved hypertension and headache, and, over time, the patient's urination increased, and edema subsided throughout the body. Furthermore, laboratory results improved, and the patient was discharged on postpartum day 11. CONCLUSION: Postpartum gallbladder wall thickening can be a diagnostic sign of PE.