E. faecalis Sepsis and Asherman's Syndrome as Complications of Sonata System Transcervical Fibroid Ablation.

The Sonata System is a minimally invasive, ultrasound-guided transcervical fibroid ablation procedure for the management of symptomatic uterine fibroids. Since its approval by the US Food and Drug Administration in 2018, this procedure has demonstrated an excellent safety profile and postprocedure satisfaction rate. We present the case of a patient treated with Sonata, who subsequently developed bacterial sepsis and Asherman's syndrome-serious complications with long-term sequelae and implications for fertility. A nulligravid woman in her 40s presented in the outpatient setting with dysmenorrhea and bulk symptoms, with imaging showing an enlarged myomatous uterus compressing the urinary bladder. She desired minimally invasive, fertility-preserving management and underwent the Sonata procedure at an outside hospital. On postoperative day 3, she was admitted to our institution with abdominal pain, fever, tachycardia, and Enterococcus faecalis bacteremia. Despite 6 days of culture-directed antibiotic therapy, the patient remained septic with worsening symptoms and imaging findings and with persistent bacteremia. On hospital day 7, the patient underwent laparoscopic myomectomy and excision of hemorrhagic, infected myometrium. She recovered appropriately after surgery and was discharged home on hospital day 11 to continue 2 weeks of intravenous antibiotics. Nine months after myomectomy, the patient was diagnosed as having Asherman's syndrome. She subsequently had an early pregnancy loss with retained products of conception, requiring hysteroscopic lysis of adhesions and dilation and curettage. Ultimately, careful patient selection is critical for the optimal application of the Sonata procedure. Limiting the extent of fibroid necrosis after treatment is a reasonable goal to minimize the risk of secondary bacterial infection and adhesiogenesis as procedural sequelae.

Safety and Feasibility of Discharge Without an Opioid Prescription for Patients Undergoing Gynecologic Surgery.

OBJECTIVE: To implement a quality-improvement intervention aimed at reducing unnecessary opioid prescriptions for patients who are undergoing gynecologic surgery. METHODS: This was a retrospective cohort study that included data from the pre- and post-quality-improvement initiative cohorts. Patients at an urban, tertiary academic medical center who were undergoing scheduled minimally invasive surgery and open abdominal surgery by a gynecologic oncologist were included. Patients underwent preoperative counseling, standardization of perioperative analgesia, and a postoperative opioid prescribing algorithm. Descriptive statistics were calculated for demographic and perioperative characteristics, process measures, and outcome measures. RESULTS: A total of 532 abdominal surgeries were analyzed. The total percentage of patients discharged with an opioid prescription decreased from 82.7% (n=229/276) to 23.1% (n=59/256) (P<.001) and was significantly reduced for all routes of surgery. The mean number of opioid tablets prescribed for all patients was significantly reduced from 7.2 tablets (SD=5.7) to 1.8 tablets (SD=4.3) (P<.001). Eighty-three percent of patients (n=97/117) who underwent minimally invasive hysterectomy and were discharged on postoperative day 0 or day 1 were not provided an opioid prescription. Fifty-one percent of patients who underwent laparotomy were discharged without an opioid prescription. The percentage of patients who required an opioid refill or new prescription in the preintervention and postintervention cohorts remained constant (6.5%, n=18/276 vs 5.9%, n=15/256, P=.75), as did postoperative calls for pain (8.3%, n=23/276 vs 10.9%, n=33/256). CONCLUSION: Patients who are undergoing scheduled abdominal gynecologic surgery can be safely discharged without opioid prescriptions with appropriate education and perioperative analgesia prescribing practices. These protocols and prescribing practices profoundly limit opioid prescriptions, which is an important factor in combating the ongoing opioid crisis.

Disease Progression-Dependent Effects of TREM2 Deficiency in a Mouse Model of Alzheimer's Disease.

Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2). Understanding TREM2 function promises to provide important insights into how neuroinflammation contributes to AD pathology. However, studies so far have produced seemingly conflicting results, with reports that amyloid pathology can be both decreased and increased in TREM2-deficient AD mouse models. In this study, we unify these previous findings by demonstrating that TREM2 deficiency ameliorates amyloid pathology early, but exacerbates it late in disease progression in the APPPS1-21 mouse model of AD. We also demonstrate that TREM2 deficiency decreases plaque-associated myeloid cell accumulation by reducing cell proliferation, specifically late in pathology. In addition, TREM2 deficiency reduces myeloid cell internalization of amyloid throughout pathology, but decreases inflammation-related gene transcript levels selectively late in disease progression. Together, these results suggest that TREM2 plays distinct functional roles at different stages in AD pathology. SIGNIFICANCE STATEMENT: Alzheimer's disease (AD) is a devastating neurodegenerative disorder and there are currently no effective treatments that modify disease progression. However, the recent identification of genetic risk factors for AD promises to provide new insight into AD biology and possible new therapeutic targets. Among these risk factors, variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2) confer greatly elevated risk for developing the disease. We demonstrate that TREM2 deficiency has opposing effects on AD-related pathologies at early and late stages of disease progression, unifying previous work in the field. In addition, we examine how TREM2 affects the function of the brain immune cell populations in which it is expressed throughout disease progression to understand possible mechanisms underlying its differential impacts on pathology.