School of Medicine

IMPORTANCE: Placement of intravenous access is challenging in pediatric patients. Complications and replacement of IV access is a common occurrence in pediatric patients. OBJECTIVE: This project evaluated a new training program for placement of pediatric USGIV lines. DESIGN: Quality improvement: pre-post cohort. SETTING: A tertiary pediatric hospital in the southwest United States. PARTICIPANTS: The pre-intervention cohort included 400 IV lines identified through retrospective chart review. A subset of 68 lines placed in the three months prior to the intervention were specific to the nurses undergoing training. The post-intervention cohort consisted of 359 lines obtained via convenience sampling. Lines were excluded if documentation lacked insertion/removal dates or reasons for removal. METHODS: The educational intervention was based on best practices, including appropriate catheter-to-vessel diameter ratios and optimal catheter length within the vessel. Training was delivered through asynchronous PowerPoint presentations, one-on-one clinical rounding, and badge card distribution. Mean dwell time and complication rates were assessed through chart review. A sample size of 353 lines was calculated to detect a 25% increase in dwell time; 359 lines were reviewed post-intervention. RESULTS: The average patient age was similar between groups (pre: 11.22 years; post: 11.28 years). A statistically significant increase in dwell time was observed post-intervention (mean 2.17 vs. 1.72 days, p = 0.0015). While overall complication rates remained stable, a significant reduction in early complications (within 0-1 day) was noted (p = 0.01778). CONCLUSIONS: These findings support integration of measurement-based decision-making in pediatric vascular access. Further multi-site studies are needed to confirm generalizability.

Objective: The objective of this study is to determine if patterns of fetal heart rate tracings (FHRT) were associated with an increased rate of composite adverse neonatal outcomes (CANO) among preterm deliveries at 32^0/7 to 36^6/7 weeks. Study Design: This was a retrospective review of intrapartum FHRT between 20 and 120 minutes before birth, among nonanomalous singletons delivered at 32^0/7 to 36^6/7 weeks. The study was conducted at a Level IV maternal center during a consecutive 15-month period. Obstetricians reviewing FHRT were blinded to the maternal characteristics, intrapartum course, and neonatal outcomes. FHRT patterns were categorized based on time spent in the final 2 hours before delivery (<50 vs. ≥50%). The primary outcome was the CANO, which included any of the following: 5-minute Apgar < 7, mechanical ventilation > 6 hours, umbilical artery pH < 7.00, bronchopulmonary dysplasia, interventricular hemorrhage, necrotizing enterocolitis, neonatal seizures, neonatal confirmed sepsis, hypoxic ischemic encephalopathy, birth injury, meconium aspiration syndrome, or neonatal death. Results: Of 5,160 patients, 672 (13%) met the inclusion criteria. CANO occurred in 57 (8.5%) newborns. Overall, FHRT patterns that differed significantly between those without versus with CANO included minimal variability (8.8 vs. 19.3%, p = 0.01, PLR = 2.2 [positive likelihood ratio], PPTP 17% [positive posttest probability]), moderate variability (76.4 vs. 52.6%, p < 0.001, NLR = 2.01 [negative likelihood ratio], NPTP 15.7% [negative posttest probability]), accelerations (58.4 vs. 40.4%, p = 0.009, NLR = 1.43, NPTP = 11.7%), and severe variable decelerations (3.5% p = 0.003, PLR = 10.79, PPTP = 50.1%). Category III FHRT pattern was also associated with an increased posttest probably of CANO (0.3 vs. 1.8%, p = 0.12, PLR = 5.39, PPTP = 27%). Conclusion: While moderate variability and accelerations were associated with significantly lower likelihood of CANO among newborns delivered at 32^0/7 to 36^6/7 weeks, minimal variability and severe variable decelerations were significantly more common in preterm newborns with CANO. Key Points: · At 32 to 36 weeks, CANO occur in approximately 8% of neonates.. · Severe variable decelerations and minimal variability increase risk of CANO.. · The PPTP of CANO is 33%, if Category III FHRT is noted before birth.. · The PPTP is 13%, if there is persistent Category II FHRT in the last 120 minutes..

Objective: ACOG publications on stillbirth or postpartum hemorrhage (PPH) do not consider stillbirth as a risk factor for postpartum hemorrhagic morbidity. This study aimed to ascertain the likelihood of composite maternal hemorrhagic outcome (CMHO) among individuals who delivered vaginally with livebirth versus a stillbirth. Study Design: This was a retrospective cohort study of all parturients greater than 20 weeks gestation who delivered vaginally at a single level IV site within 24 months. Demographic differences and baseline PPH risks were analyzed. CMHO included any of the following: estimated blood loss ≥1,000 mL, use of uterotonics (beyond prophylactic oxytocin), Bakri balloon, surgical management of PPH, blood transfusion, hysterectomy, venous thromboembolism (VTE), admission to the intensive care unit (ICU), or maternal death. Statistical analysis included chi-squared, Kruskal-Wallis, and Poisson regression with robust error variance for risk ratios, adjusting for gestational age (GA), bleeding on admission, chorioamnionitis, and prior uterine surgery. Results: Of 8,623 consecutive vaginal births ≥20 weeks gestation, 89 (1.9%) were stillbirths. Maternal age, marital status, GA at delivery, and PPH risk stratification at admission differed significantly. Bleeding at admission (p < 0.001), prior uterine surgery (p < 0.001), magnesium sulfate use (p = 0.006), chorioamnionitis (p < 0.001), platelet count <100 (p = 0.001), platelet count <50 (p < 0.001), and retained products of conception (p < 0.001) were different in the two groups. CMHO was significantly higher with a stillbirth delivery (32.6 vs. 16.8%; aRR: 1.56, 95% CI: 1.01-2.46). After adjustment, the components of the CMHO that differed significantly were estimated blood loss ≥1,000 mL and ICU admission. Tamponade, surgical intervention, VTE, hysterectomy, and maternal death did not differ between the two groups. Conclusion: Pregnancies with stillbirth, compared with livebirth, had an increased risk of hemorrhagic related morbidity. In addition to being useful in shared decision-making, our results can be nidus for intervention trials to decrease the hemorrhagic morbidity associated with stillbirth. Key Points: · The risk of CMHO was significantly higher in the stillbirth group even after adjustment for potential confounders (32.6% vs. 16.8%).. · Stillbirth was associated with a significantly higher risk of blood loss of ≥1,000 mL.. · Stillbirth was also associated with higher likelihood of uterotonic use, transfusion, and admission to ICU..

Abstract Introduction The majority of low placentation identified on first‐trimester transabdominal ultrasound resolves; however, whether this resolution is associated with adverse outcome remains poorly understood. This investigation aimed to determine whether patients with resolved first‐trimester low placentation had different delivery outcomes compared to patients who never had low placentation. Methods This is a retrospective cohort study of singleton pregnancies with low placentation, defined as low‐lying placenta or placenta covering the internal os, on first‐trimester transabdominal ultrasound between 12+0 weeks and 13+6 weeks, delivering at a single tertiary care center from January to December 2022. We compared outcomes stratified by first‐trimester low placentation that resolved by the second trimester, or those without low placentation at any point. The primary outcome was quantitative blood loss at delivery by volumetric measurement. Secondary outcomes included postpartum hemorrhage (PPH) defined as blood loss ≥1000 cc, unplanned cesarean delivery, preterm birth, 5‐min Apgar < 7, and composite maternal adverse outcomes including the use of atony device, retained products of conception, blood transfusion, peripartum hysterectomy, intensive care unit admission, or death. Results This cohort included 437 low placentation patients and 491 patients without low placentation. Resolved first‐trimester low placentation was associated with a significant increase in quantitative blood loss at delivery (405 ± 369 cc vs. 331 ± 253 cc, p  < 0.01) but no difference in incidence of PPH (6.4% vs. 4.7%, p  = 0.25). Resolved first‐trimester low placentation was also associated with increased tranexamic acid (TXA) administration (11.9% vs. 7.7%, p  = 0.03), blood transfusion (1.8% vs. 0.4%, p  = 0.04), and unplanned cesarean delivery (15.3% vs. 9.2%, p  < 0.01) without differences in the indications for unplanned cesarean delivery. In our multivariable regression, resolved first‐trimester low placentation remained associated with TXA administration (adjusted odds ratio [OR], 1.70; 95% confidence interval [CI], 1.07–2.70) and unplanned cesarean delivery (adjusted OR 1.73; 95% CI, 1.12–2.68). There were no associations with adverse neonatal outcomes or composite maternal outcome. Conclusion Resolved first‐trimester low placentation is not associated with clinically significant adverse outcomes. However, given changes in unplanned cesarean delivery rate, resolved low placentation may indicate altered uterine physiology. Future research would be valuable to better understand the relationship between resolved low placentation and unplanned cesarean deliveries.

Objective: This study aimed to compare the patterns of fetal heart rate tracings (FHRTs), and outcomes among individuals with small (birth weight [BW] <10% for gestational age [GA]; SGA) versus appropriate (BW at 10-89% for GA; AGA) newborns at term (≥37.0 weeks). Study Design: Our retrospective cohort study included consecutive deliveries over 15 months at a level IV center. FHRTs were reviewed by obstetricians blinded to maternal and neonatal outcomes. The inclusion criteria were non-anomalous singletons, cataloged as SGA or AGA birth weight using Alexander et al's nomogram. In 20-minute segments, the last 120 minutes of tracing were characterized. Rates of cesarean delivery (CD) and composite neonatal adverse outcomes (CNAOs) were compared. Results: Of 5,160 deliveries, 3,029 (58.7%) met the inclusion criteria, and among them, 422 (13.9%) were SGA and 2,607 (86.1%) AGA. There were no differences in FHRT baseline, variability, or accelerations. Compared to AGA, SGA was more likely to have prolonged decelerations (11.8 vs. 8.4%, p = 0.021), and recurrent decelerations with ≥50% of contractions (21.3 vs. 16.5%, p = 0.014). Overall, the presence of category II FHRT or not was similar between the SGA (91.2%) and AGA (88.5%; p = 0.097). Persistent category II FHRT was significantly more common among SGA (37.4%) than AGA (28.1%; aOR = 1.47; 95% CI: 1.47-1.82) newborns. The rate of CD for non-reassuring FHRT was similar among the two groups. CNAO occurred in 1.4% in both SGA and AGA neonates (p = 0.95). Conclusion: In our cohort of those with fetal monitoring prior to delivery at ≥37 weeks, persistent category II FHRT at the end of labor was significantly more common in SGA compared to AGA neonates; however, composite neonatal morbidity did not differ between the two groups. Our analysis provides data for shared decision-making that among SGA newborns, abnormalities of FHRT are not linked with adverse outcomes. Key Points: · There were no differences in FHRT baseline, variability, or accelerations between AGA and SGA.. · SGA was more likely to have prolonged decelerations and recurrent decelerations with ≥50% of contractions.. · Persistent category II FHRT before delivery is significantly more common with SGA than AGA.. · FHRT abnormalities, however, were not associated with CD for non-reassuring FHRT, or adverse outcomes..

By preserving molecular information inherited from the source cell, extracellular vesicles (EVs) can serve as biomarkers for tissue health or disease, paving the way for liquid biopsy applications. The enrichment of tissue-specific EVs (TS-EVs) from human biofluids can be challenging due to technical and methodological limitations. Here, we use single and sequential immunoaffinity capture workflows to enrich antigen-specific EVs circulating in human blood. We demonstrate the specificity, efficiency, and consistency of our approach for enriching blood plasma EV subpopulations from the nervous system, alveolar cells and hepatocytes. The enriched subpopulations are characterized by canonical EV features and markers, as well as co-localization of tissue-specific and general markers on the surface. We provide a validated workflow to derive multiple EV subpopulations from circulation, leveraging their promise as informative biomarkers of tissue status and enabling liquid biopsy and biomarker discovery.

OBJECTIVES: To challenge the perception that endometriosis uniformly regresses after menopause by presenting the case of repeated, pathology-confirmed symptomatic recurrences spanning two decades after menopause, and to emphasize key considerations for hormone therapy use and surgical management in postmenopausal endometriosis. METHODS: We report the case of a 70-year-old postmenopausal patient with prior hysterectomy, bilateral salpingo-oophorectomy, appendectomy, and pathology-confirmed endometriosis who presented with pelvic pain while receiving subcutaneous estrogen pellet therapy. Preoperative imaging was suggestive of recurrent endometriosis. The patient underwent laparoscopic excision for diagnostic and therapeutic purposes, with final pathology confirming recurrent disease. Written informed consent was obtained for publication of this case report and use of de-identified clinical images. A focused narrative literature review was performed to contextualize this case within existing data on postmenopausal endometriosis. RESULTS: Laparoscopy revealed a cystic mass arising from the right round ligament with associated retroperitoneal fibrosis and multiple peritoneal implants consistent with endometriosis. Surgical management included resection of the round ligament mass, excision of peritoneal implants, lysis of adhesions, and right ureterolysis. Histopathologic examination confirmed a round ligament adenomyoma and peritoneal endometriosis. Postoperatively, the patient experienced symptomatic improvement and was transitioned to low-dose transdermal estradiol combined with progestogen therapy. CONCLUSIONS: Endometriosis can develop, persist, or recur after menopause, particularly in the setting of unopposed and potentially supraphysiologic exogenous estrogen. This case highlights the importance of appropriate menopausal hormone therapy selection, including consideration of progestogen use regardless of uterine status, and reinforces the role of surgical excision in postmenopausal patients with suspected disease.

Ovulation is triggered by a surge in luteinizing hormone (LH) secretion from the pituitary. The LH surge is itself driven by a surge in GnRH release induced by estrogen positive feedback action in the hypothalamus. While ERα-expressing kisspeptin (Kiss1) neurons in the preoptic area (in mice, the rostral periventricular region of the third ventricle [RP3V]) are proposed to mediate this estrogen positive feedback event, the functional necessity of RP3V-derived kisspeptin for the LH surge has not been directly tested. Here we leveraged Cre/lox technology and the known high co-expression of tyrosine hydroxylase (TH) with Kiss1 in only the RP3V region to generate novel transgenic mice with selective knockout (KO) of the Kiss1 gene in just RP3V neurons (Kiss1RP3V KO mice). In situ hybridization confirmed a significant 70% reduction in cells expressing Kiss1 in the RP3V region, but not in the arcuate nucleus, along with no change in RP3V Th expression. Kiss1RP3V KO females exhibited normal pubertal timing and estrous cycles. However, functional interrogation of the ability of Kiss1RP3V KO females to generate an estradiol-induced LH surge demonstrated markedly blunted LH surges and reduced occurrence of surges, in line with the partial Kiss1RP3V knockout in this group. Correspondingly, fertility assessment revealed significant subfertility, including fewer and smaller litters. This subfertility is consistent with the observed impaired LH surges, though the downstream ovarian mechanism(s) underlying the smaller litters still needs to be determined. These findings provide direct causal evidence that RP3V-derived kisspeptin is essential for normal LH surge magnitude and optimal fertility.