The Impact of Racial, Geographic, and Socioeconomic Risk Factors on the Development of Advanced-Stage Cervical Cancer.

OBJECTIVES: Despite screening, disparities exist in cervical cancer incidence and outcomes. Demographic factors are associated with diagnosis at advanced stage (AS), but less is known about geographic factors. We sought to investigate risk factors for developing AS cervical cancer in Alabama. MATERIALS AND METHODS: We identified women treated for cervical cancer from 2005 to 2015 at our institution. Stages II-IV were considered AS. ZIP codes were categorized by federal Rural-Urban Commuting Area Codes, and 16 historically underserved counties were categorized as Black Belt rural. Using data from the American College of Obstetricians and Gynecologists, we identified women's health provider locations. We explored associations between stage and multiple factors using logistic regression. RESULTS: Of 934 patients, 29.2% were black, 52.7% had AS cancer, and 63.4% lived in urban areas. Average distance to nearest American College of Obstetricians and Gynecologists Fellow in urban, rural, and Black Belt rural areas was 5.0, 10.6, and 13.7 miles, respectively. Black race, public insurance and age of older than 65 years were associated with increased risk of AS cancer. Living in a rural area trended toward higher risk but was not significant. When stratified by race, insurance status and age were associated with AS cancer in white women only. CONCLUSIONS: Living further from a women's health provider or in a rural area was not associated with a higher risk of AS cervical cancer. Black women had a higher risk of AS than white women regardless of age, insurance status, and geography. Disparities in cervical cancer are multifactorial and necessitate further research into socioeconomic, biologic, and systems causes.

Pain Catastrophizing and Impact on Pelvic Floor Surgery Experience.

IMPORTANCE: Understanding patients' perceptions of symptoms and outcomes of urogynecologic surgery is essential for providing high-quality care. OBJECTIVE: The aim of the study was to assess association of pain catastrophizing with pelvic floor symptom distress and impact, postoperative pain, and voiding trial in patients undergoing urogynecologic surgery. STUDY DESIGN: Individuals whose self-identified gender was female and were undergoing surgery March 2020-December 2021 were included. Participants completed the Pain Catastrophizing Scale (range 0-52), Pelvic Floor Distress Inventory, and Pelvic Floor Impact Questionnaire preoperatively. Pain catastrophizing was score ≥30 and describes the tendency to magnify the overall threat of pain. Voiding trial failure was inability to void ≥2/3 of instilled volume (≤300 mL). The association between pain catastrophizing and symptom distress and impact was assessed with linear regression. A P < 0.05 is significant. RESULTS: Three hundred twenty patients were included (mean age, 60 years, 87% White). Forty-six of 320 participants (14%) had a pain catastrophizing score ≥30. The pain catastrophizing group had higher body mass index (33 ± 12 vs 29 ± 5), more benzodiazepine use (26% vs 12%), greater symptom distress (154 ± 58 vs 108 ± 60), and greater urogenital (59 ± 29 vs 47 ± 28), colorectal (42 ± 24 vs 26 ± 23), and prolapse (54 ± 24 vs 36 ± 24) subscale scores, all P ≤ 0.02. The pain catastrophizing group had greater impact (153 ± 72 vs 72 ± 64, P < 0.01) and urogenital (60 ± 29 vs 34 ± 28), colorectal (36 ± 33 vs 16 ± 26), and prolapse (57 ± 32 vs 22 ± 27) subscale scores, P < 0.01. Associations remained controlling for confounders ( P < 0.01). The pain catastrophizing group had higher 10-point pain scores (8 vs 6, P < 0.01) and was more likely to report pain at 2 weeks (59% vs 20%, P < 0.01) and 3 months (25% vs 6%, P = 0.01). Voiding trial failure did not differ (26% vs 28%, P = 0.98). CONCLUSIONS: Pain catastrophizing is associated with greater pelvic floor symptom distress and impact and postoperative pain but not voiding trial failure.

Timing and Success of Postoperative Voiding Trial After Colpocleisis With and Without Concomitant Midurethral Sling.

OBJECTIVE: The aim of this study was to compare failure rates of first voiding trial (VT) within 7 days and on postoperative day (POD) 1 after colpocleisis with versus without concomitant midurethral sling (MUS). Predictors of POD 1 VT failure were also examined. METHODS: This was a retrospective cohort study of women undergoing colpocleisis from January 2012 to October 2019 comparing VT outcomes with versus without MUS. Primary outcome was first VT failure within 7 days; outcomes of VTs performed on POD 1 were also assessed. Association between MUS and VT failure and predictors of POD 1 VT failure were assessed via logistic regression. RESULTS: Of 119 women, 45.4% had concomitant MUS. First VT was performed on mean POD 3.1 ± 2.2 in the MUS group versus POD 1.8 ± 1.8 in the no MUS group (P < 0.01). The MUS group was less likely to undergo POD 1 VT (50% vs 83%, P < 0.01). Failure of the first VT did not differ (22.2% with MUS vs 32.8% without MUS, P = 0.20); no association between VT failure and MUS was noted (adjusted odds ratio [aOR], 0.6; 95% confidence interval [CI], 0.18-2.1). There were 68.1% (81/119) of participants who underwent POD 1 VT, MUS was performed in 33.3% (27/81). The POD 1 failure did not differ between those with 33.3% versus 40.7% without MUS (P = 0.52). Midurethral sling was not associated with POD 1 VT failure (aOR, 0.93; 95% CI, 0.27-3.23). In women undergoing POD 1 VT, preoperative postvoid residual was associated with VT failure (aOR, 1.39; 95% CI, 1.01-1.92). CONCLUSIONS: In women undergoing colpocleisis, MUS was not associated with VT failure within 7 days or on POD 1. Increased preoperative postvoid residual was associated with POD 1 VT failure.

Serum Creatinine Trajectories for Community- versus Hospital-Acquired Acute Kidney Injury.

BACKGROUND: Patterns of acute kidney injury (AKI) can be distinguished by the rate of changes in the serum creation concentrations during hospitalizations. We hypothesized that the timing and values of minimum and maximum serum creatinine (sCr) could be used to distinguish between transient hospital-associated AKI (THA-AKI) and hospital-acquired AKI (HA-AKI). MATERIALS AND METHODS: We evaluated adults admitted to 2 regionally distinct academic medical centers. Peak sCr during the hospitalization was used to define AKI, using absolute changes and timing from the minimum sCr. sCr trajectories were derived based on the rate of change between the minimum and peak creatinine concentrations. RESULTS: Peak creatinine followed the minimum creatinine for HA-AKI, while the peak creatinine preceded the minimum creatinine for THA-AKI. There were 82,403 patients included in the analyses, and 53,882 (65%) did not have AKI during the index hospitalization. There were 2,611 inpatient deaths; HA-AKI had a 4.8-fold increased risk relative to those without AKI (p < 0.01), and transient AKI had a 1.6-fold increased risk for inpatient mortality relative to inpatients without AKI (p < 0.01). CONCLUSIONS: Patients with hospital-associated AKI are at an increased risk for inpatient mortality. Creatinine trajectories can be used to describe the rate of development as well as recovery from inpatient AKI. The 24- and 48-hour interval slopes may be early indicators of developing AKI. © 2016 S. Karger AG, Basel.

Prehospitalization Risk Factors for Acute Kidney Injury during Hospitalization for Serious Infections in the REGARDS Cohort.

BACKGROUND/AIMS: Acute kidney injury (AKI) frequently occurs in hospitalized patients. In this study, we determined prehospitalization characteristics associated with AKI in community-dwelling adults hospitalized for a serious infection. METHODS: We used prospective data from 30,239 participants of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a national cohort of community-dwelling adults ≥45 years old. We identified serious infection hospitalizations between 2003 and 2012. Using the Kidney Disease Improving Global Outcomes (KDIGO) criteria, we defined AKI as an increase in serum creatinine (sCr) ≥0.3 mg/dl from the first inpatient sCr measurement during the first 7 hospitalization days. We excluded individuals with a history of renal transplant or preexisting end-stage renal disease as well as individuals with <2 sCr measurements. We identified baseline characteristics (sociodemographics, health behaviors, chronic medical conditions, biomarkers, and nonsteroidal anti-inflammatory, statin, or antihypertensive medication use) independently associated with AKI events using multivariable generalized estimating equations. RESULTS: Over a median follow-up of 4.5 years (interquartile range 2.4-6.3), we included 2,074 serious infection hospitalizations among 1,543 individuals. AKI occurred in 296 of 2,074 hospitalizations (16.5%). On multivariable analysis, prehospitalization characteristics independently associated with AKI among individuals hospitalized for a serious infection included a history of diabetes [odds ratio (OR) 1.38; 95% CI 1.02-1.89], increased cystatin C (OR 1.73 per SD; 95% CI 1.20-2.50), and increased albumin-to-creatinine ratio (OR 1.19 per SD; 95% CI 1.007-1.40). Sex, race, hypertension, myocardial infarction, estimated glomerular filtration rate, high-sensitivity C-reactive protein, and the use of nonsteroidal anti-inflammatory, statin, or antihypertensive medications were not associated with AKI. CONCLUSIONS: Community-dwelling adults with a history of diabetes or increased cystatin C or albumin-to-creatinine ratio are at increased risk for AKI after hospitalization for a serious infection. These findings may be used to identify individuals at high risk for AKI.

Categories of Hospital-Associated Acute Kidney Injury: Time Course of Changes in Serum Creatinine Values.

UNLABELLED: Hospital-associated acute kidney injury (HA-AKI) is associated with increased inpatient mortality. Our objective was to categorize HA-AKI based on the timing of minimum and peak inpatient serum creatinine (sCr) and describe the association with inpatient mortality. MATERIALS AND METHODS: This study is a retrospective analysis of an administrative data set for adults admitted to a single medical center for over 4 years. Changes and timing of the minimum and peak sCr were used to define HA-AKI categories. RESULTS: Peak creatinine followed minimum creatinine for HA-AKI, and preceded the minimum value for transient HA-AKI (THA-AKI). A subset of patients developed HA-AKI after recovering from THA-AKI. Multivariable Cox regression analyses examined the association between these categories and 28-day inpatient mortality, adjusting for age, sex, race, Charlson comorbidity index, baseline kidney function, AKI recovery and renal replacement therapy. There were 50,601 patients included in the analyses, and 29,996 (59%) did not have AKI. There were 2,440 deaths; HA-AKI had a 2.24-fold (95% CI 1.99-2.51) increased risk, while THA-AKI group (12,101) had a 1.23-fold (95% CI 1.09-1.40) increased risk for inpatient mortality. THA-AKI patients who recovered and then developed HA-AKI had the same mortality risk as THA-AKI (1.27-fold [95% CI 1.07-1.51]) but longer hospitalization and less recovery from AKI. CONCLUSIONS: Risk of short-term inpatient mortality is associated with AKI, and this risk is attenuated with recovery of kidney function in the hospital. Systematic surveillance with repeated inpatient sCr values is needed to assess the short- and long-term consequences of HA-AKI.

Association of inflammatory and endothelial cell activation biomarkers with acute kidney injury after sepsis.

OBJECTIVE: Acute kidney injury (AKI) is a sequela of sepsis associated with increased morbidity and mortality. We sought to determine if individuals with elevated baseline levels of inflammation and endothelial cell activation are at increased risk for future AKI after sepsis. METHODS: We conducted an analysis of individuals developing sepsis in the national 30,239 subject REGARDS cohort. Biomarkers measured at the beginning of an 8-year observation period included high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor necrosis factor (TNF-α), E-selectin, inter-cellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and urinary Albumin-to-creatinine ratio (ACR). We defined subsequent sepsis as hospitalization for a serious infection with ≥2 Systemic Inflammatory Response Syndrome (SIRS) criteria. We excluded patients with prior dialysis or kidney transplantation, or those receiving less than two serum creatinine (sCr) measurements during hospitalization. We defined AKI as an increase in sCr ≥0.3 mg/dL from the initial sCr measurement, or the initiation of hemodialysis. Using logistic regression, we evaluated the associations between AKI and biomarker quartiles, adjusting for comorbidities. RESULTS: We identified 212 sepsis cases encompassing 41 (19.3%) AKI. Elapsed time from biomarker measurement to sepsis episode was 3.1 years (IQR 1.6-4.5). Compared with non-AKI, AKI individuals exhibited higher TNF-α (9.4 vs. 6.2 pg/mL, p = 0.003) and ACR (504.82 vs 61.81 mg/g, p < 0.001). hsCRP, IL-6, E-selectin, ICAM-1 and VCAM-1 were similar between AKI and non-AKI. After adjustment for confounders, AKI after sepsis was more likely in those with higher E-selectin (adjusted ORs 2.91 (0.95-8.93), 1.99 (0.61-6.47), 4.01 (1.30-12.35), test of linear trend p = 0.04), and higher ACR (adjusted ORs 2.29 (0.99-5.30), 10.67 (3.46-32.90), test of linear trend p < 0.001). Baseline hsCRP, TNF-α, IL-6, VCAM-1 and ICAM-1 were not associated with AKI after sepsis. CONCLUSION: Elevated baseline levels of E-selectin and ACR are associated with future AKI in the setting of sepsis. Baseline inflammatory and endothelial activation biomarkers may be useful for predicting future risk of AKI in sepsis.