Using a Frontline Staff Intervention to Improve Cervical Cancer Screening in a Large Academic Internal Medicine Clinic.

BACKGROUND: Cervical cancer is the third most common malignancy affecting women. Screening with Papanicolaou (Pap) tests effectively identifies precancerous lesions and early-stage cervical cancer. While the nationwide rate of cervical cancer screening (CCS) is 84%, our urban general internal medicine (GIM) clinic population had a CCS rate of 70% in 2016. OBJECTIVE: To improve our clinic's CCS rate to match or exceed the national average within 18 months by identifying barriers and testing solutions. DESIGN: A quality improvement project led by a multidisciplinary group of healthcare providers. PARTICIPANTS: Our GIM clinic includes 16 attending physicians, 116 resident physicians, and 20 medical assistants (MAs) with an insured and underserved patient population. INTERVENTION: Phase 1 lasted 9 months and implemented CCS patient outreach, patient financial incentives, and clinic staff education. Phase 2 lasted 9 months and involved a workflow change in which MAs identified candidates for CCS during patient check-in. Feedback spanned the entire study period. MAIN MEASURES: Our primary outcome was the number of Pap tests completed per month during the 2 study phases. Our secondary outcome was the clinic population's CCS rate for all eligible clinic patients. KEY RESULTS: After interventions, the average number of monthly Pap tests increased from 35 to 56 in phase 1 and to 75 in phase 2. Of 385 patients contacted in phase 1, 283 scheduled a Pap test and 115 (41%) completed it. Compared to baseline, both interventions improved cervical cancer screening (phase 1 relative risk, 1.86; 95% CI, 1.64-2.10; P < 0.001; phase 2 relative risk, 2.70; 95% CI, 2.40-3.02; P < 0.001). Our clinic's CCS rate improved from 70% to 75% after the 18-month intervention. CONCLUSIONS: The rate of CCS increased by 5% after a systematic 2-phase organizational intervention that empowered MAs to remind, identify, and prepare candidates during check-in for CCS.

Derivation and validation of the ED-SAS score for very early prediction of mortality and morbidity with acute pancreatitis: a retrospective observational study.

BACKGROUND: Existing scoring systems to predict mortality in acute pancreatitis may not be directly applicable to the emergency department (ED). The objective of this study was to derive and validate the ED-SAS, a simple scoring score using variables readily available in the ED to predict mortality in patients with acute pancreatitis. METHODS: This retrospective observational study was performed based on patient data collected from electronic health records across 2 independent health systems; 1 was used for the derivation cohort and the other for the validation cohort. Adult patients who were eligible presented to the ED, required hospital admission, and had a confirmed diagnosis of acute pancreatitis. Patients with chronic or recurrent episodes of pancreatitis were excluded. The primary outcome was 30-day mortality. Analyses tested and derived candidate variables to establish a prediction score, which was subsequently applied to the validation cohort to assess odds ratios for the primary and secondary outcomes. RESULTS: The derivation cohort included 599 patients, and the validation cohort 2011 patients. Thirty-day mortality was 4.2 and 3.9%, respectively. From the derivation cohort, 3 variables were established for use in the predictive scoring score: ≥2 systemic inflammatory response syndrome (SIRS) criteria, age > 60 years, and SpO2 < 96%. Summing the presence or absence of each variable yielded an ED-SAS score ranging from 0 to 3. In the validation cohort, the odds of 30-day mortality increased with each subsequent ED-SAS point: 4.4 (95% CI 1.8-10.8) for 1 point, 12.0 (95% CI 4.9-29.4) for 2 points, and 41.7 (95% CI 15.8-110.1) for 3 points (c-statistic = 0.77). CONCLUSION: An ED-SAS score that incorporates SpO2, age, and SIRS measurements, all of which are available in the ED, provides a rapid method for predicting 30-day mortality in acute pancreatitis.

Lead (Pb) exposure promotes diabetes in obese rodents.

BACKGROUND: Pb (lead) exposure occurs at elevated frequency in urban inner city populations that also have high rates of obesity and diabetes. OBJECTIVES: To determine if Pb can promote the development of diabetes in a setting of obesity, we examined the effect of Pb exposure on glucose metabolism in a rodent model of obesity. METHODS: Adult female ZDF rats were exposed to Pb in drinking water for 24 weeks. Fasting blood glucose, insulin, and glucose tolerance were measured at regular intervals. Expression of hepatic gluconeogenic genes was measured in exposed and control animals and in cultured hepatoma cells treated with Pb. RESULTS: Pb exposure induced fasting hyperglycemia after 8 weeks and glucose intolerance after 12 weeks of exposure. In addition, Pb-exposed animals showed elevated hepatic triglyceride levels and increased expression of the gluconeogenic genes PEPCK and glucose-6-phosphatase. In cultured rat hepatoma cells treatment with Pb stimulated PEPCK and glucose-6-phosphatase gene expression, suggesting a possible direct effect of Pb on hepatic gluconeogenic gene expression. CONCLUSIONS: In the setting of obesity, Pb exposure is prodiabetic, causing fasting hyperglycemia and glucose intolerance in rats. A contributing factor to the metabolic effects of Pb may be the direct stimulation of hepatic gluconeogenic gene expression.