ABSTRACT
BACKGROUND: Optimal postoperative opioid stewardship combines adequate pain medication to control expected discomfort while avoiding abuse and community diversion of unused prescribed opioids. We hypothesized that an opioid buyback program would motivate patients to return unused opioids, and surgeons will use that data to calibrate prescribing. METHODS: Prospective cohort study of postambulatory surgery pain management at a level II Veterans Affairs rural hospital (2017-2019). Eligible patients were offered $5/unused opioid pill ($50 limit) returned to our Veterans Affairs hospital for proper disposal. After 6 months, buyback data was shared with each surgical specialty. RESULTS: Overall, 934 of 1,880 (49.7%) eligible ambulatory surgery patients were prescribed opioids and invited to participate in the opioid buyback. We had 281 patients (30%) return 3,165 unused opioid pills; this return rate remained constant over the study period. In 2017, 62.4% of patients were prescribed an opioid; after data was shared with providers, prescriptions for opioids were reduced to 50.7% and 38.3% of eligible patients in 2018 and 2019, respectively (P < .0001). The median morphine milligram equivalents prescribed also decreased from 108.8 morphine milligram equivalents in 2017 to 75.0 morphine milligram equivalents in 2018 and sustained at 75.0 morphine milligram equivalents in 2019 (P < .001). Surgical providers, surgeries performed, patient characteristics, and 30-day refill rates were similar throughout the study period. CONCLUSION: A small financial incentive resulted in patients returning unused opioids after ambulatory surgery. Feedback to surgeons regarding opioids returned reduced the proportion of patients prescribed an opioid and the amount of opioid after ambulatory surgery without an increase in refills.
Subject(s)
Ambulatory Surgical Procedures/adverse effects , Analgesics, Opioid/therapeutic use , Motivation , Pain, Postoperative/drug therapy , Practice Patterns, Physicians' , Prescription Drug Monitoring Programs , Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Pain Management , Pain, Postoperative/diagnosis , Pain, Postoperative/etiology , Prospective StudiesABSTRACT
Objective. To implement an opioid buyback program after ambulatory surgery.Methods. We performed a prospective cohort study of 578 opioid-naïve patients prescribed opioids after ambulatory surgery at a rural US Veterans Affairs (VA) hospital from 2017 to 2018. We reimbursed $5 per unused opioid pill ($50 limit) returned to our VA for proper disposal. We tracked the number of participants, number of unused opioid pills returned, surgeon prescribing, and refill requests.Results. Out of 578 eligible patients, 171 (29.6%) returned 2136.5 unused opioid pills. Information shared with surgeons after 6 months led to a 27% decrease in opioid prescribing without an increase in refills.Conclusions. With this opioid buyback program, rural patients had a safe and convenient place to dispose of unused opioids. Surgeons used information about returns to adjust opioid prescribing after common ambulatory surgeries without an increase in refill requests.Public Health Implications. Although providers prescribe within state opioid guidelines, there will be variations in patient use after ambulatory surgery. An opioid buyback program helped our patients and surgeons decrease unused prescription opioids available for diversion in our rural communities.
Subject(s)
Analgesics, Opioid/therapeutic use , Practice Patterns, Physicians' , Prescription Drug Diversion/prevention & control , Ambulatory Surgical Procedures , Cohort Studies , Hospitals, Veterans , Humans , Pain, Postoperative/drug therapy , Prospective Studies , Rural Population , Surgeons , United States , United States Department of Veterans AffairsABSTRACT
Secondary hyperparathyroidism is an early complication of chronic kidney disease (CKD). Vitamin D deficiency and reduced synthesis of 1,25-dihydroxyvitamin D (calcitriol) early in the progression of CKD leads to abnormal mineral metabolism. Vitamin D deficiency leads to increased parathyroid hormone and remodeling of bone that releases calcium and phosphorus, resulting in vascular calcification. Vitamin D deficiency is associated with cardiovascular disease and contributes to the high morbidity and mortality in patients with CKD.
Subject(s)
Hyperparathyroidism, Secondary , Kidney Failure, Chronic/complications , Vitamin D Deficiency , Vitamin D/therapeutic use , Arterial Occlusive Diseases/etiology , Arterial Occlusive Diseases/pathology , Calcinosis/etiology , Calcinosis/pathology , Calcitriol/physiology , Calcitriol/therapeutic use , Cardiovascular Diseases/etiology , Causality , Cinacalcet , Disease Progression , Drug Monitoring , Ergocalciferols/therapeutic use , Glomerular Filtration Rate , Humans , Hyperparathyroidism, Secondary/diagnosis , Hyperparathyroidism, Secondary/etiology , Hyperparathyroidism, Secondary/therapy , Hyperphosphatemia/etiology , Hyperphosphatemia/prevention & control , Kidney Failure, Chronic/mortality , Naphthalenes/therapeutic use , Nurse's Role , Parathyroid Hormone/physiology , Phosphorus, Dietary/adverse effects , Proportional Hazards Models , Severity of Illness Index , Treatment Outcome , Vitamin D/chemistry , Vitamin D/physiology , Vitamin D Deficiency/diagnosis , Vitamin D Deficiency/etiology , Vitamin D Deficiency/therapyABSTRACT
BACKGROUND/AIM: Diabetic nephropathy contributes substantially to cardiovascular morbidity and mortality associated with diabetes. Urinary tumor necrosis factor (TNF) excretion is increased during diabetes and serves as an important mediator of pathological changes during the initial stages of diabetic nephropathy, including sodium retention and renal hypertrophy. We tested the hypothesis that pentoxifylline (PTF), an agent that inhibits TNF synthesis, could prevent sodium retention and renal hypertrophy during diabetes. METHODS: Proximal and distal tubule TNF expression, urinary TNF excretion, sodium retention, and renal hypertrophy were examined in control, diabetic, and PTF-treated diabetic rats. RESULTS: TNF mRNA and protein levels were increased in proximal tubule cells isolated from diabetic rats compared to control rats. In contrast, TNF expression in distal tubule cells was not increased during diabetes. PTF prevented the increase in TNF mRNA and protein in proximal tubule cells during diabetes and reduced urinary TNF excretion. PTF therapy decreased whole animal sodium retention by enhancing urinary sodium excretion in diabetic rats. In addition, PTF reduced renal hypertrophy in diabetic rats. CONCLUSIONS: The proximal tubule is an important site of TNF production during diabetes and PTF is an effective therapy for preventing the pathological changes accompanying early diabetic nephropathy.
Subject(s)
Diabetes Mellitus, Experimental/drug therapy , Diabetes Mellitus, Experimental/metabolism , Diabetic Nephropathies/drug therapy , Diabetic Nephropathies/metabolism , Kidney/metabolism , Kidney/pathology , Pentoxifylline/pharmacology , Pentoxifylline/therapeutic use , Sodium/metabolism , Tumor Necrosis Factor-alpha/biosynthesis , Animals , Hypertrophy , Kidney/drug effects , Male , Rats , Rats, Sprague-DawleyABSTRACT
Nephropathy is a major contributor to overall morbidity and mortality in diabetic patients. Early renal changes during diabetes include Na retention and renal hypertrophy. Tumor necrosis factor (TNF) is elevated during diabetes and is implicated in the pathogenesis of diabetic nephropathy. We tested the hypothesis that TNF contributes to Na retention and renal hypertrophy during diabetes. Rats with streptozotocin-induced diabetes exhibit increased urinary TNF excretion, Na retention, and renal hypertrophy through the first 20 days of diabetes. Administration of a soluble TNF antagonist (TNFR:Fc) to diabetic rats reduces urinary TNF excretion and prevents Na retention and renal hypertrophy. TNF stimulates Na uptake in distal tubule cells isolated from diabetic rats, providing a possible mechanism for TNF-induced Na retention. We conclude that urinary TNF contributes to early diabetic nephropathy and may serve as a valuable diagnostic marker. Furthermore, inhibition of TNF during diabetes may attenuate early pathological changes in diabetic nephropathy.
