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1.
J Arthroplasty ; 33(10): 3113-3117, 2018 10.
Article in English | MEDLINE | ID: mdl-29909957

ABSTRACT

BACKGROUND: Patients taking narcotics chronically are more likely to have worse outcomes after total joint arthroplasty. These negative outcomes may be avoided when modifiable risk factors such as narcotic use are identified and improved before elective joint replacement. An accurate assessment of narcotic use is needed to identify patients before surgery. This study examines the amount of reported narcotic use in patients with hip or knee osteoarthritis and compares this with the narcotic prescriptions recorded in our state's drug prescription monitoring database. METHODS: All new patients seen during a 1-year period by our adult reconstruction practice were identified. Patients' electronic health records were reviewed to determine whether narcotic use was reported. A subsequent search was performed using the Arkansas Prescription Drug Monitoring Program to determine if the patient had been previously prescribed a narcotic. RESULTS: A total of 502 patients were included in the study. One hundred seventy patients (34%) were prescribed a narcotic within 3 months of the clinic visit according to the Arkansas Prescription Drug Monitoring Program, but only 111 (22%) reported narcotic use in their electronic health record (P < .0001). Moreover, only 92 patients (54% of 170) prescribed a narcotic within 3 months reported it. Narcotic recipients were more likely to be under the age of 65 years (P = .0081), smokers (P < .0001), and current benzodiazepine users (P < .0001). CONCLUSION: This study demonstrates that patients significantly underreport their narcotic use to their physician. The availability of a state prescription drug monitoring program allows physicians to check the frequency of filled narcotic prescriptions by their patients.


Subject(s)
Analgesics, Opioid/adverse effects , Arthralgia/drug therapy , Narcotics/adverse effects , Opioid-Related Disorders/etiology , Osteoarthritis, Hip/surgery , Osteoarthritis, Knee/surgery , Adult , Aged , Aged, 80 and over , Analgesics, Opioid/therapeutic use , Arthralgia/etiology , Arthroplasty, Replacement , Databases, Factual , Elective Surgical Procedures , Female , Humans , Male , Middle Aged , Narcotics/therapeutic use , Osteoarthritis, Hip/complications , Osteoarthritis, Knee/complications , Prescription Drug Monitoring Programs , Risk Factors
2.
J Arthroplasty ; 33(9): 2774-2779, 2018 09.
Article in English | MEDLINE | ID: mdl-29705679

ABSTRACT

BACKGROUND: The use of narcotics has been found to be a modifiable risk factor for success of arthroplasty. We sought to determine the risk factors leading to increased narcotic use after total hip arthroplasty and total knee arthroplasty. METHODS: A retrospective chart review was performed on new patients presenting to an orthopedic reconstructive-service clinic. New patients aged 18 years or older with osteoarthritis of the hip or knee who presented over a 1-year period and underwent total knee arthroplasty or total hip arthroplasty were included. The Arkansas prescription monitoring program was then used to determine recent narcotic and benzodiazepine prescriptions filled within 3 months of surgery, and this was converted into morphine milligram equivalents (MME). RESULTS: One hundred seventy-nine patients met the inclusion criteria. When compared with patients who did not take any preoperative opioids, narcotic- and tramadol-only users filled an average of 86% and 38% more MME, respectively. Benzodiazepine users required an average of 81% more MME postoperative than nonusers, and smokers required an average of 90% more MME postoperative than nonsmokers. Subjects with body mass index >40 kg/m2 had 82% higher average postoperative MME than subjects with body mass index <25 kg/m2. Age and sex had no significant correlation with postoperative narcotic use. CONCLUSION: This study suggests that a patient's preoperative narcotic, tramadol, benzodiazepine, and tobacco use are correlated to the amount of postoperative narcotic prescriptions filled in the 3 months following surgery. Predisposition to substance abuse may be a characteristic which leads to increased postoperative narcotic use.


Subject(s)
Arthroplasty, Replacement, Hip/adverse effects , Arthroplasty, Replacement, Knee/adverse effects , Benzodiazepines/adverse effects , Narcotics/adverse effects , Pain, Postoperative/complications , Smoking/adverse effects , Tramadol/adverse effects , Aged , Analgesics, Opioid/adverse effects , Body Mass Index , Female , Humans , Knee Joint , Linear Models , Male , Middle Aged , Morphine/adverse effects , Opioid-Related Disorders/complications , Opioid-Related Disorders/etiology , Osteoarthritis/complications , Osteoarthritis/surgery , Pain, Postoperative/drug therapy , Postoperative Period , Retrospective Studies , Risk Factors
3.
J Appl Physiol (1985) ; 115(7): 1099-106, 2013 Oct 01.
Article in English | MEDLINE | ID: mdl-23887904

ABSTRACT

Chronic exposure to diesel exhaust particulates (DEP) increases the risk of cardiovascular disease in urban residents, predisposing them to the development of several cardiovascular stresses, including myocardial infarctions, arrhythmias, thrombosis, and heart failure. DEP contain a high level of polycyclic aromatic hydrocarbons, which activate the aryl hydrocarbon receptor (AHR). We hypothesize that exposure to DEP elicits ventricular remodeling through the activation of the AHR pathway, leading to ventricular dilation and dysfunction. Male Sprague-Dawley rats were exposed by nose-only nebulization to DEP (SRM 2975, 0.2 mg/ml) or vehicle for 20 min/day × 5 wk. DEP exposure resulted in eccentric left ventricular dilation (8% increased left ventricular internal diameter at diastole and 23% decreased left ventricular posterior wall thickness at diastole vs. vehicle), as shown by echocardiograph assessment. Histological analysis using Picrosirius red staining revealed that DEP reduced cardiac interstitial collagen (23% decrease vs. vehicle). Further assessment of cardiac function using a pressure-volume catheter indicated impaired diastolic function (85% increased end-diastolic pressure and 19% decreased Tau vs. vehicle) and contractility (57 and 48% decreased end-systolic pressure-volume relationship and maximum change in pressure over time vs. end-diastolic volume compared with vehicle, respectively) in the DEP-exposed animals. Exposure to DEP significantly increased cardiac expression of AHR (19% increase vs. vehicle). In addition, DEP significantly decreased the cardiac expression of hypoxia inducible factor-1α, the competitive pathway to the AHR, and vascular endothelial growth factor, a downstream mediator of hypoxia inducible factor-1α (26 and 47% decrease vs. vehicle, respectively). These findings indicate that exposure to DEP induced left ventricular dilation by loss of collagen through an AHR-dependent mechanism.


Subject(s)
Air Pollutants/toxicity , Cardiovascular System/physiopathology , Environmental Exposure/adverse effects , Gasoline/toxicity , Heart Ventricles/physiopathology , Vehicle Emissions/toxicity , Ventricular Remodeling/physiology , Animals , Blood Pressure/physiology , Cardiovascular System/metabolism , Diastole/physiology , Male , Rats , Rats, Sprague-Dawley , Receptors, Aryl Hydrocarbon/metabolism
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