Hospital readmission rates are considered to be an important indicator of quality of care because they may be a consequence of actions of commission or omission made during the initial hospitalization of the patient, or as a consequence of poorly managed transition of the patient back into the community. The negative impact on patient quality of life and huge burden on healthcare system have made reducing hospital readmissions a central goal of healthcare delivery and payment reform efforts. In this project, we will focus on COPD (Chronic Obstructive Pulmonary Disease) which is one of the leading causes of disability and mortality worldwide. This project will design and develop a prognostic COPD healthcare management system which is a sustainable clinical decision-support system to reduce the number of readmissions by identifying those patients who need preventive interventions to reduce the probability of being readmitted. Based on patient’s clinical records and discharge summary, our system would be able to determine the readmission risk profile of patients treated for COPD. Suitable interventions could then be initiated with the objective of providing quality and timely care that helps prevent avoidable readmission. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2014. / FAU Electronic Theses and Dissertations Collection

Orientador: Silke Anna Theresa Weber / Banca: Camila Renata Corrêa Camacho / Banca: Márcia Guimarães da Silva / Banca: Ricardo Beneti / Banca: Aline Roberta Danaga / Resumo: Introdução: A prevalência da DPOC e da SAOS e o comportamento das atividades inflamatória e metabólica destas doenças, isoladamente, já foi estudada. Entretanto, a sobreposição entre elas (Overlap) e a associação com a obesidade, ainda necessita de investigações. Objetivos: Verificar a incidência da SAOS em portadores de DPOC obeso e as atividades inflamatória e metabólica desta tríade. Métodos: Foram incluídos portadores de DPOC moderado e grave com índice de massa corpórea (IMC) ≥ 27 Kg/cm2 . Além da espirometria que classificou a DPOC, foi realizada polissonografia que diagnosticou ou não a SAOS. Foram avaliados os marcadores bioquímicos de glicemia, hemoglobina glicada (HBC), insulina, leptina, adiponectina, grelina, proteína C-reativa (PCR) e interleucina 6 (IL-6). Resultados: Este estudo transversal incluiu portadores de DPOC com (N=46) e sem (N=20) SAOS com médias de idade, IMC e VEF1, respectivamente, 61.57±11.31 x 59.75±9.68 anos, 34.00±5.67 x 33.89±6.75 kg/cm2, 57.20±16.81 x 53.85±17.65 %pred. As médias de glicemia, HBC, insulina, leptina e adiponectina com ou sem SAOS foram semelhantes. A grelina aumentou com a maior gravidade da SAOS na overlap (186.16±25.56 x 137.10±21.78 pg/ml). Não foi observado aumento da PCR para nenhum grupo. A maior gravidade da DPOC aumentou a IL-6 (5.17±5.79 x 11.18±13.10). Conclusão: A prevalência de SAOS é elevada em pacientes portadores de DPOC com obesidade. A SAOS grave elevou a atividade metabólica pelo aumento da grelina, sem influencia na expressão inflamatória, na tríade com DPOC e obesidade. A gravidade da DPOC produziu maior atividade inflamatória de IL-6. / Abstract: Introduction: The prevalence of COPD and OSA and the behaviour of inflammatory and metabolic activities of each diseases has already been studied. However, the overlap between OSA and COPD, associated to obesity, still needs investigation. Objectives: To determine the incidence of OSA in obese patients with COPD, and inflammatory and metabolic activities of this triad. Methods: moderate and severe COPD patients were included with a body mass index (BMI) ≥ 27 kg / cm2. In addition to spirometry which ranked COPD, polysomnography was performed for OSA diagnosis. Blood glucose, glycated hemoglobin (GH), insulin, leptina, adiponectin, ghrelin, C-reactive protein (CRP) and interleukin 6 (IL-6) were assesed. Results: This cross-sectional study included COPD patients with (N = 46) and without (N = 20) OSA mean age, BMI and FEV1, respectively, 61.57 ±11.31 x 59.75 ±9.68 years, 34.00 ±5.67 x 33.89 ±6.75 kg/cm2, 57.20 ±16.81 x 53.85 ±17.65% pred. Mean blood glucose, GH, insulin, adiponectin and leptin with or without OSA were similar. Ghrelin increased with greater severity of OSA in the overlap group(186.16 ±25.56 x 137.10 ±21.78 pg/ml). There was no difference for CRP, but IL-6 (5.17 ±5.79 x 18.11 ±10.13) was increased in the more severe COPD. Conclusion: The prevalence of OSA is high in COPD patients with obesity. The severe OSAS increased metabolic activity by increasing ghrelin. The severity of COPD produced greater inflammatory activity. / Doutor

by Martin Li. / Year shown on spine: 1997. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 150-157). / DECLARATION --- p.II / ABSTRACT --- p.III / ACKNOWLEDGEMENTS --- p.VII / CONTENTS --- p.VIII / LIST OF ABBREVIATIONS --- p.XIV / LIST OF TABLES --- p.XVI / LIST OF CHART --- p.XXIII / LIST OF FIGURES --- p.XXIV / Chapter CHAPTER 1 --- OBSTRUCTIVE AIRWAY DISEASE: PUBLIC HEALTH AND CLINICAL ASPECTS --- p.1 / Chapter 1.1. --- Background --- p.1 / Chapter 1.2. --- Magnitude of the problem --- p.2 / Chapter 1.2.1. --- Asthma --- p.2 / Chapter 1.2.2. --- Chronic obstructive pulmonary disease --- p.3 / Chapter 1.2.3. --- Prevalence of osteoporosis in Hong Kong --- p.4 / Chapter 1.2.4. --- History of asthma care --- p.5 / Chapter 1.2.5. --- Treatment of OAD --- p.5 / Chapter 1.3. --- Side effects of Glucocorticoid in OAD patients --- p.6 / Chapter 1.4. --- Side effccts of inhaled corticosteroids in OAD patients --- p.7 / Chapter 1.5. --- Trend of asthma therapy in Hong Kong --- p.8 / Chapter CHAPTER 2: --- OSTEOPOROSIS: PUBLIC HEALTH AND CLINICAL ASPECTS --- p.11 / Chapter 2.1. --- Bone Biology --- p.11 / Chapter 2.2. --- Skeletal Organisation --- p.11 / Chapter 2.3. --- Bone remodelling --- p.12 / Chapter 2.4. --- Effect of corticosteroids on bone remodelling --- p.13 / Chapter 2.5. --- Corticosteroids induccs osteoporosis --- p.13 / Chapter 2.6. --- Factors affecting BMD --- p.14 / Chapter 2.6.1. --- Peak bone mass --- p.14 / Chapter 2.6.2. --- Ethnic factors --- p.14 / Chapter 2.6.3. --- Aging --- p.15 / Chapter 2.6.4. --- Calcium intake --- p.15 / Chapter 2.6.5. --- Oestrogen --- p.16 / Chapter 2.6.6. --- Alcohol consumption --- p.17 / Chapter 2.6.7. --- Cigarette smoking --- p.17 / Chapter 2.7. --- Physical activity and BMD --- p.17 / Chapter 2.8. --- Body composition in Chinese subjects --- p.18 / Chapter CHAPTER 3 --- "PHASE I: BODY COMPOSITION AND BONE MINERAL DENSITY IN OBSTRUCTIVE AIRWAY DISEASE PATIENT AND NORMAL CONTROL SUBJECTS: OBJECTIVES, SUBJECTS AND METHODS" --- p.20 / Chapter 3.1. --- Objectives --- p.20 / Chapter 3.2. --- Subjects and methods --- p.21 / Chapter 3.2.1 --- OAD patients --- p.21 / Chapter 3.2.1.1 --- Disease definition and selection criteria --- p.21 / Chapter 3.2.1.2. --- Normal Control subjects --- p.21 / Chapter 3.3. --- Power of estimation --- p.22 / Chapter 3.4. --- Survey methods --- p.22 / Chapter 3.5. --- Questionnaire --- p.23 / Chapter 3.6. --- Body composition and bone mineral density measurement --- p.23 / Chapter 3.6.1. --- Body composition analysis --- p.24 / Chapter 3.6.2. --- Lumbar spine and proximal hip bone mineral density analysis --- p.24 / Chapter 3.6.3. --- Routine quality control of measurements --- p.24 / Chapter 3.6.4. --- Precision on patient repositioning --- p.25 / Chapter 3.7. --- Statistical methods --- p.25 / Chapter 3.8. --- Bone mineral density of normal control subjects --- p.25 / Chapter CHAPTER 4 --- PHASE II: FLUORIDE IN THE TREATMENT OF OSTEOPOROSIS --- p.27 / Chapter 4.1. --- Introduction --- p.27 / Chapter 4.2. --- Mechanisms of action --- p.28 / Chapter 4.2.1. --- Antiresorptive effect of fluoride --- p.28 / Chapter 4.2.2. --- Force-oriented osteogenic effect of fluoride --- p.28 / Chapter 4.2.3. --- Biochemical osteogenic effect --- p.29 / Chapter 4.3. --- Effect of fluoride salts on BMD: results of clinical trials --- p.29 / Chapter 4.4. --- Effcct of fluoride on bone histomorphology --- p.30 / Chapter 4.5. --- Compliance with sodium fluoride therapy --- p.31 / Chapter 4.6. --- Contradiction of fluoride treatment --- p.31 / Chapter 4.7. --- Sodium monofluorophosphate preparation --- p.32 / Chapter CHAPTER 5 --- PHASE II: THE EFFECTS OF FLUORIDE ON BONE MINERAL DENSITY OF OAD PATIENTS ON STEROID TREATMENT --- p.37 / Chapter 5.1. --- Objectives --- p.37 / Chapter 5.2. --- Subjects and methods --- p.37 / Chapter 5.2.1. --- Power of the study --- p.37 / Chapter 5.2.2. --- Subjects --- p.37 / Chapter 5.2.3. --- Method of randomisation --- p.38 / Chapter 5.2.4. --- Treatment modalities --- p.39 / Chapter 5.2.4.1. --- Treatment group --- p.39 / Chapter 5.2.4.2. --- Control group --- p.39 / Chapter 5.2.5. --- Bone mineral density measurements --- p.39 / Chapter 5.2.6. --- Routine quality control of measurement and precision on patient repositioning --- p.40 / Chapter 5.2.7. --- Methods of monitoring drug compliance --- p.40 / Chapter 5.2.8 --- Statistical methods --- p.40 / Chapter CHAPTER 6 --- RESULTS FOR PHASE I --- p.42 / Chapter 6.1. --- Statistical power of this phase of the study --- p.42 / Chapter 6.2. --- Clinical features of OAD subjects on inhaled steroid --- p.42 / Chapter 6.3. --- Anthropometric measurements and bone mineral density --- p.45 / Chapter 6.4. --- Analysis of covariance for BMDs differences --- p.48 / Chapter 6.5. --- Multiple regression --- p.50 / Chapter 6.6 --- Correlation --- p.51 / Chapter CHAPTER 7 --- RESULTS FOR PHASE II: FLUORIDE AND CALCIUM TRIAL --- p.81 / Chapter 7.1. --- Factors affects the power of studies --- p.81 / Chapter 7.2. --- Clinical findings --- p.82 / Chapter 7.3. --- Body measurements and bone mineral densitometry --- p.85 / Chapter CHAPTER 8: --- DISCUSSION FOR PHASE I --- p.117 / Chapter CHAPTER 9: --- DISCUSSION FOR PHASE II: TRIDIN AND CALCIUM TRIAL --- p.124 / APPENDIX 1: QUESTIONNAIRE FOR OAD BONE MINERAL DENSITY STUDY --- p.132 / APPENDIX 2: BONE SCANS FROM HOLOGIC QDR2000 --- p.137 / APPENDIX 3. TABLES AND REFERENCE CURVES FOR NORMAL HONG KONG CHINESE FEMALE OR MALE BMD --- p.142 / REFERENCE --- p.150

Interventions are needed to improve health outcomes by increasing the practice of evidence based medicine ( EBM ). Patient mediated interventions have been little studied but hold promise : they target identified barriers to EBM and particular types of patient mediated intervention have shown success. Furthermore, consumers are now being given information about evidence but the effects of this on EBM have yet to be properly assessed. The aim of this study was to show whether informing patients about research evidence leads to improved application of that evidence in their medical care. The study trialed a relatively low cost manual, developed using current best practice, which summarised Cochrane Reviews of evidence. The study focused on chronic obstructive pulmonary disease ( COPD ), a high - cost, high - burden chronic disease, showing a large gap between evidence and clinical practice. The study comprised a controlled before - and - after trial and a process evaluation. The trial assessed the success of this manual in changing medical practice for three indicator treatments ( influenza vaccination, bone density testing and pulmonary rehabilitation ) and in changing patient quality of life, knowledge, communication with doctor, satisfaction with information and anxiety. Results were analysed by median split of socioeconomic disadvantage. At 3 months the manual was associated with lower anxiety for participants with lowest socioeconomic disadvantage. At 12 months the manual was associated with higher pulmonary rehabilitation enrolment for participants with greatest socioeconomic disadvantage. Other outcome measures showed no significant change. Limitations included loss of power from unexpectedly good baseline care and adjustments for baseline differences. The process evaluation showed that the manual was read more than a control pamphlet at both 3 and 12 months but a minority of manual recipients reported talking to their doctor about topics from the manual. Very little treatment change was reported. Patient attitudes to evidence and doctor / patient communication norms appeared to be barriers for this patient group. New protocols for the design of behavioural interventions provide a framework for overcoming these barriers in future interventions. / Thesis (Ph.D.)--School of Medicine, 2006.

published_or_final_version / Public Health / Master / Master of Public Health

published_or_final_version / Nursing Studies / Master / Master of Nursing

No description available.

To investigate the possibility that malnutrition is an important factor that prolongs respiratory failure (PRF), I studied the effects of pharmacologic injections of recombinant human growth hormone (rhGH), an important anabolic stimulus, on nutritional and respiratory parameters in patients requiring mechanical ventilation for more than three days. Patients were excluded from consideration if dominating factors known to prolong ventilatory failure had not been stabilized. Over ten months, 106 patients in PRF were evaluated, but only six met the selection criteria. Three patients were randomized to receive standard nutritional support, and three into a group that received the equivalent nutrition plus 5 mg/day of rhGH for 14 days or until withdrawal of mechanical ventilation. Baseline characteristics of the selected patients were divergent as demonstrated by body mass indexes ranging from 14 to 42 (kg/m$ sp2),$ baseline maximal inspiratory pressures (PI$ sb{ max}$ from $-$15 to $-$70 cm H$ sb2$O, and Day 1 N balances from $-$13.5 to 1.2 g N/day. Despite increased plasma insulin-like growth factor-1 concentrations, the mean daily N balances of the rhGH-treated group were no better than the controls (1.3 $ pm$ 5.0 vs. 0.4 $ pm$ 2.6 g N/day; Mean $ pm$ SD), nor were there differences in PI$ sb{ max},$ level of ventilatory assistance required, and days to weaning. The persistence of respiratory failure in the overwhelming majority of patients in PRF appears to be due to factors already known to prevent weaning from mechanical ventilation. Even the carefully selected patients enrolled in the present study were insufficiently homogeneous or stable enough to allow proper testing of the experimental hypothesis.

Aim The aim of this study was to determine the contribution of occupational exposures to the burden of Chronic Obstructive Pulmonary Disease (COPD) among a sample of hospital based patients. Methods Cases (n=110) with specialist physician diagnosed COPD from the three public sector specialist respiratory clinics in KZN and controls (n=102) from other nonrespiratory chronic ailment specialist clinics at the same institutions were selected. An interviewer administered questionnaire and exposure history was obtained for each participant. In addition, a valid lung function test was obtained for each case. Data was analysed using STATA version 10. Multivariate regression models were developed to examine the relationship between COPD and occupational exposures while adjusting for age, sex, smoking and previous history of tuberculosis. The relationship of FEV1 and occupational exposures, adjusted for age, height, previous history of tuberculosis and smoking history, was investigated among cases. Results Cases and controls were similar with respect to age and sex distribution. Cigarette smoking differed significantly between cases and controls with a larger proportion of cases having ceased to smoke compared to controls (72% vs 46%, p<0.01). A higher proportion of controls reported employment in administrative, managerial and quality control positions (21.3% vs 12.0%, 7.7% vs 2.6% and 5.4% vs 0.3% respectively). Employment in the construction and shoe manufacturing industries was reported more frequently by cases (10.3% vs 3.2% and 10.0% vs 4.9% respectively). Cases were more likely than controls to have been exposed to dust (72% vs 28%, p<0.001) or to chemicals, gas or fumes (74% vs 25.5%, p<0.001) and reported exposure durations 3-4 fold higher than that of controls (p<0.001). Dust and chemical, gas or fume exposure was associated with an increased odds of developing COPD. Exposure to dusts (OR 7.9, 95% CI 3.9-15.7, p<0.001), chemicals, gas or fumes (OR 6.4, 95% CI 3.2-12.8, p<0.001) were significantly associated with odds of developing COPD. In addition, previous history of tuberculosis, as well as smoking were associated with an increased odds of COPD (OR 5.7, 95% CI 1.2-27.4 p<0.001 and OR 6.4, 95% CI 2.3-17.7, p<0.001). Discussion and Conclusion This is one of the first hospital based case-control studies looking at occupational contribution to COPD undertaken in South Africa. In this sample of participants, strong associations were observed between self-reported occupational exposures to dust, and chemicals, gas or fumes, and physician’s diagnosis of COPD. The study also demonstrated a strong association between smoking and previous history of tuberculosis, and risk of COPD. The findings suggest that persons with known occupational exposures to respiratory irritants should be monitored to detect the onset of respiratory ill-health and that preventive strategies should reduce exposure to these agents in the workplace. / Thesis (M.Med.)-University of KwaZulu-Natal, Durban, 2009.

The objective of this study was to assess the oxygen cost of various intensities of steady-state cycling. VO2 (ml·min -1·kg-1) was measured at rest, during unloaded cycling (UL), 20 Watts, 50% (SS50) & 65% (SS65) of peak watts in 40 COPD patients (64 +/- 9 yrs; FEV1/FVC: 48 +/- 17 % predicted; FEV1:36 +/- 14 % predicted) and 28 age-matched healthy controls (CTRL). Despite higher VE (L·min -1) in COPD vs. CTRL (UL: 20.6 +/- 3.4 vs. 15.4 +/- 4.1; 20W: 24.3 +/- 4.5 vs. 17.8 +/- 4.2), VO2 at rest, at UL and 20W was not higher in COPD compared to CTRL. In addition, comparable slope and intercept coefficients for the VO2 vs. Watt relationship were obtained in COPD and CTRL for submaximal cycling of low to moderate intensity. (Abstract shortened by UMI.)