Measurement of individual clinical productivity in an academic anesthesiology department.
(25/801)
BACKGROUND: The ability to measure productivity, work performed, or contributions toward the clinical mission has become an important issue facing anesthesiology departments in private practice and academic settings. Unfortunately, the practice and billing of anesthesia services makes it difficult to quantify individual productivity. This study examines the following methods of measuring individual productivity: normalized clinical days per year (nCD/yr); time units per operating-room day worked (TU/OR day); normalized time units per year (nTU/yr); total American Society of Anesthesiologists (ASA) units per OR day (tASA/OR day); and normalized total ASA units per year (ntASA/yr). METHODS: Billing and scheduling data for clinical activities of faculty members of an anesthesiology department at a university medical center were collected and analyzed for the 1998 fiscal year. All clinical sites and all clinical faculty anesthesiologists were included unless they spent less than 20% of their time during the fiscal year providing clinical care, i.e., less than 0.2 clinical full-time equivalent. Outliers, defined as faculty who had productivity greater or less than 1 SD from the mean, were examined in detail. RESULTS: Mean and median values were reported for each measurement, and different groups of outliers were identified. nCD/yr identified faculty who worked more than their clinical full-time equivalent would have predicted. TU/OR day and tASA/OR day identified apparently low-productivity faculty as those who worked a large portion of their time in obstetric anesthesia or an ambulatory surgicenter. tASA/OR day identified specialty anesthesiologists as apparently high-productivity faculty. nTU/yr and ntASA/yr were products of the per-OR day measurement and nCD/yr. CONCLUSION: Each of the measurements studied values certain types of productivity more than others. By defining what type of service is most important to reward, the most appropriate measure or combination of measures of productivity can be chosen. In the authors' department, nCD/yr is the most useful measure of individual productivity because it measures an individual anesthesiologist's contribution to daily staffing, includes all clinical sites, is independent of nonanesthesia factors, and is easy to collect and determine. (+info)
Iron deficiency and reduced work capacity: a critical review of the research to determine a causal relationship.
(26/801)
The causal relationship between iron deficiency and physical work capacity is evaluated through a systematic review of the research literature, including animal and human studies. Iron deficiency was examined along a continuum from severe iron-deficiency anemia (SIDA) to moderate iron-deficiency anemia (MIDA) to iron deficiency without anemia (IDNA). Work capacity was assessed by aerobic capacity, endurance, energetic efficiency, voluntary activity and work productivity. The 29 research reports examined demonstrated a strong causal effect of SIDA and MIDA on aerobic capacity in animals and humans. The presumed mechanism for this effect is the reduced oxygen transport associated with anemia; tissue iron deficiency may also play a role through reduced cellular oxidative capacity. Endurance capacity was also compromised in SIDA and MIDA, but the strong mediating effects of poor cellular oxidative capacity observed in animals have not been demonstrated in humans. Energetic efficiency was affected at all levels of iron deficiency in humans, in the laboratory and the field. The reduced work productivity observed in field studies is likely due to anemia and reduced oxygen transport. The social and economic consequences of iron-deficiency anemia (IDA) and IDNA have yet to be elucidated. The biological mechanisms for the effect of IDA on work capacity are sufficiently strong to justify interventions to improve iron status as a means of enhancing human capital. This may also extend to the segment of the population experiencing IDNA in whom the effects on work capacity may be more subtle, but the number of individuals thus affected may be considerably more than those experiencing IDA. (+info)
Commentary on "evidence that iron deficiency anemia causes reduced work capacity".
(27/801)
This commentary assesses the strength of the causal evidence presented by Haas and Brownlie in this supplement and examines the potential magnitude of iron-deficiency anemia on welfare. From both the laboratory and field experiments, the evidence is strong and suggests that the potential magnitude of the effect of iron-deficiency anemia on work productivity is substantial. This commentary briefly discusses some of the limitations of using the estimates of effects on physiological capacity for measuring the effect on the social and economic well-being of individuals and society. Biological data are relevant to social and economic development, but additional field studies may be as important as the laboratory experiments to answer questions that also affect work productivity, household maintenance and child raising activities, and hence affect social and economic development. We extend the critical evidence review of human field studies that received disproportionately less attention than the laboratory studies in Haas and Brownlie. We provide some estimates of the magnitude of effects on well-being based on how this information has been used. Future field studies that examine the effect of iron-deficiency anemia and work output in an economic sense should measure increases in productivity but should complement this information with data on wages, income or some measure of profits to derive a money metric measure of increased productivity. Additional information on individual time allocation in household work, child care and leisure may also be required to capture social benefits deriving from improved work capacity. (+info)
Iron-deficiency anemia: reexamining the nature and magnitude of the public health problem. Summary: implications for research and programs.
(28/801)
This paper provides summary judgments about the strength of the evidence that iron deficiency or anemia causes the six functional outcomes that were reviewed in the preceding papers, highlights priority research needs and discusses the implications of these conclusions for advocacy and programs. A significant body of evidence supports a causal relationship between iron deficiency and deficits in work productivity and child development, and between severe anemia and maternal and child mortality. Causal evidence is lacking or contradictory for iron deficiency and low birth weight and infectious disease, and for mild-to-moderate anemia and child or maternal mortality. Future research is required to expand or refine these conclusions. In the meantime, advocacy should focus on the outcomes supported by substantial causal evidence. These causal relationships can be separated into a problem of severe anemia (which causes mortality) and tissue iron deficiency (which causes deficits in work performance and child development). The simple model depicting severe anemia and tissue iron deficiency as distinct but overlapping entities with distinct functional outcomes is presented and may be useful in designing and evaluating programs. (+info)
Productivity and economic burden associated with diabetes.
(29/801)
OBJECTIVES: This report assessed the cost and burden of diabetes in broad terms of economic status, underlying disability, and barriers to health care--that is, as reflected in employment, income, disability days, general health status, and access to medical care. METHODS: We used the 1990 to 1995 Behavioral Risk Factor Survey in Oklahoma to compare persons with diabetes with age-, sex-, and race/ethnicity-matched respondents without diabetes. RESULTS: Persons with diabetes were significantly and substantially worse off on all economic, disability, and access measures. CONCLUSIONS: Compared with nondiabetic persons, diabetic persons have fewer resources to deal with higher levels of disability and poorer health status. (+info)
Social costs of untreated opioid dependence.
(30/801)
Using cost-of-illness methodology applied to a comprehensive survey of 114 daily opiate users not currently in or seeking treatment for their addiction, we estimated the 1996 social costs of untreated opioid dependence in Toronto (Ontario, Canada). The survey collected data on social and demographic characteristics, drug use history, physical and mental health status, the use of health care and substance treatment services, drug use modality and sex-related risks of infectious diseases, sources of income, as well as criminality and involvement with the law enforcement system. The annual social cost generated by this sample, calculated at Canadian $5.086 million, is explained mostly by crime victimization (44.6%) and law enforcement (42.4%), followed by productivity losses (7.0%) and the utilization of health care (6.1%). Applying the $13,100 cost to the estimated 8,000 to 13,000 users and 2.456 million residents living in Toronto yields a range of social cost between $43 and $69 per capita. (+info)
Indirect cost of ischemic heart disease to employers.
(31/801)
BACKGROUND: The management of healthcare programs by employers requires accurate information about the indirect and direct costs of important chronic diseases. OBJECTIVE: To determine the indirect costs of ischemic heart disease from the perspective of the employer in private industry in the United States. DESIGN: Indirect cost of illness analysis using the human capital approach, taking the perspective of the employer rather than that of society. METHODS: Ischemic heart disease was identified in a proprietary claims database of 3.1 million insured persons using an algorithm based on administrative codes. Economic data were derived from the Bureau of Labor Statistics, the Employment Management Association, and published sources. Work-loss data were taken from the National Center for Health Statistics' Health Interview Survey. The indirect cost was calculated as the sum of the costs due to morbidity and mortality. From the perspective of the employer, morbidity costs come from lost productivity, idle assets, and nonwage factors resulting from absenteeism and mortality costs are expenditures for replacing and retraining workers. This differs from calculations from the societal perspective, in which indirect costs are the value of an individual's lost income--both current and potential. RESULTS: The total indirect cost of ischemic heart disease to employers in private industry was $182.74 per enrollee. Ninety-five percent of the indirect cost was the consequence of work loss due to morbidity rather than of mortality costs. CONCLUSION: From the perspective of the employer, the indirect cost of ischemic heart disease is overwhelmingly due to morbidity costs. (+info)
Short-term efficiency and safety of gene delivery into canine kidneys.
(32/801)
BACKGROUND: Gene delivery of biologically active molecules to the kidney may have potential therapeutic applications in renal and cardiovascular diseases. Recombinant adenovirus is one of the most efficient vectors for in vivo gene delivery. However, in vivo toxicity at the site of administration has to be evaluated for the successful use of adenovirus-mediated gene transfer. The aim of this study was to document precisely the short-term safety of different routes of intra-renal adenoviral administration and to compare their transduction efficiency. METHODS: Dog puppies were injected with an adenoviral vector expressing the beta-galactosidase reporter gene in both kidneys via three different routes, i.e. intra-renal-ureteral route (IU) and intra-renal-arterial route with (IAC) or without (IA) clamping of the renal vein. Toxicity of viral administration was assayed on day 4 at both physiological and histological levels. Renal samples were monitored for the presence of nuclear beta-galactosidase-expressing cells. RESULTS: All renal physiological parameters (glomerular filtration rate, effective renal plasma flow, and electrolyte excretion fractions) remained stable whatever the route of viral administration. No histological lesion was detected in any of the haematoxylin-eosin-stained kidney sections, and there was no evidence of ischaemia-reperfusion injury in the kidneys subjected to venous clamping. Efficient transgene expression was obtained in dog kidneys following IAC and IU injection of adenoviral vectors. Gene transfer via the IAC route induced gene expression predominantly in the cortical interstitial cells. Retrograde IU adenoviral injection resulted in reduced transduction efficiency compared with the IAC route, with transgene expression occurring mainly in the distal tubular and pyelic epithelial cells. CONCLUSIONS: The two major findings of this study were (i) the absence of acute histological and functional renal alteration following intra-arterial and intra-ureteral injections of adenoviral vectors in both kidneys of healthy dogs, and (ii) the efficiency of transgene expression with specific cellular targeting according to the route of administration. (+info)