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An important question is what happens after long-term – Etidronate: the regimen recommended by the producer treatment 10mg fluoxetine amex breast cancer quote. A study of 7-years administration of alendronate is 400 mg daily orally for 2 weeks every 3 months buy genuine fluoxetine line menstruation jokes arent funny period. Actually the turnover – Risedronate: the recommended regimen is 5 mg daily stays at a constant level generic fluoxetine 20 mg with amex breast cancer drugs, the BMD still goes up, and the orally or 35 mg once weekly. Therefore there is until now no in- dication that one would have to stop the treatment because As is the case in animals, studies in humans have revealed of an increase in osseous fragility. Whether it would be of advantage of bisphosphonates, especially those containing a nitrogen to interrupt treatment for a certain time is not known. Glorieux FH, Bishop NJ, Plotkin H, Cauley JA, Thompson DE, Nevitt MC, E, Emkey RD, Greenwald M, Zizic Chabot G, Lanogu G, Travers R (1998) Bauer DC, Genant HK, Haskell WL, TM, Wallach S, Sewell KL, Lukert BP, Cyclic administration of pamidronate Marcus R, Ott SM, Torner JC, Quandt Axelrod DW, Chines AA (1999) Rise- in children with severe osteogenesis SA, Reiss TF, Ensrud KE (1996) Ran- dronate therapy prevents corticosteroid- imperfecta. N Engl J Med 339:947– domized trial of effect of alendronate induced bone loss. Arthritis Rheum 42: 952 on risk of fracture in women with ex- 2309–2318 10. De Groen PC, Lubbe DF, Hirsch LJ, McKeever CD, Hangartner D, Keller 1535–1541 Daifotis A, Stephenson W, Freedholm M, Chesnut CH, Brown J, Eriksen EF, 2. Boivin GY, Chavassieux PM, Santora D, Pryor-Tillotson S, Seleznick MJ, Hoseyni MS, Axelrod DW, Miller, PD AC, Meunier PJ (2000) Alendronate Pinkas H, Wang KK (1996) Esophagi- (1999) Effects of risedronate treatment increases bone strength by increasing this associated with the use of alen- on vertebral and nonvertebral fractures the mean degree of mineralization of dronate. N Engl J Med 355:1016–1021 in women with postmenopausal osteo- bone tissue in osteoporotic women. JAMA 14:1344–1352 Bone 27:697–694 bone disease – from the laboratory to 11. Academic, San Diego Minne HW, Quan H, Bell NH, Brun J, Crouzet B, Arnaud F, Delmas 7. Fleisch H, Russell RGG, Francis MD Rodriguez-Portales J, Downs RW Jr, PD, Meunier PJ (1992) Vitamin D and (1969) Diphosphonates inhibit hydroxy- Dequeker J, Favus M, Seeman E, calcium to prevent hip fractures in the apatite dissolution in vitro and bone Recker RR, Capizzi T, Santora AC II, elderly. Lombardi A, Shah RV, Hirsch LJ, Science 165:1262–1264 Karpf DB (1995) Effect of oral alen- 8. Francis MD, Russell RGG, Fleisch H dronate on bone mineral density and (1969) Diphosphonates inhibit forma- the incidence of fractures in post- tion of calcium phosphate crystals in menopausal osteoporosis. N Engl J vitro and pathological calcification in Med 333:1437–1443 vivo. Schnitzer T, Bone HG, Crepaldi G, A, Gilchrist NL, Eisman J, Weinstein Stepan J, Munoz-Torres M, Wilkin TJ, Adami S, McClung M, Kiel D, Felsen- RS, El Hajj Fuleihan G, Reda C, Yates Qin-sheng G, Galich AM, Vandormael berg D, Recker RR, Tonino RP, Roux AJ, Ravn P (1998) Alendronate pre- K, Yates AJ, Stych B (1999) Multina- C, Pinchera A, Foldes AJ, Greenspan vents postmenopausal bone loss in tional, placebo-controlled, randomized SL, Levine MA, Emkey R, Santora women without osteoporosis. Ann In- trial of the effects of alendronate on AC, Kaur A, Thompson DE, Yates J, tern Med 128:253–261 bone density and fracture risk in post- Orloff JJ (2000) Therapeutic equiva- 13. Meunier PJ, Boivin GY (1997) Bone menopausal women with low bone lence of alendronate 70mg once- mineral density reflects bone mass but mass: results of the FOSIT study. Reginster JY, Minne HW, Sorensen Clin Exp Res 12:1–12 373–377 OH, Hooper M, Roux C, Brandi ML, 24. Mortensen L, Charles P, Bekker PJ, Lund B, Ethgen D, Pack S, Roumag- Rodriguez-Portales JA, Menkes CJ, Digennaro J, Johnston CC (1998) Rise- nac I, Eastell R (2000) Randomized Wasnich RD, Bone HG, Santora AC, dronate increases bone mass in an early trial of the effects of risedronate on Wu M, Desai R, Ross PD (2000) postmenopausal population: two years vertebral fractures in women with es- Skeletal benefits of alendronate: 7-year of treatment plus one year of follow- tablished postmenopausal osteoporosis. Mühlbauer RC, Russell RGG, the molecular mechanisms of action Metab 85:3109–115 Williams DA, Fleisch H (1971) the of bisphosphonates. Eur J Clin RL, LaCroix AZ, Kooperberg C, Ste- of 4-amino-1-hydroxybutylidene bis- Invest 1:336–344 fanick ML, Jackson RD, Beresford SA, phosphonate on bone biomechanics in 16. J Bone Miner Res 7:1399–1406 Prince R, Gaich, GA, Reginster YI, JM, Ockene J, Writing Group for the 26. JAMA cyclical etidronate treatment of post- 1444 288:321–333 menopausal osteoporosis. Saag KG, Emkey R, Schnitzer TJ, Med 323:73–329 Brown JP, Hawkins F, Goemaere F, Thamsborg G, Lieberman UA, Delmas PD, Malice M-P, Czachur M, Daifotis AG (1998) Alendronate for the preven- tion and treatment of glucocorticoid-in- duced osteoporosis. Schenk R, Merz WA, Mühlbauer R, Russell RGG, Fleisch H (1973) Effect of ethane-1-hydroxy-1:1-diphospho- nate (EHDP) and dichloromethylene diphosphonate (Cl2MDP) on the calci- fication and resorption of cartilage and bone in the tibial epiphysis and meta- physis of rats. The approach to osteoporosis can favor- load necessary to cause a vertebral ably alter the disease. Lin · structure, mineral content, and qual- Osteoporosis · Bisphosphonates · M. Radiographic techniques PTH (1–34) · Falls Metabolic Bone Disease Service, centered on dual X-ray absorptiome- Hospital for Special Surgery, try (DXA) permit a determination of New York, New York, USA bone mass and fracture risk. Lane bisphosphonate and pulsatile PTH Department of Orthopaedic Surgery, profoundly decrease the risk of frac- Hospital for Special Surgery, 535 East 70th Street, ture (50+%). Fall prevention strate- NY 10021 New York, USA gies can further decrease the possi- have been developed that may decrease the fragility frac- Introduction ture rate by up to 50% compared with controls treated only with calcium [7, 24, 40, 70, 79]. During the same time pe- Osteoporosis is a serious problem in the United States, af- riod, two minimally invasive procedures have been devel- fecting as many as 13–18% of women and 3–6% of men oped to rapidly address painful vertebral fractures – verte- [49, 55, 64, 68, 89]. Details regarding these proce- than half of all Caucasian white women will sustain an os- dures are the subject of separate articles within this issue. Approx- imately one-half of these fractures are related to the verte- bral bodies, with two-thirds being silent and one-third Fracture etiology: factor of risk symptomatic. Epidemiological studies have demonstrated that multiple vertebral fractures increase morbidity [67, Vertebral bodies sustain fractures under two different me- 69], and the presence and increasing numbers of fractures chanical environments: repetitive loading that fatigues the significantly increase mortality rates [11, 23, 41, 48]. De- cancellous bone and leads to the accumulation of mi- spite the recognition that osteoporotic fractures increase crofractures, or single traumatic events may overload the the risk for additional vertebral fractures as well as hip frac- vertebral body and lead to fracture [58]. To understand the tures, the majority of individuals with these fractures re- etiology of vertebral fracture, information about the loads main undiagnosed and untreated [28, 31, 74]. Radiographic methods have been enhanced and represents the ratio of the load applied to the bone to aid in the diagnosis of osteoporosis. The load 66 necessary to cause a vertebral fracture is determined by the DXA scan can be performed in a lateral or antero- the characteristics related to the vertebral body structure posterior (AP) mode. However, with the presence of osteophytes and scoliosis, the preci- sion decreases and may be artificially elevated, particu- the determinants of bone failure load larly with osteosclerotic facet joints [62]. Above the age of 60, lateral DXA avoids the posterior elements of the the ability of the vertebral body to bear certain loads de- spine, and may address this problem in patients typically pends on both the material properties of the bone and on with evidence of osteoarthritis of the spine. However, the the geometrical distribution of the tissue components overhanging ribs and the superior projection of the iliac which are able to withstand load [39]. Vertebral fractures wing often obscure the L1 and L2, and L4 and L5 verte- occur in cancellous bone, which has a complex microstruc- bral bodies, respectively, leaving one or two vertebral ture. The volume of tissue contained within cancellous bone bodies available for analysis. This may significantly de- is the bone volume fraction, and the mass of the bone crease the precision of the methodology. As a consequence, tissue within a given volume is the apparent density. Since represents the failure load per cross-sectional area is pro- the hip has a greater content of cortical bone, there may be portional to the square of the apparent density [9].
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Considering the different tools discussed purchase discount fluoxetine online pregnancy ovulation calendar, what are some of their key common elements? The Improvement Guide: A Practical Approach to Enhancing Organizational Performance order fluoxetine 10mg overnight delivery menopause 11hsd1. Reducing the Cost of Poor Quality Through Responsible Purchasing Leadership discount fluoxetine master card ximena herrera women's health. Baldrige National Quality Program Health Care Criteria for Performance Excellence. The Six Sigma Way: How GE, Motorola, and Other Top Companies Are Honing Their Performance. Total Quality Management Performance and Cost Measures: the Strategy for Economic Survival. PART II ORGANIZATION AND MICROSYSTEM This page intentionally left blank CHAPTER 5 THE SEARCH FOR A FEW GOOD INDICATORS Robert C. Lloyd Increasingly, healthcare professionals are using Shewhart control charts to analyze the variation that resides within data. Yet, many still struggle with an essential aspect of quality measurement—identifying and developing appropriate indicators to be placed on control charts. Control charts based on inappropriate or poorly developed indicators are of no value; they merely provide chart junk. To obtain good data, therefore, it is necessary to approach its collection in a systematic way. This chapter provides a template and prac- tical recommendations for selecting and developing indicators. Seven milestones in the quality measurement journey are discussed, and recom- mendations for avoiding pitfalls along the way are offered. This chapter also reviews the leading national indicator initiatives and the data expectations related to each initiative. It may seem hard to believe, but there actually was a time when the only group that cared about measuring the efficiency and effectiveness of healthcare services was providers themselves. While providers are more focused than ever on performance meas- urement, they must balance their own measurement efforts against those being demanded by the following: • Purchasers of care (individuals and companies) • Business coalitions (representing companies within defined geo- graphical areas) • Insurance companies interested in structuring contractual agree- ments around quality outcomes • Accrediting organizations. This is a fundamental switch from how healthcare data have historically been treated. Prior to the early 1980s, the only way one could obtain data on hospitals or physicians was through the subpoena process. Such data can be obtained from various Internet sites, state data commissions, CMS, Consumer Reports, and various proprietary vendors. The basic theory behind such releases is that they will make providers more accountable for the outcomes they pro- duce, improve quality, and help to contain costs. National Indicator Initiatives Along with the growing interest in reporting healthcare performance data to the public has come a related challenge. Specifically, those who endorse the public release of provider data have quickly realized that the indicators being reported must be 1. Standardized across all providers (common definitions and data col- lection procedures); 2. Produced within reasonable time frames (which has been a widely debated issue); 3. Developed at a reasonable cost to both providers and those assem- bling the data; and 4. In my 20-plus years in the healthcare field, I have never seen one set of indicators satisfy all four of these criteria simultaneously. Numerous groups and organizations have sponsored national indi- cator sets. Several of the more well known indicator initiatives are sum- marized below. Minimum Data Set the idea of creating a small set of indicators that captures the essential aspects of any healthcare experience is very appealing. As healthcare has become more complex, the idea of a minimum data set (MDS) has gained even more appeal than it had when it was first introduced in the late 1960s. What started as a general concept has emerged, over time, into a variety of specific data sets. MDSs have been proposed for everything from inpatient services to ambulance services. The basic idea behind an MDS is that a the Search for A Few Good Indicators 91 small core set of indicators is defined and used for mandatory collection and reporting at the state, regional, or national level. The basic problem with implementing this concept, however, is that agreement on what con- stitutes a minimum set of indicators has been elusive. The other major challenge has been determining who will be the end user of the MDS. Providers have different data needs than policymakers, and both groups have different needs than the purchasing managers of large corporations or the public. In the long and interesting history associated with the development of MDSs, several key developments and structures deserve to be mentioned. In 1969, the National Committee on Vital and Health Statistics developed the first formal outline for an MDS for hospital discharge data elements. This led to the creation of the Uniform Hospital Abstract Minimum Data Set in 1973. The Uniform Hospital Discharge Data Set (UHDDS) emerged in the early 1970s as the standard MDS referent for hospital-based services. The 14 data elements contained in the original UHDDS were then used to create the first Uniform Bill (UB) for hospital services, popularly known as UB-82 (82 refers to 1982, when the structure of the UB was first accepted). This one-page form contains 86 fields, some of which allow for multiple entries or subcategories. While UB-92 is used primarily for pro- cessing Medicare claims, the format has been adopted by other groups. The elements included in UB-92 were determined by the National Uniform Billing Committee (NUBC),1 which was established in 1975. Each state has its own UBC that can recommend limited revisions to UB-92. In terms of physician billing, the CMS-1500 form (originally called HCFA-1500) is the standard reference. This form was last revised in 1992 and is accepted by nearly all insurance plans. An area that has been particularly active has been the nursing profession. Today, the Nursing Management Minimum Data Set is undergoing research and development (Huber et al.
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Results at rest ((b) generic fluoxetine 10 mg without a prescription menstruation after childbirth, (f ) buy fluoxetine cheap women's health questions answered, during tonic dorsiflexion (torque at 4 Nm order 20 mg fluoxetine free shipping women's health clinic greenville tx, (c), (g)), tonic plantar flexion (torque at 4 Nm, ((d ), (h)), and simultaneous co-contraction of both ankle flexors and extensors ((e), (i)). The observation that reciprocal Ia inhibi- ing control of motoneurones and Ia interneurones, tion is depressed during co-contraction with respect in contrast with the linkage seen during simple to rest further suggests that the pathway medi- flexion–extension movements. This decoupling is ating reciprocal Ia inhibition is actively inhib- reminiscent of studies in the monkey suggesting ited during such contractions. Two spinal candi- that the descending control of the spinal motor sys- dates probably contribute to this depression of tem is conveyed by different descending pathways the transmission in the reciprocal Ia pathway. An impor- Changes in reciprocal Ia inhibition during tant functional role of this increased presynaptic postural activity inhibition could be to decrease the Ia input to Ia interneurones to allow the parallel activation of the With the initiation of a fast stepping movement by two antagonistic muscles (see Chapter 11,p. Peroneal- induced (1 × MT, 2 ms ISI) reciprocal Ia inhibition of the soleus H reflex is enhanced with a time course similar to that of the soleus H reflex depression. In Functional implications contrast, the D1 presynaptic inhibition was found There was no significant difference in the amount to be only marginally and inconsistently increased. However, there was a decrease the similar time courses of both the increased recip- in reciprocal Ia inhibition when the subjects were rocal Ia inhibition of the soleus H reflex and the tib- forced to make a co-contraction of dorsi- and plan- ialis anterior H reflex facilitation would then provide tar flexors in order to maintain balance, e. Changes in reciprocal Ia inhibition during gait Depression of reciprocal Ia inhibition during TheamountofreciprocalIainhibitionbetweenankle contraction of remote muscles flexors and extensors is modulated during walking, albeit by less than during voluntary contractions at A depression of peroneal-induced reciprocal Ia inhi- equivalent levels of EMG activity (Petersen, Morita & bition of the soleus H reflex has also been described Nielsen, 1999;Fig. The manoeuvre produces reflex reinforce- ment, akin to the classical Jendrassik manoeuvre, Methodology and the H reflex is facilitated in both the soleus and the tibialis anterior, in proportion to biting force. In some subjects, it has been possible to investigate Under these circumstances, the question arises the changes in reciprocal inhibition of the soleus about whether depression of reciprocal Ia inhibition Hreflex throughout the step cycle. In addition, the is merely the result of a subliminal co-contraction of modulation of reciprocal inhibition seen in the on- ankle flexors and extensors or is related to the mech- goingrectifiedEMGofthesoleusandtibialisanterior anisms responsible for the generalised reflex rein- was explored during the stance and swing phases of forcement (cf. The amplitude of the conditioned H reflex (as a percentage of its unconditioned value) is plotted against the time after heel contact. The intensity of the posterior tibial nerve (PTN) stimulation was adjusted to maintain the control H reflex at ∼5% of Mmax. The lower part of (c) shows the Sol and TA EMG activity (average of 30 sweeps); abscissa time after heel contact. The amount of reciprocal inhibition of Sol EMG during the stance phase (e) and of TA EMG during the swing phase (f ) (expressed as a percentage of the amount of inhibition observed during a voluntary contraction at equivalent EMG) is plotted against the time after heel contact. This suggests that the pat- ternofafferentfeedbackcannotexplaintheobserved modulation. Modulation of reciprocal Ia inhibition In the subject illustrated in Fig. Around the onset of the swing phase, stance phase of gait, and that from plantar flexors to reciprocal inhibition became greater than at rest, dorsiflexorsissmallinswing. This suggests that help ensure that antagonistic motoneurones are not transmission in the pathway of reciprocal Ia inhi- activated inappropriately during the walking cycle. Peroneal-induced inhibition of the on-going need to stabilise the ankle during the stance phase soleusEMGwasmuchsmalleratheelstrikethandur- of walking (see Chapter 11,p. It progres- sively increased through the stance phase, though always smaller than during the voluntary contrac- Studies in patients and clinical tion-MACROS-. Reciprocalinhibitionoftheon- implications going tibialis anterior EMG during the swing phase was similarly much smaller than during voluntary Methodology dorsiflexion. Because it is unusual reciprocal Ia inhibition for a sizeable H reflex to be recordable in tibialis (i) Presynaptic inhibition of Ia terminals on soleus anterior, peroneal-induced reciprocal Ia inhibition motoneurones is decreased during dynamic volun- ofthesoleusHreflexisusuallyexplored(however,see tary contractions of soleus but strongly increased p. Care is necessary to ensure that the condi- throughout the stance phase of walking (Chapter 8, tioning stimulus activates only the deep peroneal pp. Methodological reasons, in particular in patients with incomplete spinal cord injury who inadvertent stimulation of the superficial peroneal had recovered sufficient function to walk with some nerve,mayaccountforsomediscrepantfindings(see assistance than in healthy subjects. Tanaka & Ito (1976) found that a train of three shocks (ii) An early facilitation replacing the early inhi- totheperonealnervehadnoeffectin6of11patients bition was seen in two of four patients with incom- with hemiplegia, but produced an early inhibition in pletespinalcordinjuryandfourofthesevenpatients two patients and an early facilitation in the other withacompletespinallesionreportedbyCroneetal. Del- Perez&Field-Fote (2003)reported that, recipro- waide (1985) mentioned an early peroneal-induced cal inhibition tested at the 3-ms ISI was slightly facilitation in a few spastic patients, but gave no decreased. The absence lations show that the clear reciprocal Ia inhibi- of reciprocal inhibition on the unaffected side rep- tion observed in normal subjects was absent in the resents further evidence that spinal mechanisms patients. This is also illustrated in the are not normal on the clinically unaffected side of histogramsofFig. In patients in whom serial recordings the early facilitation that often replaces the early were obtained there was an increase in Ia inhibition inhibition could be due to Ib excitation duringtherecoveryperiodfollowingstroke,afinding not confirmed by Crone et al. It is possible that this facilitation in spastic patients could be due to the fact that a normal Ib excitation is moreeasilydisclosedbecauseofthedecreasedrecip- Patients with traumatic spinal cord injury rocal Ia inhibition. Studies in patients 231 (a) (b) Normal Spastic Corticospinal 120 100 Ia INs 80 TA Sol MN α MN Ia ISI (ms) Ia (c) Normal Spastic 40 TA Soleus 20 0 -60 -45 -30 -15 0 15 Difference between conditioned and control reflexes (% of control) Fig. Changes in reciprocal Ia inhibition of ankle muscles in patients with spasticity due to multiple sclerosis. The tonic corticospinal facilitation of tibialis anterior (TA)-coupled Ia interneurones (INs) is presumably interrupted in spastic patients (horizontal double-headed arrow). This produces both a reduction of the reciprocal Ia inhibition to soleus (Sol) motoneurones (MN), and a disinhibition of opposite soleus-coupled INs mediating reciprocal Ia inhibition to TA MNs. The size of the conditioned H reflex (expressed as a percentage of its unconditioned value) is plotted against the interstimulus interval (ISI). Average data from 74 normal subjects (●) and 39 patients with multiple sclerosis (❍). The number of subjects (expressed as a percentage of the total number of subjects in each population) is plotted against the difference between the size of the conditioned and control reflexes (expressed as a percentage of the control reflex size; negative values: inhibition, positive values: facilitation, at the 2 ms ISI). Changes during voluntary contraction soleus motoneurones (see Chapter 8,p. Themain ever, in functional terms, given the relatively weak abnormality in the patients was an absence of the sensitivity of the stretch reflex to presynaptic inhi- increase in peroneal-induced reciprocal Ia inhibi- bition of Ia terminals (see Chapter 8,pp. With the absence of modu- be a major factor in the unwanted stretch reflex lation of presynaptic inhibition of Ia terminals on activity triggered by the dynamic contraction of 232 Reciprocal Ia inhibition tibialis anterior in spastic patients (see Chapter 12, in normal subjects the excitabilities are similar (see pp. Mechanisms underlying changes in reciprocal Ia inhibition in spasticity Conclusions In normal subjects, the dominant excitatory effect Theresultsare,ingeneral,toovariabletoallowauni- of corticospinal volleys on ankle muscles is directed fying statement. However, putting aside the results to tibialis anterior (Brouwer & Ashby, 1991). If there was normally a tonic corticospinal disfacilitation of Ia interneurones to ankle extensor drive to tibialis anterior-coupled Ia inhibitory motoneurones by the corticospinal lesion removes interneurones, as exists in the baboon (Hongo et al. However, this is not a major ticularly in those patients with a focal lesion and factor causing spasticity at rest, since normalisation significant motor impairment, and (ii) explain the of reciprocal inhibition after frequent peroneal sti- increased reciprocal Ia inhibition from ankle exten- mulation is not accompanied by significant changes sorstotibialisanteriormotoneurones(seethesketch in spasticity (see below). Interruption of the corticospinal facilitation of the relevant Ia interneu- rones by corticospinal lesions probably accounts for Reciprocal Ia inhibition from ankle why reciprocal Ia inhibition is not increased at the extensors to flexors onset of voluntary dorsiflexion in multiple sclerosis In contrast to data on reciprocal Ia inhibition of patients. In investi- gations using PSTHs, reciprocal inhibition was also Evidenceforplasticityhasbeenfoundinnormalsub- greaterinpatientswithincompletespinalcordinjury jects(Perez,Field-Fote&Floeter,2003). This was attributed to relative excitability of these two neuronal popula- potentiation of the glycinergic synapse of Ia tions. In patients with spinal cord injury the reflex interneurones, and/or recruitment of subliminal effects of Ia inhibitory interneurones were obtained interneurones, as has been described in the goldfish at lower threshold than the soleus H reflex, whereas (Oda et al.
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