The fetal matrix. Evolution, development and disease. Peter Gluckman, Mark Hanson. Cambridge: Cambridge University Press, 2005 (xiv + 257 pp). ISBN 0 521 54235 9. This is a remarkable book by two authors who have both worked at the very top of fetal and perinatal biology for decades. They hypothesise that much of adult chronic disease can be explained by a series of predictive adaptive responses made by the fetus during intrauterine life. By these responses, triggered by changes in the intrauterine environment, the fetus attempts to change aspects of its growth and development in a way that may favour postnatal survival. In a sense, the intrauterine environment is taken to be a predictor of life outside the womb, which may well be very different from the fetal prediction. It is put forward that these interactions of gene and environment are ultimately responsible for many of the health problems of adulthood including obesity, hypertension, diabetes and the vascular consequences of atherosclerosis, stroke and myocardial infarction. The story does not require an in-depth understanding of either genetics or fetal physiology. In fact, the authors gently introduce some of their concepts with basic information about reproduction and the influence of genes on embryonic development, before developing their ideas in greater detail. The narrative writing style is easy to follow and there is an extensive bibliography for anyone interested in further study in this field. The book ends with a discussion of how a better understanding of these concepts might help to prevent adult disease, and the possibilities that may exist from manipulating both the prenatal and postnatal environments. While some of this is speculative, the authors develop a compelling argument for governments to fund research in the field of developmental biology. They argue strongly that there needs to be a “big science” approach, with the funding of long-term studies that begin long before pregnancy and continue into adulthood. If the authors are correct, this kind of investment may also pay dividends for other scourges of modern civilisation such as breast and prostate cancer, and Alzheimer’s disease. This work has the potential to be recognised as a landmark publication that influences scientific thinking for decades. It should be of interest to anyone who is involved in any aspect of human medicine and biology, particularly those working in the field of perinatal medicine. David A EllwoodProfessor of Obstetrics and Gynaecology The Canberra Hospital, ACT

David A Ellwood

Objective: To estimate the risks of maternal and perinatal morbidity and mortality in a second pregnancy, attributable to caesarean section in a first pregnancy.Design and setting: Cross-sectional analytic study of hospital births in New South Wales, based on linked population databases.Participants: 136 101 women with one previous birth who gave birth to a singleton infant in NSW in 1998–2002.Main outcome measures: Crude and adjusted odds ratios (aOR) and 95% confidence intervals (95% CI) for maternal and perinatal morbidity and mortality.Results: 19% of mothers had a caesarean section in their first pregnancy. Compared with mothers who had had primary vaginal births, mothers who had had primary caesarean section and undewent labour in the second birth were at increased risk of uterine rupture (aOR, 12.3; 95% CI, 5.0–30.1; P < 0.0001), hysterectomy (3.5; 1.5–8.4; P < 0.01), postpartum haemorrhage (PPH) following vaginal delivery (1.6; 1.4–1.7; P < 0.0001), manual removal of placenta (1.3; 1.1–1.6; P < 0.01), infection (6.2; 4.7–8.2; P < 0.0001) and intensive care unit (ICU) admission (3.1; 2.1–4.7; P < 0.0001); among mothers who did not undergo labour (ie, had an elective caesarean section), there was a lower risk of PPH (0.6; 0.5–0.7; P < 0.0001) and ICU admission (0.4; 0.3–0.5; P < 0.0001). For infants there was increased risk of preterm delivery (1.2; 1.1–1.3; P < 0.0001) and neonatal intensive care unit admission following labour (1.6; 1.4–1.9; P < 0.0001) in the birth after primary caesarean section. The occurrence of stillbirth was not modified by labour.Conclusions: Caesarean section in a first pregnancy confers additional risks on the second pregnancy, primarily associated with labour. These should be considered at the time caesarean section in the first pregnancy is being considered, particularly for elective caesarean section for non-medical reasons.

Lee K Taylor DRANZCOG, FAFPHM · Judy M Simpson PhD, CStat · Christine L Roberts DrPH, FAFPHM · Emily C Olive FRANZCOG, DDU · David J Henderson-Smart FRACP, PhD

Physical activity can significantly reduce the risk of cardiovascular disease, diabetes, some forms of cancer, osteoporosis, obesity, falls and fractures, and some mental health problems. While the benefits of physical activity are clear, there is a slightly increased risk of sudden death while exercising (compared with while sedentary), especially in untrained people undertaking unaccustomed vigorous activity. Routine exercise testing yields a significant number of false-positive results, and has not been shown to prevent exercise-related acute cardiac events. There is no convincing evidence that exercise is itself associated with osteoarthritis, but significant joint injury which occurs during sport is associated with an increased risk of subsequent development of osteoarthritis.

Peter D Brukner MB BS, FACSP · Wendy J Brown BSc(Hons), MSc, PhD

“SNAP” is a model for the general practice management of four common behavioural risk factors: smoking, nutrition, alcohol and physical activity. The SNAP program was developed for the Australian Government in 2002. In 2003 and 2004, a feasibility study was conducted in one urban and one rural division of general practice (DGP) in NSW, in partnership with their local area health services. Information technology support and referral directories were developed, based on an initial needs assessment, SNAP guidelines, a clinical summary chart, patient education materials, and general practitioner and staff training. GPs reported that the SNAP approach fitted general practice consultations well. After its implementation, they were more confident in using motivational interviewing and SNAP interventions and referred more frequently. The impact and sustainability of the SNAP program were limited by a lack of effective practice teamwork, poor linkages with referral services, and the lack of a business model to support SNAP in the practices. DGPs could play an important role in providing practice visits and resources to improve communication, education and collaboration to support SNAP programs.

Mark F Harris DRACOG, FRACGP, MD · Coletta Hobbs BSc(Psych)(Hons), PhD · Gawaine Powell Davies BA, MHP · Sarah Simpson BA(Hons), BAppSci(Health Ed), MPH · Diana Bernard BSocStud, Grad Dip Early Childhood Studies, MPH · Anthony Stubbs BA(Health Ed)

The Sharing Health Care Initiative (SHCI) demonstration project, which aimed to improve management of chronic diseases, was implemented in four small remote communities in the Katherine region which are serviced by the Katherine West Health Board, a remote Aboriginal-community-controlled health organisation in the Northern Territory. We reviewed the project proposal, final report, evaluation reports and transitional funding proposal, and supplemented these with in-depth interviews with key individuals. We determined factors critical to the sustainability of the SHCI project in relation to context, community engagement, systems flexibility and adaptability, the availability and effect of information systems, and the human nature of health care and policy. The project had a significant impact on community awareness of chronic disease and an improvement in clinic processes. We found that a number of interrelated factors promoted sustainability, including: An implementation strategy sufficiently flexible to take account of local conditions; A high level of community engagement; Appropriate timeframes, timing and congruence between national policy and local readiness to implement a chronic disease project; Effective communication between participating organisations; Project champions (key individuals) in participating organisations; Effective use of monitoring and evaluation data; and Adequate and ongoing funding. The absence of a number of these factors, such as poor communication, inhibited sustainability. Other factors could both promote and inhibit. For example, the impact of key individuals was important, but could be idiosyncratic and have negative effects.

John Wakerman MTH, FAFPHM, FACRRM · Elizabeth M Chalmers MPH, FAFPHM, FACRRM · Christine L Clarence BPE, MICD, DipTeaching · John S Humphreys BA, Dip Ed, PhD · Andrew I Bell MB BS, FAFPHM, FACRRM · Ann Larson BA, MA, PhD · David Lyle MB BS, FAFPHM, PhD · Dennis R Pashen MPHTM, FRACGP, FACCRM

Objective: To estimate the incremental effects on cost and quality of life of cardiac rehabilitation after an acute coronary syndrome.Design: Open randomised controlled trial with 1 year’s follow-up. Analysis was on an intention-to-treat basis.Setting: Two tertiary hospitals in Sydney.Intervention: 18 sessions of comprehensive exercise-based outpatient cardiac rehabilitation or conventional care as provided by the treating doctor.Participants: 113 patients aged 41–75 years who were self-caring and literate in English. Patients with uncompensated heart failure, uncontrolled arrhythmias, severe and symptomatic aortic stenosis or physical impairment were excluded.Main outcome measures: Costs (hospitalisations, medication use, outpatient visits, investigations, and personal expenses); and measures of quality of life. Incremental cost per quality-adjusted life year (QALY) saved at 1 year (this estimate combines within-study utility effects with reported 1-year risk of survival and treatment effects of rehabilitation on mortality). Sensitivity analyses around a base case estimate included alternative assumptions of no treatment effect on survival, 3 years of treatment effect on survival and variations in utility.Results: The estimated incremental cost per QALY saved for rehabilitation relative to standard care was $42 535 when modelling included the reported treatment effect on survival. This increased to $70 580 per QALY saved if treatment effect on survival was not included. The results were sensitive to variations in utility and ranged from $19 685 per QALY saved to rehabilitation not being cost-effective.Conclusions: The effects on quality of life tend to reinforce treatment advantages on survival for patients having postdischarge rehabilitation after an acute coronary syndrome. The estimated base case incremental cost per QALY saved is consistent with those historically accepted by decision making authorities such as the Pharmaceutical Benefits Advisory Committee.

Tom G Briffa PhD, MSc · Simon D Eckermann PhD(Ec), MSc, GradDipHEc · Alison D Griffiths BA Hons · Anthony C Keech MB BS, MScEpid, FRACP · Phillip J Harris MB BS, DPhil, FRACP · M Rose Heath RN · Saul B Freedman PhD, FRACP, FACC, FESC · Lana T Donaldson RN, MPH · N Kathryn Briffa BAppSc(Physio), PhD

Strict control of blood glucose levels should be pursued before conception and maintained throughout the pregnancy (glycohaemoglobin [HbA1c] level as close as possible to the reference range). Before conception: high-dose (5 mg daily) folate supplementation should be commenced; oral hypoglycaemic agents should be ceased; and diabetes complications screening should take place. Management should be by a multidisciplinary team experienced in the management of diabetes in pregnancy. Blood glucose monitoring is mandatory during pregnancy, and targets are: fasting 4.0–5.5 mmol/L; postprandial < 8.0 mmol/L at 1 hour; < 7 mmol/L at 2 hours. A first trimester nuchal translucency (possibly with first trimester biochemical screening with pregnancy-associated plasma protein A and β-human chorionic gonadotropin) should be offered. Ultrasound should be performed for fetal morphology at 18–20 weeks, if required, for cardiac views at 24 weeks and for fetal growth at 28–30 and 34–36 weeks. Induction of labour or operative delivery should be based on obstetric and/or fetal indications. Level 3 neonatal nursing facilities may be required and should be anticipated when birth occurs before 36 weeks, or if there has been poor glycaemic control. Insulin requirements fall rapidly during labour and in the puerperium. At this time, close monitoring and adjustment of insulin therapy is necessary.

Aidan McElduff MB BS, PhD, FRACP · N Wah Cheung MB BS, FRACP, PhD · H David McIntyre MB BS, FRACP · Janet A Lagström BSc, RM, GradCertDiabetesEd · Barry N J Walters FRACP, FRANZCOG · Jeremy J N Oats MB BS, DM, FRANZCOG · Peter Wein MB BS, FRANZCOG · Glynis P Ross MB BS(Hons), FRACP · David Simmons MD, FRACP

Soft-tissue injuries are injuries to skin, fascia, ligament, muscle, and tendon. Currently, many therapeutic medications are commonly used in the management of soft-tissue injuries, including: analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, prolotherapy sclerosant agents, aprotinin, glyceryl trinitrate, botulinum toxin, and glucosamine. Despite their regular use for soft-tissue injury, few medications have strong evidence of a consistent therapeutic effect. In this article, we review the proposed mechanisms of action, side effects, and the evidence base (based on National Health and Medical Research Council levels of evidence1) for common soft-tissue injury treatments. We also suggest appropriate circumstances for using therapeutic medications, with emphasis on the Hippocratic principle of primum non nocere (first do no harm). Non-steroidal anti-inflammatory drugs for ligament and muscle injuryNSAIDs are among the most widely used medications for common soft-tissue injuries such as muscle contusions, muscle tears, and ligament tears. The mechanism of action of NSAIDs is through non-specific cyclo-oxygenase inhibition, thereby blocking the production of prostaglandins from arachidonic acid. Prostaglandin inhibition by NSAIDs decreases the inflammatory response, which can have both positive and negative effects. For example, the arachidonic acid “overflow” pathway may lead to increased leukotriene production and potential tissue damage. Other known negative NSAID class side effects include hypertension, altered renal function, gastrointestinal disturbance (including peptic ulceration), and the recently discovered increased rates of myocardial infarction with non-selective NSAIDs, such as diclofenac and ibuprofen (evidence level III-2 [E32]).2 Potentially desirable class effects of NSAIDs include reduced risk of bowel cancer and increased blood clotting times. Side effects, whether positive or negative, are generally far more relevant for long-term use (such as in patients with rheumatoid arthritis) than with short-term use for sports injury. Many NSAIDs are available as topical preparations. Although the results of tissue penetration studies are variable, for injured body structures which are close to the surface (eg, limbs), topical NSAIDs may offer the advantages of higher local tissue concentrations with reduced risk of systemic side effects. The balance of evidence suggests that NSAID use is associated with a short-term mild to moderate decrease in pain in “minor sports injury” (E2),3 ankle sprains and knee pain (E2),4 and shoulder pain (E1).5 The number needed to treat (NNT) for a positive effect greater than placebo for most conditions is 3–4 patients. There is no evidence that NSAIDs improve muscle function after injury. NSAIDs (and corticosteroids) are catabolic in nature, particularly having their effect on tissues such as the soft-tissue structures of muscles, ligaments, tendon, and fascia, with very little effect on neural tissue. Therefore, in conditions where the pathological disorder is entrapment or impingement of nerves because of soft-tissue proliferation, such as carpal tunnel syndrome, Morton’s neuroma, thoracic outlet syndrome, and intervertebral disc prolapse, there is a strong theoretical basis to support the use of anti-inflammatory medications like NSAIDs (and corticosteroids). There is level II evidence of efficacy of NSAIDs on the inflammatory components of disorders such as bursitis in rotator cuff disease or iliotibial band friction syndrome,6 and synovitis in Morton’s neuroma7 or carpal tunnel syndrome.8 Case study — a torn tendon and bursitis in the shoulder A 46-year-old left-handed woman with a 6-month history of left shoulder pain initially injured the shoulder while playing tennis. She felt a dull ache in the lateral arm immediately after the game, and now has night pain, and pain with activities of daily living. Examination showed restricted range of shoulder motion, muscle weakness, and positive impingement signs. Her x-rays were unremarkable. Ultrasound showed a supraspinatus tendon tear with bursal thickening, and supraspinatus tendon tear with supraspinatus bursitis was diagnosed. Therapy is dictated by the patient’s activity level. If she requires strong overhead function then the goal of treatment should be healing of the tendon tear. However, if she generally only requires use of the arm for activities below shoulder height, then relief of impingement is the primary goal of treatment. Anti-inflammatory treatment for 6 weeks and/or subacromial corticosteroid and local anaesthetic injections (Figure A) are among the best therapeutic options for giving pain relief. These will generally provide analgesia, but may have potentially deleterious effects on tendon healing. Regular use of ice and paracetamol may be used for analgesia as alternatives if healing is considered important. Topical glyceryl trinitrate patches (1.25 mg/24 h) are an appropriate option to help relieve symptoms and increase function with chronic injury (Figure B). Exercise rehabilitation is the cornerstone of managing tendinopathies to regain function — in this situation, concentrating on scapula stabilisation and rotator cuff strengthening. This may be managed by the general practitioner confident in exercise prescription for this shoulder injury, or with the assistance of a sports physician or physiotherapist with experience in rehabilitating such injuries. Surgery may have a role if other treatments are not successful. If the patient requires high levels of shoulder function, direct repair of a tendon tear has a good rate of success, but requires prolonged rehabilitation. Arthroscopic acromioplasty is a procedure with quicker recovery which, like anti-inflammatory agents, is directed at providing pain relief rather than maximising shoulder function. A: Corticosteroid injections for tendon injuries, such as this subacromial injection, provide a short term reduction in pain of 6–8 weeks duration in most soft-tissue conditions. B: Quartered 5 mg/24 h glyceryl trinitrate patch, used for treatment of shoulder tendinopathy. Thus, current evidence does not support NSAID use as solo therapy or long-term therapy for soft-tissue injury, except when the primary disorder is soft-tissue impingement, or predominantly inflammatory (such as bursitis or synovitis). NSAIDs should not be used routinely in soft-tissue injury, as they are, at best, an adjunct to treatment through symptom relief, most notably analgesia (see Case study), and these benefits must be weighed against the risks of gastrointestinal side effects, especially with prolonged use. Non-steroidal anti-inflammatory drugs for tendinopathyThe abnormality in chronic tendinopathy in most cases is degeneration, with no evidence of inflammation (Box 1). Despite this, there is level II evidence that NSAIDs provide short-term mild to moderate decreases in pain in lateral epicondylosis,9 increased abduction in rotator cuff disease,10 but have no efficacy in treating Achilles tendinopathy.11 The mechanism of action of NSAIDs in tendinopathy is unclear. NSAID use decreases fibroblast proliferation and increases “overflow” leukotriene production in tendon both at rest and during exercise, which is additive to the normal effect of increased leukotriene production with cyclic tendon loading. So, there is potential for NSAIDs to cause tendon damage through increased leukotriene formation. Further, as tendinopathies have a tendency to chronicity, the side effects of NSAIDs with prolonged use are an even greater limitation than with other soft-tissue injuries. Thus, the evidence does not support the use of NSAIDs in pure tendinopathy, given their small effect on relieving symptoms and potential adverse effects. Short-term use of ice and paracetamol should provide an equivalent analgesic effect without serious side effects. Non-steroidal anti-inflammatory drugs compared with paracetamol for soft-tissue injuryParacetamol is an analgesic with a centrally mediated mechanism of action. With comparable efficacy to NSAIDs for pain in soft-tissue injury (E2),12 and being both opioid-sparing and NSAID-sparing, it can be used in combination analgesia. It also has a low cost, low side-effect profile, and no risk of local soft-tissue injury. It is often the analgesic of choice for soft-tissue injury. Cyclo-oxygenase-2 (COX-2) inhibitors for soft-tissue injuryCOX-2 inhibitors were developed to selectively block the COX-2 enzyme and the inflammatory process without inhibiting the effects of prostaglandins on gastroprotection or the effects of thromboxane on bleeding time and platelet aggregation. The use of these agents is currently under review because of increased rates of myocardial infarction, with rofecoxib withdrawn from the market and celecoxib only recommended for use in rheumatoid arthritis and osteoarthritis at low dosages. Given the lack of evidence of efficacy for these agents in soft-tissue injury, and significant cardiovascular safety concerns that are yet to be adequately researched, COX-2 inhibitors should generally not be used for treating soft-tissue injuries. They would only be recommended for patients in whom nerve or mechanical impingement is predominant, and non-specific NSAIDs are contraindicated because of a coexisting gastric disorder. They should not be used in patients at high risk of cardiovascular disease. Corticosteroid injections for tendinopathyCorticosteroids are injectable anti-inflammatory medications that inhibit the accumulation of neutrophils and the synthesis of inflammatory mediators, and prevent phagocytosis and lysosomal enzyme release. They have short-term efficacy in symptom relief for degenerative tendinopathies, bringing decreased pain in lateral epicondylosis (E1),13 decreased pain and increased abduction in rotator cuff tendinopathy (E1),14 and decreased pain and increased function in trigger finger (E2).15 However, there does not appear to be a positive effect of peritendinous injections in Achilles tendinopathy (E2).16 Positive results noted in studies occur in, at most, 80% of patients, and are generally limited to 6–8 weeks after injection (Box 1). Longer-term studies (12 months’ follow-up) of the effects of corticosteroid injections in lateral epicondylitis show inferior results to physiotherapy (E2).17 Studies have not shown clinically significant improvements in function with corticosteroid injections (E1) or greater efficacy than NSAIDs for shoulder pain. The demonstrated effect of corticosteroids in decreasing pain of tendinopathies may be the result of improvements in the inflammatory components of tendon injuries such as bursitis in shoulder tendinopathy, and tenosynovitis in trigger finger. The mechanism of any effect of corticosteroid injections in reducing symptoms in purely degenerative tendinopathies is unknown. There is Level IV evidence of tendon rupture with both local corticosteroid injection and oral corticosteroid treatment. This risk may be overstated in view of the frequent use of corticosteroid injections, a lack of evidence of increased rates of tendon rupture with corticosteroid use, and the endstage tendon degeneration noted in tendon ruptures.18 Animal studies indicate that cortico-steroids weaken tendon whether injected into or proximal to the tendon, and it is possible that corticosteroid injections do lead to partial rupture of tendon substance. In non-weight-bearing tendons or patients who place little demand on the affected tendon through heavy loading at work or playing sport, this may lead to symptom abatement through a “medical tenotomy”, with surprisingly little functional loss. Partial tendon rupture in weight-bearing tendons or patients who place higher demand on the tendon is much more significant, and frequently necessitates surgery. Thus, the evidence suggests that a single corticosteroid injection for symptomatic tendon injuries may achieve a mild, short-term reduction in pain for up to 6 weeks, particularly for “non-critical” tendons where rupture may not be a deleterious outcome. This injection should be coupled with a tendon-specific rehabilitation program. Where actual tendon healing is critical to a good outcome, such as overuse injuries to major weight-bearing tendons like the Achilles, corticosteroid injections are probably contraindicated. Prolotherapy and aprotinin injectionsProlotherapy generally refers to the injection of a sclerosant such as phenol, or hypertonic glucose. Theoretically, sclerosants may be useful for soft-tissue conditions, such as ligament injuries, in which joint laxity is an issue. There are no controlled studies examining prolotherapy as a treatment for soft-tissue injury, although there is some low-level evidence supporting prolotherapy for back pack pain and osteoarthritis.19 Given the lack of evidence of efficacy, prolotherapy cannot yet be recommended for treating soft-tissue injury. Its major advantage is that side effects of treatment are likely to be minimal. Aprotinin is a broad-spectrum metalloprotease (MMP) inhibitor used to treat many conditions, but particularly in preventing blood loss during cardiac surgery. Its use in chronic tendinopathy is attractive, as aprotinin may act as a collagenase inhibitor. Certain MMPs have been shown to be present in excessive proportions in patellar tendinopathy and rotator cuff tendinopathy, and aprotinin could potentially normalise the concentration of MMPs in chronic tendinopathy, which may help healing. In treatment for tendino-pathy as a series of two to four injections into the peritendinous space, aprotinin provides superior analgesia when compared with corticosteroid injections and placebo in patella tendinopathy (E2),20 and in Achilles tendinopathy (E3).21 Potential side effects include allergy and anaphylaxis, although death has only been reported when used intravenously for cardiac surgery; the “test dose” of 3–5 mL for major procedures is similar to the therapeutic dose for tendinopathy.22 The use of aprotinin injections for tendon injuries is currently an “off-label” indication. Botulinum toxin for tendinopathyBotulinum toxin type A is a neurotoxin which inhibits the release of the neurotransmitter acetylcholine at the neuromuscular junction, and inhibits skeletal muscle contraction. It results in reduced muscular spasticity, reduces pain and increased function in “whiplash-associated disorder” (E2).23 The use of multiple botulinum injections around the musculotendinous junction as a “last option” in the treatment of lateral epicondylosis has comparable results to extensor release surgery (E2);24 however, placebo injections demonstrate equal efficacy.25 These treatments may all induce local tissue healing responses. Side effects of botulinum injections include allergic reactions, and permanent muscle and tendon injury. Current evidence does not support the use of botulinum toxin injections for tendon injuries. An exception may be in chronic recalcitrant cases of lateral epicondylosis where surgery is considered. Glyceryl trinitrate treatment for tendinopathyGlyceryl trinitrate is a donor of nitric oxide (the endothelium-derived relaxing factor), but the mechanism of action of topical glyceryl trinitrate therapy on tendon is unknown. Nitric oxide inhibition decreases collagen content and collagen synthesis by fibroblasts,26 and nitric oxide donation may stimulate collagen synthesis by fibroblasts. In acute shoulder pain, there is evidence of an analgesic effect of 3 days duration (E2),27 which is of lesser efficacy than corticosteroid injections (E2).28 In chronic tendinopathies, topical glyceryl trinitrate therapy with 1.25 mg per 24 hours has level II clinical evidence of decreased pain, increased tendon force, improved functional measures, and improved symptom resolution in Achilles tendinopathy,29 lateral epicondylosis,30 and supraspinatus tendinopathy.31 Glyceryl trinitrate has a long history of therapeutic use in humans, and the common side effects of rash and headache are rapidly reversible on discontinuation of topical treatment. It should not be used concomitantly in patients taking phosphodiesterase inhibitors such as sildenafil (Viagra; Pfizer), as the additive effect may cause life-threatening hypotension. The use of topical glyceryl trinitrate for tendon injuries is currently an “off-label” indication, although medical practitioners may legally exercise discretion in prescribing this treatment for tendon conditions, provided likely effects, and side effects, such as rash and headache, are explained to the patient. Topical glyceryl trinitrate therapy has robust evidence of efficacy in treating common chronic tendinopathies, the side-effect profile is known and reversible, and this therapy should be used as an adjunct to tendon rehabilitation in chronic tendinopathies (Box 1). Glucosamine and soft-tissue injuriesGlucosamine has a significant analgesic effect in treating osteoarthritis, and it has been suggested that it may aid wound healing through enhanced fibroblastic production of hyaluronate (E5).32 There are no studies on glucosamine in treating soft-tissue injury. ConclusionBox 2 provides a flowchart summarising the evidence-based options for medical treatment of soft-tissue injuries. The widespread use of NSAIDs and corticosteroid injections in the treatment of most soft-tissue injuries requires reassessment based on current evidence, while new drugs such as aprotinin and glyceryl trinitrate hold promise as effective adjunctive treatment for chronic tendinopathies. Evidence-based guidelines on newer therapies There is evidence for the efficacy of topical glyceryl trinitrate therapy in treating common chronic tendinopathies (Achilles tendinopathy, lateral epicondylosis, and supraspinatus tendinopathy) (E2),27-29 and it can be used as an adjunct to tendon rehabilitation. Aprotinin provides superior analgesia compared with corticosteroid injections and placebo in patella tendinopathy (E2).18 This therapy may be particularly useful for chronic tendinopathy of the major weightbearing tendons, where the use of cortisone is contraindicated. Given the lack of controlled efficacy studies, prolotherapy cannot yet be recommended for treating soft-tissue injuries. Current evidence does not support the use of botulinum toxin injections for tendon injuries.23 There are no studies on the use of glucosamine in treating soft-tissue injuries. 1 Tendinopathies Tendon injuries, such as in lateral epicondylosis (tennis elbow, top) and tibialis posterior tenosynovitis (bottom), can be recalcitrant to treatment; conventional treatments such as non-steroidal anti-inflammatory drugs and corticosteroid injections may have a short term analgesic effect, while there is some evidence of efficacy with newer treatments such as topical glyceryl trinitrate therapy. 2 Evidence-based medical management of soft–tissue injuries NSAIDs = non-steroidal anti-inflammatory drugs.

Justin A Paoloni PhD, MSpMed, FACSP · John W Orchard MB BS, PhD, FACSP

Obesity is shaping up to be the major health care problem and one of the most frequent causes of preventable death in Western countries in the 21st century. Bariatric surgery is the only current treatment that has been shown to achieve major and durable weight loss. Major weight loss in the severely obese leads to total or partial control of a wide range of common and serious diseases, such as diabetes, heart disease and hypertension. Laparoscopic adjustable gastric banding is the most common type of obesity surgery performed in Australia. It is effective, relatively safe and minimally invasive. The blocks to broader application of bariatric surgery should be identified and resolved.

Paul E O’Brien MD, FRACS · Wendy A Brown MB BS, PhD, FRACS · John B Dixon MB BS, PhD, FRACGP

In late 1995, a treatment program for renal disease and hypertension was introduced into a remote Aboriginal community. Over the next 3.5 years, mean blood pressure levels were markedly reduced, renal function stabilised, and rates of both renal and non-renal deaths declined significantly. In 1999–2000, responsibility for the program was passed to the community’s local Health Board, which subsequently faced deficiencies in clinical information systems and a shortfall in funding. After the handover, the intensity of the program declined, and compliance with medicines fell. Blood pressures in the treatment cohort increased, renal function deteriorated, and rates of deaths from natural causes subsequently rose. From 2002 to mid-2003, the adjusted risks of renal and non-renal deaths in the treatment cohort were three and 9.5 times the respective risks of people during the first 18 months of treatment in the systematic phase of the program. Sustained vigorous activity, both in treatment of people already identified and in community screening for treatment eligibility, is required to maintain good results in any chronic disease program. Adequate resources and well supported staff are essential, and constant evaluation is needed to follow outcomes and modify strategies as necessary.

Wendy E Hoy FRACP · Srinivas N Kondalsamy-Chennakesavan MB BS, MPH · Jennifer L Nicol BSc(Hons), MSc(Stats)