Volume 173 Issue 8

Medicine and the Community Diagnoses and treatment recommendations on workers compensation medical certificates Eva Schönstein and Dianna T Kenny MJA 2000; 173: 419-422 For editorial comment, see Bogduk Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Occupational health Abstract Objective: To review the diagnostic descriptions and treatment recommendations for back and neck pain on the new workers compensation medical certificates and compare these with evidence-based guidelines. Design: Retrospective analysis of 251 medical certificates of workers with compensable neck and back pain held by a workers compensation insurer. Main outcome measures: Diagnoses given and treatments prescribed by the nominated treating doctors. Results: The diagnoses most frequently used were "sprain/strain" and "pain/ache". Physiotherapy was the most frequently prescribed treatment, followed by rest and medication. Rest was prescribed for 68 (27%) workers, 87% of whom were classified as having an acute injury. Activity-based treatments were prescribed for 45 (18%) workers. Conclusions: Not all doctors used diagnostic terms consistent with recommended anatomical taxonomy. The drug therapy prescribed was consistent with current evidence-based treatment guidelines. However, the prescribing of rest, and the omission, in most cases, of explicit recommendations to resume normal activities, including work, are not consistent with current guidelines. The cost of managing workplace back injuries is increasing. Figures for 1997-98 show that back injuries accounted for 30% of the cost of all workplace injuries (gross cost, $224 million),1 while comparable figures for 1996-97 were 36% and $212.5 million.1,2In an effort to reverse the growing WorkCover Authority (WCA) debt ($1.7 billion at the time of writing),3 the 1997 Grellman Report4 made recommendations which resulted in the Workplace Injury Management and Workers Compensation Act 1998 (NSW). A new medical certificate intended to streamline reporting and management of compensable work-related injuries was introduced, as well as the concept of the "nominated treating doctor" (NTD) -- a general practitioner nominated by the injured worker who agrees to provide continuity of care until a return to work is achieved (Box 1). In recent years, national and international guidelines and systematic reviews -- some evidence-based -- have established standards for diagnosis and treatment of people with back or neck pain,5-10 including the most recent National Health and Medical Research Council (NHMRC) guide to acute pain management11 and the definitive publication on classification of pain by the International Association for the Study of Pain (IASP).12 To streamline management and reduce the costs associated with prolonged disability and time off work, it is important that the NTDs' diagnoses and treatment recommendations conform with evidence-based guidelines. We compared the diagnoses and treatments given on Part 1 of a sample of medical certificates of workers (who had work-related back or neck pain) with the taxonomic guidelines for diagnosis and the emerging guidelines for management. Methods We examined retrospectively all the medical certificates related to neck and back pain of a NSW workers compensation insurer for the period 1 October 1998 - 15 February 1999. Medical certificate entries were de-identified. Diagnosis and treatment were coded according to the most common wording used by doctors. Diagnoses were further grouped into those indicating and those not indicating a specific pathological condition. Treatments were further coded according to the amount of rest and/or activity prescribed. Active treatments involved exercise, work conditioning/work hardening, and maintenance of normal activity (including work). Diagnoses were then compared with taxonomic guidelines, and treatments were compared, wherever possible, with evidence-based guidelines for the management of spinal pain. According to the time between the date of injury on the certificates and the date of the medical certificate, the worker's condition was classified as acute (< 6 weeks), subacute (6-12 weeks) or chronic (> 12 weeks). Ethical approval: Approval for the study was obtained from the Human Ethics Committee, The University of Sydney. Results Diagnosis On 227 of 251 certificates examined (90%), doctors did not specify a patho-anatomical diagnosis: on 92 certificates (37%) the diagnosis was sprain/strain; on 68 (27%) ache/pain; and on 67 (26%) injury (mechanical, lumbago, dysfunction, whiplash, discopathy, myalgia). The location of the pain was lumbar spine (131; 52%), back (42; 17%), cervical spine (39; 16%), and other (39; 16%). Thirty-four doctors (14%) used at least two diagnostic descriptors, and, of these, six used at least three. Examples included "back pain due to low back strain", "thoracolumbar spinal pain, right sciatica", and "lumbar disc degeneration, right low back pain, and right sciatica pain". Treatment The most frequently prescribed treatments (Box 2) were physiotherapy (116; 46%); rest (68; 27%); non-steroidal anti-inflammatory drugs (NSAIDs) (64; 25%); and analgesia, analgesics or "painkillers" (56; 22%). Specific active management advice, such as exercise, a return to work, suitable duties, work conditioning, hydrotherapy or work rehabilitation, was recommended for 45 (18%) workers. Many had more than one treatment prescribed, with the total sample of 251 being prescribed 455 treatments. Most workers were seen by their doctors in the acute phase of injury (208; 83%), with the remainder in the subacute (18; 7%) or chronic (21; 8%) categories. Of the workers prescribed rest, 87% were classified as having an acute injury. Fifty-six workers (22%) were certified fit for suitable duties, 24 of these (43%) on their initial visit to their NTD. Ninety-two workers (37%) were deemed unfit for work. This information was not included on the remaining certificates. Of the 92 workers deemed unfit for work, 59 (64%) were on their first visit to their doctor, 13 (14%) were being issued with a progress medical certificate, and 8 (9%) were making their final visit. The remaining 20 (22%) certificates did not have this information. The treatments prescribed on the medical certificates and available evidence for their efficacy are summarised in Box 3. Wherever possible, the evidence is presented according to the NHMRC level-of-evidence ratings. Discussion We found that doctors completing medical certificates for workers with back and neck pain generally did not indicate a specific pathoanatomical diagnosis. This is consistent with epidemiological evidence:6,7 in 85%-90% of back complaints, a pathoanatomical diagnosis can not be made from the history, examination or even medical imaging. One of the primary aims of the initial assessment is to exclude "red flag" conditions such as tumours, fractures, disc prolapses, herniations, or infections. According to the NHMRC,11 this exclusion is the key to managing acute spinal pain, and for this purpose the history is the most valid tool.13 The diagnoses given on medical certificates for back and neck pain should explicitly reflect the exclusion of "red flag" conditions, and the presence of a benign, self-limiting condition which generally resolves within four weeks of onset of pain.14The certificates showed that the doctors used a variety of (implicit) taxonomic systems to describe "non red flag pain"; for example, anatomical (eg, "back pain", "thoracolumbar spinal pain"), aetiological or mechanical (eg, "mechanical back pain", "injury"), or descriptive pathological (eg, "sprain", "tear", "degeneration"). Only anatomical classification is consistent with the IASP classification.12 However, the precise terminology used to describe pain of this type is contentious. Terms such as "non-specific back pain",6,15 "simple back pain",14 or "back pain of unknown or uncertain origin"12 have been proposed. NSAIDs and analgesics were the most frequently prescribed medical therapy. Their use for spinal pain is consistent with current evidence-based practice,9 but support for the use of NSAIDs is limited and applies only in the short term.9,11 Although physiotherapy, either alone or in combination with other treatments, was the most frequently prescribed treatment, the NTD generally did not specify the exact nature of the physiotherapy intervention. While scientific evidence for the efficacy of specific physiotherapy treatments for neck and back pain has been published,8,9,16 there is great variability in treatments among physiotherapists,17,18 and the extent to which they adhere to evidence-based practice has not been studied. The Australian Physiotherapy Association has made a concerted effort to educate and inform its members by producing position statements on neck pain and back pain. These as yet unpublished statements are based on randomised controlled trials and systematic reviews (some by the Cochrane Collaboration). A Physiotherapy Evidence Database has also been created (PEDro).19 When reviewing their patients, doctors need to consider the evidence for the efficacy of the specific physiotherapy treatment received. "Rest" was the second most common word included in treatment recommendations (27% of cases), and most workers for whom rest was prescribed were in the acute phase of their injury. In contrast, activity-based treatments were recommended in only 18% of cases. Both in terms of what was prescribed and what was omitted, this is contrary to current evidence. There is now Level I evidence that bed rest should not be prescribed for acute back pain;20 and Level II evidence that advising patients to return to normal activity (including work),21-24 providing reassurance, and discouraging fear of activity and illness behaviour, are effective for managing acute and subacute spinal pain. It is acknowledged that the use of the word "rest" may not necessarily mean "bed rest". However, even when used in combination with an activity-based treatment, the word "rest" may be construed to mean a cessation of all, most, or some of a person's normal functional and work activities. Recommendations As a result of our study, we recommend that: The new workers compensation medical certificates should be changed to assist nominated treating doctors (NTDs) to indicate that "red flag" conditions have been excluded. The use of the word "rest" on medical certificates should be restricted and the resumption of normal functional and work activities should be explicitly included. There should be a taxonomic standard for describing neck and back pain which clearly communicates that the condition is benign and has a good prognosis. This should reduce fear-avoidance and illness behaviours in workers,25 and assist employers to provide suitable temporary duties for workers. The medical profession and other appropriate authorities need to encourage dissemination and use of evidence-based guidelines and best practice in the management of compensable spinal pain. Acknowledgements We thank HIH Insurance (Injury Management Department) for providing access to workers compensation medical certificates, and Dr C Maher and Dr J Latimer, from the School of Physiotherapy, Faculty of Health Sciences, The University of Sydney, for their support and helpful comments. Competing interests: No conflict of interest exists and the study received no funding. References WorkCover NSW. Statistical bulletin. NSW workers compensation. Sydney: WorkCover NSW, 1997-1998. WorkCover NSW. Back injuries statistical profile, 1996/1997. WorkCover NSW, 1997/98 Annual Report. Sydney: WorkCover NSW, 1998. Grellman RJ. Inquiry into workers compensation system in NSW. Sydney: KPMG, 1997. Agency for Health Care Policy and Research (AHCPR). Clinical Practice Guidelines Number 14. Acute low back problems in adults. Rockville, Md: AHCPR, 1994. Fordyce WE, editor. Back pain in the workplace. Management of disability in nonspecific conditions. International Association for the Study of Pain. Seattle, Wash: IASP Press, 1995. Victorian WorkCover Authority. Guidelines for the management of employees with compensable low back pain. Melbourne: Victorian WorkCover Authority, 1996. Gross A, Aker P, Goldsmith CH, Peloso P. Conservative management of mechanical neck pain: systematic overview and meta-analysis. BMJ 1996; 313: 1291-1296. Van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspecific low back pain. A systemic review of randomized controlled trials of the most common interventions. Spine 1997; 22: 2128-2156. Waddell G, Feder G, McIntosh A, et al. Low back pain evidence review. London: Royal College of General Practitioners, 1998. National Health and Medical Research Council. Acute pain management: scientific evidence. Canberra: NHMRC, 1999. Merskey H, Bogduk N, editors. Classification of chronic pain. International Association for the Study of Pain. Seattle, Wash: IASP Press, 1994. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992; 268: 760-765. Croft PR, Macfarlane GJ, Papageorgiou AC, et al. Outcome of low back pain in general practice: a prospective study. BMJ 1998; 316: 1356-1359. Cedraschi C, Nordin M, Nachemson AL, Vischer TL. Health care providers should use a common language in relation to low back pain patients. Baillieres Clin Rheumatol 1998; 12: 1-15. Gross A, Aker P, Goldsmith C, Peloso P. Physical medicine modalities for mechanical neck disorders (Cochrane Review). Cochrane Library; Issue 1, 2000. Van der Valk RWA, Dekker J, van Baar ME. Physical therapy for patients with back pain. Physiotherapy 1995; 81: 345-351. Jette AM, Smith K, Haley SM, Davis KD. Physical therapy episodes of care for patients with low back pain. Phys Ther 1994; 74: 101-114. The Physiotherapy Evidence Database (PEDro). May 2000. <http://ptwww.cchs.usyd.edu.au/pedro/> (accessed 6 September 2000). Koes BW, van den Hoogen HMM. Efficacy of bed rest and orthoses of low back pain. A review of randomized clinical trials. Eur J Phys Med Rehabil 1994; 4: 96-99. Malmivaara A, Hakkinen U, Aro T, et al. The treatment of acute low back pain -- bed rest, exercise or ordinary activity? N Engl J Med 1995; 332: 351-355. Indahl A, Velund L, Reikeraas O. Good prognosis for low back pain when left untampered. A randomized clinical trial. Spine 1995; 20: 473-477. Lindstrom I, Ohlund C, Eek C, et al. Mobility, strength, and fitness after a graded activity program for patients with subacute low back pain. A randomized prospective clinical study with a behavioural therapy approach. Spine 1992; 17: 641-652. Lindstrom I, Ohlund C, Eek C, et al. The effect of graded activity on patients with subacute low back pain: a randomized prospective clinical study with an operant-conditioning behavioural approach. Phys Ther 1992; 72: 279-293. Loeser JD, Sullivan M. Doctors, diagnosis and disability: a disastrous diversion. Clin Orthop Rel Res 1997; 336: 61-66. (Received 3 Sep 1999, accepted 31 Jul 2000) Authors' details Faculty of Health Sciences, The University of Sydney, Sydney, NSW. Eva Schönstein, BAppSc(Phty), MHPEd, Lecturer, School of Physiotherapy. Dianna T Kenny, PhD, MAPsS, Associate Professor of Psychology. Reprints will not be available from the authors. Correspondence: Ms Eva Schönstein, School of Physiotherapy, Faculty of Health Sciences, University of Sydney, PO Box 170, Lidcombe 1825. E. SchonsteinATcchs.usyd.edu.au Make a comment 1: The new medical certificate Part 1: Requires the nominated treating doctor (NTD) to give a diagnosis, recommend treatment and determine the worker's fitness for work and suitable duties, including specific restrictions. It must be completed for those who are likely to return to pre-injury or suitable duties within 7 days of injury. Part 2: Requires doctors to specify nature and restrictions to proposed suitable duties (only completed for workers expected to return to work after more than 7 days from the date of injury). Part 3 (Return to Work Form): Requires recommendations on when the worker should resume work and the restrictions on activities arising from the work-related injury (must be completed for all workers who need a graded return to pre-injury or other permanent duties). Back to text 2: Treatments most commonly prescribed on the 251 medical certificates Treatment (examples) Number (%) Physiotherapy only 48 (19%) Physiotherapy + activity 12 (5%) (Physiotherapy and exercise, or rehabilitation, or hydrotherapy, or modified duties, or graded return to work) Physiotherapy + passive treatment 56 (22%) (Physiotherapy and medication or rest or massage or heat or ice or a combination of these) Medication only 25 (10%) (Analgesics, NSAID, drug not specified, Brufen [Knoll], Voltaren [Novartis], Panadeine Forte [Sanofi- Synthelabo]) Medication + activity 9 (4%) (Analgesia and home exercises , paracetamol and back exercises, NSAID and light duties) Medication + rest 24 (9%) (NSAID or analgesics and rest) Rest only 6 (2%) (Rest, bed rest) Rest + activity 12 (5%) (Rest and exercise or modified duties or return to work) Specified single treatment other than rest, medication or physiotherapy 17 (7%) (Acupuncture, chiropractic, manipulation) Other combinations of two or more treatments 8 (3%) (NSAID and heat and massage, rest and local heat and massage) Other treatment descriptors not elsewhere classifiable 17 (7%) ("Conservative management", "restricted daily", "nil", "rehabilitation medicine") Treatment not specified 17 (7%) Total 251 (100%) Back to text 3: Treatments recommended on more than one of the 251 medical certificates and NHMRC levels of evidence for their efficacy (wherever possible)* Treatment prescribed n (%) RCGP10 Van Tulder et al9 Physiotherapy 116 (46%) -- -- Rest, bed rest 68 (27%) Ineffective, Level I Ineffective, Level I NSAID 64 (25%) Effective, Level I Effective, Level I Analgesics, analgesia 56 (22%) Effective, Level III Effective, Level II Exercise, swimming 29 (12%) Ineffective, Level I Ineffective, Level I Light, modified duties, gradual return to work 13 (5%) Effective, Level IV -- Massage 11 (4%) -- -- Manipulation, mobilisation, chiropractic 11 (4%) Effective, Level I Effective, Level III Heat (electromagnetic or source unspecified) 9 (7%) -- -- Ice 4 (2%) -- -- Muscle relaxants 3 (1%) Effective, Level I Effective, Level I Ultrasound 3 (1%) -- -- Work conditioning 2 (0.8%) Effective, Level III -- Acupuncture 2 (0.8%) -- -- Victorian WCA7 Gross et al8 IASP6 AHCPR5 Beneficial -- -- -- Beneficial (48 hours) -- Ineffective Ineffective, Level I Beneficial Inconclusive Effective Effective, Level II Beneficial Inconclusive Effective Effective, Level III Beneficial -- Effective Effective, Level III Beneficial -- Effective Effective, Level IV Beneficial -- -- -- Beneficial Effective short term, Level I Effective Effective, Level II Beneficial Effective short-term Level I Ineffective Self-application, Level IV Beneficial -- -- Self-application Level IV Beneficial short term Inconclusive Ineffective Effective, Level III -- -- -- -- -- -- -- -- Beneficial Inconclusive Ineffective Ineffective, Level IV *For some of the guidelines cited (IASP6 and Victorian WCA7) levels of evidence were not given. For others (RCGP10 and AHCPR5), the levels of evidence given were converted to match the NHMRC levels. Back to text

Eva Schonstein · Dianna T Kenny

Medicine and the Community The impact of domestic violence on individuals Jill Astbury, Judy Atkinson, Janet E Duke, Patricia L Easteal Susan E Kurrle, Paul R Tait and Jane Turner MJA 2000; 173: 427-431 See Articles 1, 3 and 4 of this series Abstract - Children - Pregnant women - Elderly people - Indigenous people - People of non-English-speaking background - The need for change - References - Authors' details - - More articles on Aboriginal health Abstract There is extensive evidence of the adverse effects of domestic violence across all age groups and cultural backgrounds. The impact of domestic violence may be long-term, affecting emotional adjustment, physical health and subsequent relationships. Health professionals should be aware of the confounding effect of youth, age and cultural diversity on presentation. Shame and isolation militate against disclosure. Specific, sensitive questioning that incorporates awareness of cultural and social issues is essential to detect domestic violence and initiate appropriate assistance. If the idea of "home" implies physical and psychological safety and security as well as shelter, then a child, adult or older person affected by domestic violence experiences a hidden "homelessness".1 Domestic violence occurs across the lifespan2 and across most cultures. Women are at a disproportionately high risk of physical, sexual and psychological violence from an intimate person such as a partner or ex-partner.3 Many children, too, are likely to experience violence from someone they know or be witnesses to violence within their families.4 Domestic violence may be physical, sexual or psychological, but all three can be present. What is subjectively defined and identified as "domestic violence" by victims can be strongly mediated by cultural beliefs, values and previous experience of abuse and may not coincide with standard clinical or research definitions. Domestic violence is always characterised by the use of coercive control and psychological abuse.5,6 Victimisation is associated with alterations in the perception of the perpetrator, especially a belief in his or her omnipotence, and alterations in the victim's perception of self. Feelings of self-blame, shame and loss of self-esteem are extremely common. At the same time, psychological defenses used to cope with violence include denial of its existence and minimisation of its severity.7 Acts of contrition and intermittent kindness by the perpetrator can maintain the relationship and give false hope to the abused person that the violence will end. In addition to the common features of domestic violence, there are important aspects of domestic violence that are characteristic of specific groups in society, such as children, pregnant women, the elderly, Indigenous people, and people of non-English-speaking background. Here we examine some of the specific problems of each of these groups in more detail. Children Children can be at risk of experiencing and witnessing violence within the family or from those known to them.8 The perpetrator is usually in a caring role or a position of trust in relation to the child. Children can be the direct targets of physical violence or can get hurt when they try to protect another family member, often the mother, or try to stop their parents from fighting. It is becoming increasingly apparent that domestic violence results in a similar outcome for many children, whether they are direct victims or only witnesses of the violence. A number of authors have pointed to a clear link between domestic violence and child abuse, with one being a predictor of the other: it has been estimated that children living in domestic violence situations are up to 15 times more likely to be abused or neglected than children from non-violent homes.9-11 Behavioural and psychological consequences of childhood violence include poor school performance, bedwetting, aggression (particularly among males), temper tantrums, oppositional behaviour, self-blame, guilt for the violence between parents, isolation from peers, self-harming behaviour, running away, psychosomatic symptoms, stealing, over-eating, depression, sleep disturbances and excessive anxiety symptoms (see Box 1). Violence by a person in a position of trust impairs the child's ability to trust others and increases the risk of victimisation in later life.12 Recent research has shown that there are significant and possibly persistent neurobiological effects of trauma experienced in early childhood. Work by Perry and others13,14 has demonstrated the importance of critical periods of exposure to secure parenting: exposure to recurring traumatic experiences in early childhood places a child at much greater risk of long-term psychological, emotional and behavioural problems. The type of violence is not the primary factor determining long-term outcome. More important predictors are the duration of violence, its severity and frequency. The cumulative impact of exposure to multiple adverse experiences (eg, violence, psychological or sexual abuse, substance misuse) in childhood is predictive of adverse health outcomes in adult life. In a large US study it was found that exposure to four or more categories of adverse childhood experiences was associated with a 4-12-fold increased risk of alcoholism, drug abuse, depression and attempted suicide.15 Protective factors include a healthy relationship with a primary carer, good social support and positive subsequent life experiences.8,12 Pregnant women The number of unwanted or unplanned pregnancies and terminations is higher among women experiencing domestic violence.16,17 Pregnancy itself is a time of heightened risk and the abdomen is targeted more frequently and more severely in pregnant women.18,19 The Women's Safety Australia survey4 found that, of all the women who reported violence occurring at some time in their lives, 42% were pregnant at the time. Twenty per cent reported that violence occurred for the first time during the pregnancy, although the strongest predictor of violence occurring during pregnancy is a prior history of abuse.12 Furthermore, women abused during pregnancy are at even greater risk of violence in the postpartum period.19 Women experiencing violence during pregnancy often obtain minimal or late antenatal care.20 They are at increased risk of having poor weight gain, anaemia, infections, or preterm labour; of bearing a low birthweight infant; and experiencing postnatal depression.18,21-23 They are also more likely to engage in behaviours harmful to health, such as smoking, drinking excessive amounts of alcohol, and substance misuse.18,21-23 Elderly people Abuse of elderly people is the most recent form of familial violence to come to public attention but it remains a largely hidden problem. Most community-based studies have shown that similar proportions of older men and women are victimised (in contrast to the younger population, in which the number of women experiencing domestic violence is greater than the number of men).24 Close family members (the victim's spouse, adult child or other relative) constitute the majority of abusers and usually live with the victim.25 The reasons for elder abuse are often related to their dependence on others (due to physical or mental impairment, particularly dementia), psychopathology in the abuser, or a long history of family violence26 (see Box 2). Many instances of elder abuse are "victim-victim" situations in which abusers may themselves be worn-out carers. Physical consequences include the actual injuries inflicted (eg, bruising, lacerations, fractures, or burns) as well as the results of neglect, such as malnutrition, decubitus ulceration, and inappropriate use of medication. Older people who are frail may sustain major injuries from an apparently minor cause -- for instance, a shove leading to a fall may result in a fatal subdural haemorrhage. Abuse may also have psychological consequences: feelings commonly experienced are a sense of powerlessness, shame at having to admit that the abuse is occurring at the hands of close family members, fear of retaliation from the abuser, and particularly fear of institutionalisation if the abuse is reported. Such fears increase the victim's reluctance to report abuse,27 often causing a self-imposed isolation. Control by the abuser may be exercised financially through the improper use of an older person's property or finances or misuse of a power of attorney, or may take the form of neglect whereby the necessities of life (adequate food, clothing, medication, or other care) are withheld by a caregiver.28 Indigenous people Domestic violence in Indigenous families and communities in Australia is presently at a level for serious concern.29,30 In 1990, an Aboriginal and Torres Strait Islander Commission briefing document advised the Australian Aboriginal Affairs Council that "the increasing injuries and fatalities as a result of interpersonal violence have risen to levels which not only impair life but also threaten the continued existence of Australian Indigenous peoples".31 Physical assault is commonly associated with psychological abuse, and Indigenous victims of domestic violence (who are mainly women) may view themselves as being of little worth, incompetent, and deserving of abuse.32 The situation becomes more complex when racism and discrimination in social control structures are intertwined with domestic violence32 (see Box 3). Domestic violence in Indigenous communities can only be understood in the context of the historical, political, social and cultural environments in which it occurs.34 Colonisation has had a disastrous impact on the lives of Indigenous people: it has created complex and cumulative forms of traumatic stress that may be articulated as physical, emotional and spiritual distress; misuse of alcohol and other drugs; and violent behaviour arising from a rage that is directed towards the self and other close family members.35 With the breakdown of cultural lore, behaviours that were previously functional in conflict resolution processes have become unstructured and damaging when used under the influence of alcohol or other drugs.36 John Cawte, a psychiatrist and anthropologist, identifies Indigenous communities as suffering from "gross stress", a form of post-traumatic stress disorder in which individuals express their loss and bewilderment as emotional and behavioural disorders.37 Indigenous women are less likely than non-Indigenous women to report an assault, and less likely to seek medical help unless they have severe injuries.38 Historical interactions with police, who were used by the state to forcibly remove Indigenous children under government assimilation policies, and deaths of Indigenous people in custody continue to engender a deep mistrust of law enforcement officials.39 Indigenous women fear for their own safety40 and the safety of other family members if police or social welfare officials become involved. While some Indigenous women may call the police to intervene in violent situations, they are less likely than non-Indigenous women to want to lay charges, and there is a general belief that charging or incarcerating Indigenous men does not reduce male violence. Indigenous women are more likely to ask for other interventions in which their partner also receives help for his drinking and/or violent behaviour.32 People who have been traumatised through violence are more likely to be treated as if they are mentally ill or unstable than to be provided with programs that will meet their needs; however, recent program initiatives in Australia are beginning to respond to the specific and unique needs of Indigenous peoples.29 People of non-English-speaking background The extent of domestic violence experienced in Australia by people of non-English-speaking background has not been extensively studied. However, research suggests that overseas-born males are more likely to commit partner homicide than would be expected from their numbers in the general community.41 This may reflect a higher rate of domestic violence among overseas-born women. Alternatively, these women may be less likely to leave violent situations, and therefore experience escalating violence. For those who are migrants, the strain of migration may compound the problem. However, in most cases in which a couple migrated together, the abuse preceded migration.42 Once in Australia, however, the migrant family may undergo further stresses as traditional gender roles shift. This may encompass unemployment or downward shifts in employment status for men, and paid employment for women. Assimilation of the younger generation into the broader Australian culture may further erode traditional hierarchies based on age and sex. Women who may be at particular risk include Asian women sponsored by non-Asian men,43 and Middle Eastern women brought to Australia for arranged marriages to Middle Eastern men already residing here.42 Such women have not only left behind their family and supports, but have joined partners whose established community networks may not recognise their needs. In some instances, their partner's extended family may collude in the violence, overtly or indirectly, by not offering support.42 Disclosure of domestic violence towards women of non-English-speaking background is inhibited if they have poor command of English (Box 4). For some women, however, the issue is more fundamental -- their concept of sexual assault within marriage may be very different from current Australian values and norms.44 Over 70% of migrant women have minimal knowledge of the legal rights of victims of domestic violence,45 which further inhibits disclosure, and many know little about support services or refuges. Women from Middle Eastern and Latin American cultural backgrounds who experience domestic violence are often reluctant to contact police, in part because they have witnessed oppression or torture at the hands of police in their country of origin.42 Domestic violence often creates a feeling of shame. There may be considerable pressure for a woman to maintain a marriage, and she may fear being deported.46 She may feel the burden of providing financial support for family in her country of origin,47 and consider that their plight outweighs any consideration of personal needs. The erosion of self-esteem accompanying domestic violence is compounded if the woman is isolated by virtue of limited English and lack of family and friends in whom to confide. The adverse health effects are similar to those experienced by abused women in the broader Australian society, although they may be exacerbated by longer delay in disclosure. The need for change Each of the specific groups examined has characteristic issues related to their experience of domestic violence. Nevertheless, the need for change applies equally to all groups. Patients are reluctant to disclose violence if not asked,48 but sensitive questioning can legitimate and encourage disclosure. As the Council on Scientific Affairs of the American Medical Association has observed, knowledge of a history of abuse can provide "the starting point from which to disentangle a confusion of presenting complaints and symptoms".49 Clinical practice and medical education programs in Australia have been slow to respond to the large body of research confirming the harmful health effects of domestic violence. Failure by healthcare providers to detect and treat those affected by domestic violence exacerbates the harm done in several ways. Firstly, the complexity of violence-related negative health outcomes increases if abuse remains undetected. Secondly, the drain on healthcare resources increases as victims present repeatedly to primary and emergency healthcare providers. (Conversely, victims' uptake of preventive healthcare is considerably lower than average, and the role of violence in their "non-compliance" with preventive health behaviours can easily be missed.) Thirdly, non-detection ensures that treatments are necessarily directed at the symptoms rather than the cause.1 A thorough understanding of the multiple adverse health effects and high rate of physical and psychological comorbidity associated with domestic violence must be acquired by all healthcare professionals. Training is required in every aspect of treatment, including initial questioning, counselling and responding to those who do disclose violence, and providing appropriate assistance, including safety plans and advocacy on behalf of patients. A number of our medical colleges have begun this necessary task. In clinical care, the concept of meaningful assistance to patients with health needs associated with domestic violence deserves to be strongly promoted. References Burke T. Housing and poverty. In: Fincher R, Nieuwenhuysen J, editors. Australian poverty. Melbourne: Melbourne University Press, 1998: 165-184. Kleinschmidt KC. Elder abuse: a review. Ann Emerg Med 1997; 30: 463-472. Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52: 1048-1060. Australian Bureau of Statistics. Women's safety, Australia, 1996. Canberra: ABS, 1996. Ratner P. The incidence of wife abuse and mental health status in abused wives in Edmonton, Alberta. Can J Public Health 1993; 84: 246-249. Campbell JC, Lewandowski LA. Mental and physical health effects of intimate partner violence on women and children. Psychiatr Clin North Am 1997; 20: 353-374. Martin J, Anderson J, Romans S, et al. Asking about child sexual abuse: methodological implications of a two-stage survey. Child Abuse Negl 1993; 17: 383-392. Anderson J, Martin J, Mullen P, et al. Prevalence of childhood sexual abuse experiences in a community sample of women. J Am Acad Child Adolesc Psychiatry 1993; 32: 911-919. McKay MM. The link between domestic violence and child abuse: assessment and treatment considerations. Child Welfare 1994; 73: 29-39. Bowker LH, Arbittel M, McFerran J. On the relationship between wife-beating and child abuse. In: Yllo K, Bograd M, editors. Feminist perspectives on wife abuse. Newbury Park, California, Sage Publications, 1988. Stacy W, Sharpe A. The family secret: domestic violence in America. Boston: Beacon Press, 1983. Resnick HS, Acierno R, Kilpatrick DG. Health impact of interpersonal violence. 2: Medical and mental health outcomes. Behav Med 1997; 23: 65-78. Hart S, Brassard M. A major threat to children's mental health: psychological maltreatment. Am Psychol 1987; 42: 160-165. Perry BD. Neurobiological sequelae of childhood trauma: post-traumatic stress disorders in children. In: Murburg M, editor. Catecholamine function in post-traumatic stress disorder: emerging concepts. Washington, DC: American Psychiatric Press, 1994. Felitti VJ, Anda RF, Nordenberg D, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. Am J Prev Med 1998; 14: 245-258. Evins G, Chescheir N. Prevalence of domestic violence among women seeking abortion services. Women's Health Issues 1996; 6: 204-210. Glander SS, Moore ML, Michielutte R, Parsons LH. The prevalence of domestic violence among women seeking abortion. Obstet Gynecol 1998; 91: 1002-1006. Parker B, McFarlane J, Soeken K. Abuse during pregnancy: effects on maternal complications and birth weight in adult and teenage women. Obstet Gynecol 1994; 84: 323-328. Gielen AC, O'Campo P, Faden R, et al. Interpersonal conflict and physical violence during the childbearing year. Soc Sci Med 1994; 39: 781-787. Norton LB, Peipert JF, Zierler PH, et al. Battering in pregnancy: an assessment of two screening methods. Obstet Gynecol 1995; 85: 321-325. Adams-Hillard PJ. Physical abuse in pregnancy. Obstet Gynecol 1985; 66: 185-190. McFarlane J, Parker B, Soeken K, Bullock L. Assessing for abuse during pregnancy: severity and frequency of injuries and associated entry into prenatal care. JAMA 1992; 267: 3176-3178. Berenson AB, Wiemann CM, Wilkinson GS, et al. Perinatal morbidity associated with violence experienced by pregnant women. Am J Obstet Gynecol 1994; 170: 1760-1766. Kleinschmidt KC. Elder abuse: a review. Ann Emerg Med 1997; 30: 463-472. Kurrle S, Sadler P, Lockwood K, Cameron ID. Elder abuse: prevalence, intervention and outcomes in patients referred to four Aged Care Assessment Teams. Med J Aust 1997; 166: 119-122. Kurrle S, Sadler P, Cameron ID. Patterns of elder abuse. Med J Aust 1992; 157: 673-676. Kurrle S. Responding to elder abuse -- a follow-up study of interventions and outcomes. Aust J Ageing 1993; 12: 5-9. Kurrle S, Sadler P. Assessing and managing abuse of older people. Sydney: NSW Office on Ageing, 1994. Report of the Aboriginal and Torres Strait Islander Women's Task Force on Violence. Brisbane: Queensland Government, 1999: 91. Ferrante A, Morgan F, Indermaur D, Harding R. Measuring the extent of domestic violence. Sydney: Hawkins Press, 1996: 28-34. Aboriginal and Torres Strait Islander Women's Task Force on Violence Report Brisbane: Queensland Government, 1999: 3. Aboriginal and Torres Strait Islander Women's Task Force on Violence Report. Brisbane: Queensland Government, 1999: 45-81, 156-200. Lawrence D, editor. Future directions. Proceedings of the Future Directions Queensland Domestic Violence Conference. Yeppoon, Queensland, July 1995. Rockhampton, Central Queensland University, 1995: 235. Mow KE. Tjunpami: family violence in Indigenous Australia. A report and literature review for the Aboriginal and Torres Strait Islander Commission. Canberra: ATSIC, 1992. Aboriginal Coordinating Council. Submission to the Royal Commission into Aboriginal Deaths in Custody. Cairns: ACC, 1991. Atkinson J. Lifting the blankets -- the transgenerational effects of trauma in Indigenous Australia [PhD thesis]. Brisbane: Queensland University of Technology, 2000. Cawte J. Medicine is the law: studies of psychiatric anthropology of Aboriginal tribal societies. Honolulu: University Press of Hawaii, 1974: 193. Bolger A. Aboriginal women and violence. Darwin: Australian National University North Australia Research Unit, 1991. Payne S. Aboriginal women and the law. In: Cunneen C, editor. Aboriginal perspectives on criminal justice. Sydney: Institute of Criminology, University of Sydney Law School, 1992. Kiss J. A matter for regret. Australian Lawyer 1996; 31(2): 14. Easteal P. Killing the beloved: homicide between adult sexual intimates. Canberra: Australian Institute of Criminology, 1993: 47. Easteal P. Shattered dreams -- marital violence among the overseas-born in Australia. Melbourne: Bureau of Immigration and Multicultural Population Research, 1996. Elliott and Shanahan Research. Summary of background research for the development of a campaign against domestic violence, conducted for the Office of the Status of Women, Department of the Prime Minister and Cabinet. Canberra: 1988. Quarter way to equal. A report on barriers to access to legal services for migrant women. Sydney: Law Foundation of New South Wales, 1994. Public violence: a report of violence in Victoria. Melbourne: Victorian Community Council against Violence, 1992. Hansen D, Le Sueur M. Separating mothers and children: Australia's gendered immigration law and policy. Alternative Law Journal 1996; 21: 203-206. Lawton K. Needs of NESB women in women's refuges: a perspective from a remote rural area in the north west of Western Australia. BIR Bulletin 1992; 6: 30-33. Mazza D, Dennerstein L, Ryan V. Physical, sexual and emotional violence against women: a general practice-based prevalence study. Med J Aust 1996; 164: 14-17. American Medical Association, Council on Scientific Affairs. Violence against women: relevance for medical practitioners. JAMA 1992; 267: 3184-3189. Authors' details Key Centre for Women's Health in Society, University of Melbourne, Carlton, VIC. Jill Astbury, MEd, PhD, Associate Professor. Cooperative Research Centre for Rainforest Ecology and Management, Cairns, QLD. Judy Atkinson, PhD, Senior Research Officer, Aboriginal Liaison. Harley Medical Chambers, Fitzroy, VIC. Janet E Duke, FRANZCOG, FRCOG. Faculty of Law, Australian National University, Canberra, ACT. Patricia Easteal, PhD, Visiting Fellow. Rehabilitation and Aged Care Service, Hornsby Ku-ring-gai Hospital, Hornsby, NSW. Susan E Kurrle, MB BS, DipGerMed, Director and Senior Staff Specialist. Child Protection Unit, New Children's Hospital, Westmead, NSW. Paul R Tait, MB BS, FRACP, Head. Department of Psychiatry, Royal Brisbane Hospital, Herston, QLD. Jane Turner, MB BS, FRANZCP, Senior Lecturer. Reprints will not be available from the authors. Correspondence: Associate Professor J Astbury, Key Centre for Women's Health in Society, 720 Swanston Street, Carlton, VIC 3053. j.astburyATkcwh.unimelb.edu.au ©MJA 2000 Make a comment Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 2000 Medical Journal of Australia. We appreciate your comments. 1: Illustrative case of domestic violence involving children Nine-week-old baby "Lee" was taken to the family's general practitioner by her mother, "Anna", who stated that Lee was waking throughout the night and hard to settle. The GP noted some old and new bruising on Lee's head and trunk and asked Anna about these. She stated that Lee had tipped out of a bassinet down some stairs and also tended to bruise easily. Concerned about the possibility of child abuse, the GP referred Lee to the local hospital emergency department and notified the Department of Community Services. Lee was found to have skull and rib fractures and a subdural haematoma. Coagulation studies were normal. Anna was depressed and tearful on presentation. She admitted to the social worker that on several occasions she had "lost it" with Lee and thrown her down into her cot. She said her husband was away for long hours at work and she felt isolated. She later disclosed a long history of verbal, physical and sexual assault by her husband. He was often short-tempered and verbally intimidating towards her and their two-year-old son (who was described as being "very scared" of his father). She had had postnatal depression following the delivery of her first child. It was later learned that Anna had grown up in a family where domestic violence had occurred regularly. Back to text 2: Illustrative case of domestic violence involving an elderly person "Mrs Jones" is an 84-year-old widow with moderate Alzheimer disease. Until recently, she had been living alone, and was managing quite well with assistance from community services and regular visits from her general practitioner. Then her daughter moved in with her, ostensibly to care for her. Her daughter cancelled all services and suggested to the GP that his regular visits were unnecessary. Three months later, one of Mrs Jones' neighbours contacted her GP. He was concerned that Mrs Jones appeared to have lost a lot of weight and was often seen in her backyard crying. The GP visited and was reluctantly admitted to the house by Mrs Jones' daughter. The GP noted that Mrs Jones had indeed lost weight, and she appeared unkempt and had facial bruising. Her mental state had markedly deteriorated. Arrangements were made for Mrs Jones to be admitted to hospital, where she was found to be malnourished, to have an untreated wrist fracture and to have bruising over her trunk and face. Back to text 3: Illustrative case of domestic violence involving Indigenous people "Eva" has been married for nearly 25 years and has been beaten many times and subjected to different forms of abuse by her husband. She has seven children, and prides herself on being a strong Aboriginal woman, a "survivor". She stays in the relationship because "all kids need a father". Calling the police has therefore never been an option when she is being assaulted. Nor would calling the police be of any help. They are already constantly involved in her life, and judge her as being "a bad mother", "a troublemaker" and "emotionally unstable". Her sons are all in trouble with the law for their public behaviour, which is often violent. They are either in jail or in juvenile detention centres, on remand or parole. On release from jail they go back into a family environment that provokes distress and anger. Her eldest son has just served his second jail term for assault, after stabbing a person who said something against his father. He unsuccessfully attempted suicide in jail. He grieves for the loss of relationship with his father and continually attempts to establish some nurturing communication. He says he wants to get married and have a happy life, but all his relationships with young women have ended because of his violence. His mother, whom he has seen bashed many times, is angry at the juvenile justice system, Corrective Services and other state agencies because they just lock her children up without helping them to stop their offending behaviours. She is more involved with her own day-to-day survival than being able to think through how she can help them "break their cycle".33 Back to text 4: Illustrative case of domestic violence involving a woman of non-English-speaking background presenting in general practice "Ruziye" is a Turkish migrant sponsored by her Turkish-Australian husband, to whom she has been married for 18 months. She presents to a general practitioner with a complaint of rectal bleeding and extreme pain. Her husband enters the surgery with her. Background Ruziye's file indicates that she has seen the doctor for vaginal bleeding on several prior occasions. Consultation GP: Mr Amir, I would prefer to see your wife alone. Husband: Her English is not good. I can do translating. GP: That's OK. I have learned to talk to patients from non-English-speaking backgrounds and require that the consultation takes place between Ruziye and myself. [Husband reluctantly leaves the office] GP: When did the bleeding and soreness begin? Ruziye: A few days ago. GP: How did it start? Ruziye: My husband he likes to, you know, that part of me. This is hard to say. Where I come from, we do not talk about these things. GP: I understand that it is not easy for you. To help you though I do need to have an understanding of what has happened. Ruziye: Yes, I see. He does push hard and it hurts. GP: Do you ask him to stop? Ruziye: I tried once but he said it is my duty as his wife. GP: Well, Ruziye, in Australia, it is actually not your duty. In fact, we have laws that say you can say "no" to your husband and if he still does it, he is breaking the law. Ruziye: I did not know this. But in my family, you have to stay married and I have nowhere to go anyway. GP: There is help for you, Ruziye. If you decide that he is hurting you and that you want to leave, I can give you a pamphlet that lists places and people that will help you. Ruziye: Thank you doctor. Ruziye returned to the doctor several times over the next year with similar problems. Each time, the doctor gently talked to her about marital rape and other types of violence. Back to text

Jill Astbury · Judy Atkinson · Janet E Duke · Patricia L Easteal · Susan E Kurrle · Paul R Tait · Jane Turner

New Drugs, Old Drugs COX-2 inhibitors Peter M Brooks and Richard O Day MJA 2000; 173: 433-436 Abstract - Adverse gastrointestinal events - Coxibs - The future of COX-2 - Practical issues - References - Authors' details - - More articles on General medicine Abstract Cyclooxygenase-2 (COX-2) inhibitors constitute a new group of non-steroidal anti-inflammatory drugs (NSAIDs) which, at recommended doses, block prostaglandin production by cyclooxygenase-2, but not by cyclooxygenase-1. Two COX-2 inhibitors are currently available in Australia -- celecoxib, which is taken twice daily, and rofecoxib, which is taken once daily. Both drugs act rapidly in providing pain relief and their anti-inflammatory analgesic effect in osteoarthritis and rheumatoid arthritis is equivalent to standard doses of non-selective NSAIDs. Celecoxib and rofecoxib show significantly lower incidences of gastrotoxicity (as measured by endoscopic studies and gastrointestinal ulcers and bleeds) than non-selective NSAIDs. There is Level 2 evidence that COX-2 inhibitors: reduce pain in classic pain models -- third-molar extraction, dysmenorrhoea and after orthopaedic surgery; reduce pain and disability in osteoarthritis of the hip and knee; and reduce pain and disability in rheumatoid arthritis. Other adverse effects, such as interference with antihypertensive agents and the potential to produce renal dysfunction in patients with compromised renal function by COX-2 inhibitors, seem similar to those of non-selective NSAIDs. Traditional non-steroidal anti-inflammatory drugs (NSAIDs) constitute one of the largest groups of pharmaceuticals, with a world market in excess of $13 billion per annum.1 Although primarily used to treat pain and inflammation in musculoskeletal disease, NSAIDs may also have a role in the management of such widely differing conditions as chronic pain associated with conditions other than musculoskeletal disorders, Alzheimer disease and colorectal cancer.2 Although NSAIDs have been extraordinarily useful in controlling signs and symptoms of musculoskeletal disease, it is now appreciated that their use is associated with significant morbidity, primarily because of gastrointestinal toxicity,3 but also because of renal dysfunction4 and cardiac failure.5Until 10 years ago, it was accepted that NSAIDs acted by reducing prostaglandin synthesis through inhibition of cyclooxygenase (COX). Over the last decade the finding that cyclooxygenase activity increases in inflammation led to the identification of a new COX isoform, and the elucidation of its molecular structure.6 Recognition that cyclooxygenase consisted of two isoforms, COX-1 and COX-2, spawned an active, molecular-based drug development program for specific inhibitors of COX-2. The isoforms differ in that glucocorticoids inhibit synthesis of COX-2, but not COX-1, and COX-2 has a larger active site and a side pocket into which the new specific inhibitors fit.7 Inhibition by traditional NSAIDs and the selective COX-2 inhibitors (now classified as a separate class of NSAIDs -- the coxibs) is compared in Box 1. Coxibs should have the same efficacy as a traditional NSAID, but without the effects on haemostasis and gut mucosa. Adverse gastrointestinal events and NSAID therapy Indigestion, mucosal erosion, ulceration, bleeding and perforation of the stomach are all associated with NSAID use, and serious side effects can be asymptomatic. The risk of adverse gastrointestinal events increases with age and dose. Other risk factors for gastrointestinal adverse effects include the simultaneous use of two or more NSAIDs, a history of peptic ulcer or gastrointestinal bleeding, comorbid conditions such as cardiac and renal dysfunction, and concomitant use of corticosteroids or anticoagulants.8 Up to 2% of patients who take an NSAID for 12 months develop an ulcer or a significant gastrointestinal bleed, and this imposes a significant burden on individuals and the community.3 Coxibs Two COX-2 inhibitors are currently available in Australia, and their drug profiles are given in Box 2. Rofecoxib has a longer half-life than celecoxib and is suitable for once-daily dosing, while celecoxib usually needs to be given twice daily. These two drugs also have significantly different effects on the cytochrome P450 (CP450) enzyme system, which is important in the metabolism of drugs. Celecoxib inhibits CP450 (CYP2C9) enzymes and thus may cause elevation of plasma concentrations of any drug metabolised by this isoenzyme, such as some β-blockers, antidepressants and antipsychotics. Rofecoxib does not inhibit this enzyme system and has fewer potential metabolic interactions. Like conventional NSAIDs, both rofecoxib and celecoxib may diminish antihypertensive effects of angiotensin-converting enzyme (ACE) inhibitors and diuretic effects of frusemide and thiazides. Both coxibs have the potential to increase plasma lithium levels. Warfarin levels and, more importantly, prothrombin times can be increased by both drugs. Plasma concentrations of methotrexate were increased by just over 20% when coadministered with rofecoxib, while celecoxib did not significantly increase methotrexate levels.9 The clinical significance of this interaction is unclear, but increased care with methotrexate monitoring is appropriate after introducing a coxib. Efficacy Pain relief: Rofecoxib (50 mg) has been shown to be superior to placebo and equivalent to naproxen sodium (550 mg) in the 12 hours after being taken for orthopaedic surgical pain relief (E2) (see Box 3 for an explanation of level-of-evidence codes) and for dysmenorrhoea (E2), and equivalent to ibuprofen (400 mg) after third-molar tooth extraction (E2). Celecoxib in a dose of 100 mg or 200 mg was significantly better than placebo for pain after third-molar extraction, and no different than ibuprofen 400 mg or naproxen sodium 550 mg (E2).10 Osteoarthritis of hip and knee: In a 12-week trial of more than 1000 patients comparing 50 mg, 100 mg and 200 mg celecoxib twice daily with 500 mg naproxen twice daily or placebo, the 100 mg and 200 mg doses of celecoxib were as effective as the naproxen. Although 50 mg celecoxib twice daily was better than placebo, it was not as effective as the higher doses.11 Rofecoxib in doses of 12.5 mg and 25 mg once daily has been shown to be significantly better than placebo, as effective as 2.4 g of ibuprofen daily (over six weeks)12 and as effective as 150 mg of diclofenac daily (over one year) for osteoarthritis of the knee (E2).13 Rheumatoid arthritis: A three-month, double-blind, placebo-controlled study comparing naproxen 500 mg twice daily, placebo and celecoxib in doses of 100 mg, 200 mg or 400 mg twice daily in more than 1100 patients with rheumatoid arthritis showed that all celecoxib doses and naproxen were effective for pain and inflammation throughout the 12 weeks (E2).14 Interestingly, only 60% of patients completed this study. The reasons for failure to complete were not different between the active treatment groups, although those taking placebo showed a higher treatment failure rate. These patients also underwent endoscopy within a week of commencing treatment and at the end of the three months. The peptic ulceration rate (defined as any break in the mucosa at least 3 mm in diameter with unequivocal depth) was 4% for those taking placebo, and 6%, 4% and 6% for those taking 100 mg, 200 mg and 400 mg celecoxib, respectively; these incidences were not significantly different. However, the rate was significantly higher (26%) for those taking 500 mg naproxen (E2).14 A six-month study comparing 200 mg celecoxib twice daily with 75 mg diclofenac twice daily in 655 patients with adult-onset rheumatoid arthritis showed that celecoxib had similar efficacy to diclofenac, with a significantly lower incidence of gastrointestinal side effects. In this study 430 patients underwent endoscopy within seven days of the last treatment, and gastroduodenal ulcers (defined as any break in the mucosa of at least 3 mm in diameter with unequivocal depth) were found in 33 patients (15%) treated with diclofenac and eight (4%) in the celecoxib group. In this study, the rate of withdrawal for any gastrointestinal-related adverse event (most commonly abdominal pain, diarrhoea and dyspepsia) was nearly three times higher in the diclofenac-treated group than in the celecoxib group, and this was significant at P < 0.001 (E2).15 In an eight-week study, 648 patients with rheumatoid arthritis were randomly assigned to groups receiving either placebo or 5 mg, 25 mg or 50 mg of rofecoxib once daily. In this study the 5 mg dose was no different to placebo, while both larger doses were significantly better than placebo. No clinically significant oedema, hypertension or serious gastrointestinal effects were reported.16 Adverse events Gastrointestinal: Carefully conducted endoscopy studies show a significantly lower incidence of endoscopically proven ulcers with up to 12 months of treatment with COX-2-specific agents. In patients with rheumatoid arthritis, celecoxib is associated with significantly less gastroduodenal ulceration than naproxen14 or diclofenac (E2).15 In a combined analysis of eight trials in patients with osteoarthritis, treatment with rofecoxib was associated with a significantly lower incidence of perforations, ulcers or bleeds than treatment with ibuprofen, diclofenac or nabumetone (E1).17 An endoscopic study in osteoarthritis showed an ulcer incidence at 12 weeks for rofecoxib equivalent to that for placebo and significantly lower than for ibuprofen.18 Large studies of gastrointestinal outcomes with both celecoxib and rofecoxib are currently in progress, and these data should be available in the next few months. There are also data suggesting that small bowel permeability is not affected by COX-2-specific agents, whereas it is increased with non-selective NSAIDs. Renal: Although it was initially felt that COX-2-specific agents might be renal-sparing, there is COX-2 in the kidney19 and it can be induced in circumstances such as sodium depletion or in patients taking ACE inhibitors. COX-2-specific inhibitors may affect renal function in much the same way as traditional NSAIDs, and particular care should be taken in prescribing these drugs to patients with renal dysfunction or in those taking diuretics or antihypertensive agents, particularly ACE inhibitors. Cardiovascular: The inhibitory effect on platelet function by traditional non-selective NSAIDs may play a contributory role in gastric bleeding. However, prostacyclin (PGI2) is also thought to play an important role as an antithrombotic and vasodilator, and COX-2 is thought to play a role in the biosynthesis of both systemic and renal prostaglandin (PGE2),20 thus influencing PGI2 synthesis. This may have important connotations in vascular disease. The implications of specific COX-2 inhibition on thrombosis are not known, although there have been several case reports of thromboses in patients with the antiphospholipid syndrome treated with celecoxib.21 As the COX-2 story unfolds it will be important to explore the effect of combinations of low-dose aspirin and specific COX-2 inhibitors in a wide range of patients. Reproduction COX-1 and COX-2 are both involved in various aspects of ovulation, implantation and parturition.22 COX-2-deficient mice are infertile and COX-2-specific inhibitors should not be taken by women wishing to become pregnant. The future of COX-2 inhibitors Large studies of gastrointestinal outcomes are currently in progress with both these agents to further examine clinical gastrointestinal events. Patients with a previous history of peptic ulceration (although not in the previous six months) and patients up to and over the age of 90 years have been included in outcome studies so far completed. As COX-2 is involved in ulcer healing, it is important to know whether use of these agents will retard this process. It will also be important to see, in large clinical trials, whether coxibs will have any effect on the incidence of vascular disease. With the knowledge that COX-2 is overexpressed in bowel cancer and in Alzheimer disease and that non-selective NSAIDs retard both of these conditions comes the tantalising prospect that coxibs may have potential for wider use in the future.1,7 Celecoxib has been approved in the US for patients with familial polyposis coli after a randomised placebo-controlled trial showed a 28% reduction in the number of polyps in patients who took 400 mg celecoxib twice daily.23 Practical issues An algorithm for prescribing specific COX-2 inhibitors is shown in Box 4, and important messages for patients are shown in Box 5. Cost-effectiveness studies (which are dependent on the local price of the drug), based on current US prices, suggest that use of COX-2 inhibitors would be cost effective in high risk patients -- those with a history of peptic ulceration, those taking high doses of NSAIDs or corticosteroids, and those aged over 65.24The release of COX-2 inhibitors in Australia appears to be good news for sufferers of musculoskeletal conditions.25 As with the introduction of any new drug, doctors should assess patients carefully, asking whether there are specific reasons for changing therapy (such as ineffectiveness or adverse events), and review patients taking the new drug at frequent intervals. In this way these drugs can be introduced cost effectively and benefit the maximum number of patients. Disclaimer: Peter Brooks serves on Advisory Boards for Merck Sharp and Dohme for rofecoxib, and in the past has consulted and been a member of Advisory Boards for Pfizer and Searle. Richard Day serves on Advisory Boards on rofecoxib for Merck Sharp and Dohme and on Advisory Boards for celecoxib for Pfizer and Searle. References Brooks PM. COX-2 inhibitors. Aust Prescriber 2000; 23: 30-32. Dubois RN, Abramson SB, Crofford L, et al. Cyclooxygenase in biology and disease. FASEB J 1998; 12: 1063-1073. Fries JF. NSAID gastropathy: the second most deadly rheumatic disease? Epidemiology and risk appraisal. J Rheumatol 1991; 18 Suppl 28: 6-10. Henry D, Page J, Whyte I, Nanra R, Hall C. Consumption of non-steroidal anti-inflammatory drugs and the development of functional renal impairment in elderly subjects. Results of a case-control study. Br J Clin Pharmacology 1997; 44: 85-90. Heerdink ER, Leufkens HG, Herings RMC, et al. NSAIDs associated with increased risk of congestive heart failure in elderly subjects taking diuretics. Arch Intern Med 1998; 158: 1108-1112. Luong C, Miller A, Barnett J, et al. The structure of human cyclooxygenase-2; conservation and flexibility of the NSAID binding site. Nat Struct Biol 1996; 3: 927-933. Hawkey CJ. Cox-2 inhibitors. Lancet 1999; 353: 307-314. Wolfe NM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of non steroidal antiinflammatory drugs. N Engl J Med 1999; 340: 1888-1899. Karim A, Tolbert DS, Hunt TL, et al. Celecoxib, a specific COX-2 inhibitor, has no significant effect on methotrexate pharmacokinetics in patients with rheumatoid arthritis. J Rheumatol 1999; 26: 2539-2543. Geis GS. Update on clinical developments with celecoxib, a new specific Cox-2 inhibitor: what can we expect? J Rheumatol 1999; 26 Suppl 56: 31-36. Bensen WG, Fiechther JJ, McMirren JI, et al. Treatment of osteoarthritis with celecoxib, a cyclooxygenase-2 inhibitor: a randomized controlled trial. Mayo Clin Proc 1999; 74: 1095-1105. Ehrich EW. Effect of specific Cox-2 inhibition in osteoarthritis of the knee: a 6 week double blind placebo controlled pilot study of rofecoxib. J Rheumatol 1999; 26: 2438-2447. Cannon GW, Caldwell JR, Holt P, et al. Rofecoxib, a specific inhibitor of cyclooxygenase 2, with clinical efficacy comparable with that of diclofenac sodium: results of a one-year, randomized, clinical trial in patients with osteoarthritis of the knee and hip. Rofecoxib Phase III Protocol O35 Study Group. Arthritis Rheum 2000; 43: 978-987. Simon LS, Weaver AL, Graham DY, et al. Anti-inflammatory and upper gastro-intestinal effects of celecoxib in rheumatoid arthritis. JAMA 1999; 282: 1921-1928. Emery P, Zeidler H, Kviem TK, et al. Celecoxib versus diclofenac in long term management of rheumatoid arthritis: randomised double blind comparison. Lancet 1999; 354: 2106-2111. Schnitzer T. The safety profile, tolerability and effective dose range of rofecoxib in the treatment of rheumatoid arthritis. Clin Ther 1999; 21: 1688-1702. Langman MJ, Jensen DM, Watson DJ, et al. Adverse upper gastrointestinal effects of rofecoxib compared to NSAIDs. JAMA 1999; 282: 1929-1933. Hawkey C, Laine L, Simon T, et al. Comparison of the effects of rofecoxib (a cyclooxygenase 2 inhibitor), ibuprofen and placeo on gastroduodenal mucosa of patients with osteoarthritis. Arthritis Rheum 2000; 43: 370-377. Komhoff M, Grone H-J, Klein T, et al. Localisation of cyclooxygenase-1 and -2 in adult and fetal human kidney: implications for renal function. Am J Physiol 1997; 272: 460-468. McAdam BFF, Catella-Lawson IA, Mardini A, et al. Systemic biosynthesis of prostacyclin by cyclo-oxygenase (Cox-2); the human pharmacology of a selective inhibitor of Cox-2. Proc Natl Acad Sci USA 1999; 96: 272-277. [Published erratum appears in Proc Natl Acad Sci USA 1999 May 11; 96: 5890.] Crofford LJ, Oates JC, McCune WJ, et al. Thrombosis in patients with connective tissue diseases treated with specific COX-2 inhibitors: a report of four cases. Arthritis Rheum 2000; 43: 1891-1896. Richards JS, Fitzpatrick SL, Clemens JW, et al. Ovarian cell differentiation: a cascade of multiple hormones, cellular signals and regulated genes. Rev Prog Hormone Res 1995; 50: 223-254. Steinbach G, Lynch PM, Phillips RKS. The effect of celecoxib, a cyclo oxygenase-2 inhibitor, in familial adenomatous polyposis. N Engl J Med 2000; 342: 1946-1952. Peterson WL, Cryer B. Cox-1 sparing NSAIDs -- is the enthusiasm justified? JAMA 1999; 282: 1961-1963. Schachna L, Ryan PFJ. Cox-2 inhibitors: the next generation of non-steroidal anti-inflammatory drugs. Med J Aust 1999; 171: 175-176. Authors' details University of Queensland, Royal Brisbane Hospital, Brisbane, QLD. Peter M Brooks, MD, FRACP, Executive Dean of Health Sciences. University of New South Wales, St Vincent's Hospital, Sydney, NSW. Richard O Day, MD, FRACP, Professor of Clinical Pharmacology. Reprints will not be available from the authors. Correspondence: Professor P M Brooks, Faculty of Health Sciences, University of Queensland, Edith Cavell Building, Royal Brisbane Hospital, Herston, QLD 4029. Make a comment 1: Action, regulation and inhibition of cyclooxygenase-2 Regulation: mainly constitutive, but increases 2-4 - fold with inflamatory stimuli. Expressed by most tissues, particularly platelets, stomach, intensive and kidney. Inhibition: by non-steroidal anti-inflammatory drugs. Regulation: mainly inducible (10-20-fold). Induced by inflammatory stimuli in macrophages, monocytes, synoviocytes, chondrocytes, fibroblasts and endothelial cells. Hormonally induced in ovaries and fetus. Constitutive in central nervous system, kidney, testes and trachea. Inhibition: by non-steroidal anti-inflammatory drugs and selective COX-2 inhibitors. Back to text 2: Drug profiles of celecoxib and rofecoxib Action At therapeutic plasma concentrations, coxibs block COX-2 but do not significantly interfere with COX-1. Onset of action Analgesia: 1 hour. Anti-inflammatory effect: less than 2 weeks after starting therapy. Dosing Celecoxib, 200-400 mg, orally, twice daily. Rofecoxib, 12.5-50 mg, orally, once daily. Metabolism Celecoxib: by cytochrome P450; half-life, 12 hours; protein binding, 97%. Rofecoxib: by metabolic reduction; half-life 17 hours; protein binding, 85%. Adverse effects Reduction in gastrointestinal events (ulcers, bleeds and erosions) compared with non-selective non-steroidal anti-inflammatory drugs (NSAIDs). Effects on renal function (potential for mild fluid retention, insufficiency in renally compromised patients and those taking ACE inhibitors) similar to those of non-selective NSAIDs. Drug interactions Celecoxib Rofecoxib Effect Clinically significant Warfarin Yes Yes Increased prothrombin time Yes Methotrexate No Yes Increased methotrexate levels Probably not Lithium Yes Yes Increased lithium levels Yes Angiotensin-converting enzyme inhibitors Yes Yes Reduced antihypertensive effects (potential for renal impairment) Yes Inhibitors of CYP2C9* Yes No Increased plasma concentrations of celecoxib Yes Substrates of CYP2D6† Yes No Increased plasma concentration of substrate Probably Frusemide and thiazides Yes Yes Reduced diuretic effect Yes Codeine and oxycodeine Yes No Potential for reduced pain efficacy of substrates Possibly Antacids Yes ? Reduced celecoxib plasma concentrations Probably *Amiodarone, cimetidine, fluoxetine, fluconazole, metronidazole, fluvastatin. †ß-Blockers, antidepressants (amitryptyline, desipramine, clomipramine, fluoxetine), antipsychotics (haloperidol, thioridazine), perhexiline. Back to text 3: Level-of-evidence codes Evidence for the statements made in this article is graded according to the NHMRC system7 for assessing the level of evidence: E1 Level I: Evidence obtained from a systematic review of all relevant randomised controlled trials. E2 Level II: Evidence obtained from at least one properly designed randomised controlled trial. E31 Level III-1: Evidence obtained from well-designed pseudo-randomised controlled trials (alternate allocation or some other method). E32 Level III-2: Evidence obtained from comparative studies with concurrent controls and allocation not randomised (cohort studies), case-control studies, or interrupted time series without a parallel control group. E33 Level III-3: Evidence obtained from comparative studies with historical control, two or more single-arm studies, or interrupted time series without a parallel control group. E4 Level IV: Evidence obtained from case-series, either post-test, or pre-test and post-test. Back to text 4: When to prescribe a COX-2 inhibitor Prescribe for patients with rheumatoid arthritis or osteoarthritis who are: Not responding to conventional non-steroidal anti-inflammatory drugs (NSAIDs) and/or At risk of gastrointestinal (GI) toxicity because they: have had previous NSAID-associated GI toxicity; are aged over 65 years; have severe arthritic disease; are taking a high dose of NSAIDs. Back to text 5: Important messages for patients COX-2 inhibitors produce many effects of non-steroidal anti-inflammatory drugs (NSAIDs) but with a reduced incidence of gastrotoxicity. COX-2 inhibitors are no better than NSAIDs in reducing musculoskeletal pain and inflammation but are safer. COX-2 inhibitors may interfere with antihypertensive or diuretic medication. Back to text

Peter M Brooks · Richard O Day

Viewpoint Economic sanctions and public health: the case of Iraq Susan J Wareham We have a duty to speak out MJA 2000; 173: 438-439 Economic sanctions have often been thought of as a humane alternative to war, a way of bringing undesirable governments into line without the loss of innocent lives. The situation in Iraq, however, demonstrates that comprehensive economic sanctions can, in effect, be a weapon of mass destruction, with devastating consequences for public health. Sanctions were imposed against Iraq in August 1990 after Iraq invaded Kuwait, and they were reimposed to force Iraq's disarmament after the 1991 Gulf War. All goods entering Iraq require authority from the United Nations Security Council Sanctions Committee, and Iraq's exports of oil are severely limited. (While the Security Council has now removed the ceiling on Iraq's oil exports, the oil industry is severely damaged and lacking essential supplies.) The effects of the sanctions on the health of the people of Iraq, particularly the children, have been documented repeatedly by the UN's humanitarian agencies and other bodies, and ignored repeatedly by policymakers. In July 1993, the Food and Agriculture Organization and the World Food Programme reported that the sanctions had ". . . generated persistent deprivation, chronic hunger, endemic undernutrition, massive unemployment and widespread human suffering" and that ". . . a grave humanitarian tragedy is unfolding".1 A World Health Organization study released in March 1996 stated that health conditions were deteriorating at an alarming rate, and that malnutrition among young children was widespread.2 In 1999, UNICEF conducted a child and maternity mortality survey of nearly 40 000 households throughout Iraq. The child mortality results indicated a major increase in mortality rates in the preceding decade, both in infants and in children under five years.3 This should be seen in the context of the steady reductions in child mortality before the imposition of sanctions, from an under-five mortality rate of 127 per 1000 livebirths in 1970, to 83 in 1980 and to 50 in 1990. The rates then rose to 117 per 1000 livebirths in 1995 and to 125 in 1998. On the basis of these results, Executive Director Carol Bellamy reported UNICEF's conclusion: if the substantial reduction in child mortality throughout Iraq during the 1980s had continued through the 1990s, there would have been half a million fewer deaths of children under five.4 In April 1999, I took part in an international delegation to Iraq, with representatives of the United States, Canada, the United Kingdom, Palestine and Australia, sponsored by International Physicians for the Prevention of Nuclear War. The purposes were to observe conditions, to deliver medical and pharmaceutical supplies, and to make contact with professional colleagues who have been internationally isolated. In the hospitals we visited, most of the basic drugs and medical and surgical supplies, including antibiotics and intravenous fluids, were in short supply or unavailable. At Saddam Paediatric Hospital, in Baghdad, clinicians we spoke to said that cholera, gastroenteritis, tuberculosis, measles, pertussis, rubella, poliomyelitis and other infectious illnesses have become more common since the imposition of sanctions. Vaccination programs have suffered from a lack of refrigerated transport. A nauseating stench from blocked and broken sewerage pipes pervaded many hospital wards. With adequate plumbing supplies and chlorine and other chemicals for water purification either blocked by the sanctions5 or unaffordable, it is very difficult to control faecal-oral spread of infections. Colleagues we met at Baghdad University College of Medicine also spoke of the major effect that the lack of textbooks, and even paper for photocopying, had had on medical education. For the medical profession in Iraq, such shortages and Third World conditions are a new phenomenon. Before the sanctions, Iraq, with its vast oil wealth, had an abundance of medical supplies and one of the best healthcare systems in the region. Malnutrition was not a major public health problem in Iraq before 1990.6 The Harvard Study Team that visited Iraq in April and May 1991 reported that many of the young physicians they spoke to had never seen a case of marasmus before the 1991 Gulf Crisis, and even the older physicians had not seen many.7 We heard several reports from doctors that the incidence of childhood leukaemia and of major congenital abnormalities has risen sharply, especially in southern Iraq near the 1991 war zone. Some suspected that depleted uranium weapons used in that war may be a contributing factor. (Depleted uranium, a by-product of the uranium enrichment process, was used in armour-piercing shells both in the 1991 Gulf War and against Serbia in 1999.) UN cancer statistics for southern Iraq between 1989 and 1994 have shown a sevenfold increase in cancer rates.8 Professor Doug Rokke, a health physicist at Jacksonville State University, Alabama, who was responsible for the clean-up of US depleted uranium equipment in Iraq, argues strongly that its use should be banned.9 Research on this subject is urgently needed. Most of the Iraqi children with leukaemia die. According to Professor Karol Sikora, Professor of International Cancer Medicine, Imperial College School of Medicine, London, radiotherapy equipment, chemotherapy drugs and analgesics for Iraq are consistently blocked by the United States and Britain.10 Morphine is generally unavailable, and even aspirin is severely rationed. Denis Halliday was the UN Humanitarian Coordinator in Iraq until his resignation in 1998 in protest at the effects of the sanctions. (His successor, Hans Von Sponeck, resigned in February this year for precisely the same reason.) Halliday was in Australia in April this year, at the invitation of the Medical Association for Prevention of War, for discussions with the Australian government, which still supports the sanctions policy. He says that the sanctions are a form of genocide, that they have done nothing but target civilians, and that they strengthen Saddam Hussein. The elimination of Iraq's weapons of mass destruction is an essential step towards peace in the Middle East. However, while such weapons remain elsewhere in the region, and the ongoing suffering, degradation, humiliation and resentment of the Iraqis is ignored, peace prospects remain grim. For our profession, the defence and promotion of public health is one of the greatest contributions we can offer humanity. Policies which deprive whole populations of food, clean water and basic healthcare are anathema to public health principles and must be condemned outright. For all those who suffer the effects of this deprivation -- those who die needlessly and their relatives and our professional colleagues who must watch them die -- we have a duty to speak out. References Food and Agriculture Organization of the United Nations. Special Alert No. 237 -- FAO/WFP Crop and Food Supply Assessment Mission to Iraq. Rome: FAO/WFP, July 1993. World Health Organization. Health conditions in Iraq "serious", WHO study finds. Press release WHO/23. Geneva: WHO, 25 March 1996. UNICEF/Ministry of Health. Child and Maternal Mortality Survey 1999: Preliminary report. Iraq: UNICEF, July 1999. UNICEF. Iraq surveys show "humanitarian emergency". Press release. UNICEF, 12 August, 1999. Office of the Humanitarian Co-ordinator, Baghdad. The Secretary-General's 90-Day Report to the UN Security Council, 15 March 1999. Situation analysis of children and women in Iraq. UNICEF Report. 30 April 1998. The Harvard Study Team. The effect of the Gulf crisis on the children of Iraq. Special report. N Engl J Med 1991; 325: 977-980. Ciment J. Iraq blames Gulf war bombing for increase in child cancers. BMJ 1998; 317: 1612. Rokke D. Depleted uranium and its effects in Iraq. Proceedings of the conference hosted by the Campaign Against Sanctions on Iraq. Cambridge, UK, 13-14 November 1999. Cambridge, UK: Campaign Against Sanctions on Iraq, 2000. (Distributed by Barque Press.) Sikora K. Cancer services are suffering in Iraq [personal view]. BMJ 1999; 318: 203. Authors' details Medical Association for Prevention of War (Australia), Canberra, ACT. Susan J Wareham, MB BS, President. Reprints will not be available from the author. Correspondence: Dr S J Wareham, 3 Katz Place, Spence, ACT 2615. warehamsATozemail.com.au Make a comment

Susan J Wareham