Issues
Volume 166 Issue 2
Editorials Childhood sexual abuse: concerns and consequences Sarah E Romans, Paul E Mullen (MJA 1997; 166: 59)Do anabolic-androgenic steroids enhance sporting performance? Michael C Kennedy, Anthony J OSullivan (MJA 1997; 166: 60)Guidelines: in search of certainty Deborah Saltman (MJA 1997; 166: 62)Peanut allergy Richard G Douglas, Robyn E OHehir (MJA 1997; 166: 63) Research Prevalence of childhood sexual abuse in a community sample of Australian women Jillian M Fleming (MJA 1997; 166: 65)Abstract - ArticleClinical practice guidelines in general practice: a national survey of recall, attitudes and impact Leena Gupta, Jeanette E Ward, Robert S A Hayward (MJA 1997; 166: 69)Visual impairment in nursing home residents: the Blue Mountains Eye Study Paul Mitchell, Phillip Hayes, Jie Jin Wang (MJA 1997; 166: 73)Perinatal exposure to HIV in Australia, 1982-1994 Ann M McDonald, Marilyn Cruickshank, John B Ziegler, Elizabeth Elliott, John M Kaldor (MJA 1997; 166: 77) Notable Cases Plasmodium vivax malaria acquired in far north Queensland Dianne L Brookes, Scott A Ritchie, Andrew F van den Hurk, Julie R Fielding, Mark R Loewenthal (MJA 1997; 166: 82) For Debate The epidemic of post-traumatic stress disorder: a passing phase? John H T Ellard (MJA 1997; 166: 84)Post-traumatic stress disorder: the importance of clinical objectivity and systematic research Alexander C McFarlane (MJA 1997; 166: 88) Clinical Practice The role of the general practitioner in the treatment of schizophrenia: general principles Vaughan J Carr (MJA 1997; 166: 91) Update TChanges to postgraduate medical training in the United Kingdom: implications for Australasian doctors Steve R Kisely (MJA 1997; 166: 95) MJA Practice Essentials - Rheumatology Osteoarthritis Lyn M March (MJA 1997; 166: 98)
Editorials
Do anabolic-androgenic steroids enhance sporting performance?
A recent study has provided evidence that testosterone increases muscle strength, but does this translate to enhanced performance? 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". strength increased considerably in subjects who received placebo, but who were told they were receiving anabolic steroids For almost half a century, athletes have believed that use of anabolic-androgenic steroids can improve sporting performance. The United States physician John Zeigler was so convinced of their positive effects that on his return from the World Powerlifting Championships in Vienna in 1954 he worked on the development of methandrostenolone as a means of enhancing sporting performance. 1 This belief has persisted, leading to the widespread and much-publicised use of these drugs at all levels of sport (professional and amateur). It has been promoted by the banning of these drugs by sporting bodies to ensure fair competition. 2 Media reports and "underground" guides to anabolic steroids have also propagated the use of anabolic-androgenic steroids, which has spread from elite athletes to recreational bodybuilders, amateur athletes and adolescents. 3 Are the athletes and their coaches mistaken in their belief? Theoretically, anabolic-androgenic steroids should improve athletic performance by increasing muscle mass (via increased protein synthesis, nitrogen retention and antiglucocorticoid actions), as well as by increasing aggression and motivation. Moreover, recent isotope uptake studies in humans indicate that androgens may increase muscle protein synthesis, possibly through stimulation of intramuscular insulin-like growth factor-I (IGF-I) gene expression. 4 However, clinical studies have, in general, been inconclusive, partly because of the many unique methodological problems in studying the effects of anabolic-androgenic steroids (see below). In 1991, 16 randomised, placebo-controlled studies that used objective measures of performance were analysed by Elashoff et al. 5 They concluded that, while the possibility of anabolic-androgenic steroids improving sporting performance could not be excluded, "the data are insufficient to allow any firm conclusion about the efficacy of anabolic steroids in enhancing overall athletic performance". Since then, apart from a non-placebo-controlled study that showed an increase in lean body mass in healthy male volunteers receiving weekly injections of testosterone enanthate, 6 there were few real developments in the area until Bhasin et al. 7 published their study in July 1996. This study will probably become, in time, one of the most-cited articles on drugs and sport. Funded by the National Institutes of Health (US), the study examined the effect of high doses of testosterone enanthate in sesame oil (600 mg/week intramuscularly for 10 weeks); the authors made every attempt to remove confounding variables (such as diet, training, and weightlifting experience), and used standardised measures. Forty-three experienced weightlifters were randomly assigned to one of four groups (placebo with or without exercise, or testosterone with or without exercise). Strength was measured by two single weightlifts -- upper-body strength by benchpress, and lower-body strength by squatting. Fat-free body mass was measured by underwater weighing, and muscle size by magnetic resonance imaging. Forty subjects completed the study. Body weight increased only in the two testosterone-treated groups, and fat-free body mass only in the exercise groups, with the greatest change in fat-free mass in the testosterone plus exercise group (increase, 6.1 kg). Percentage body fat did not change in any group. Muscle size increased more in the testosterone groups than in either placebo group. Strength increased in both testosterone groups, as well as in the exercise group receiving placebo, but was greater in the exercise group with testosterone than in the exercise group with placebo. No significant adverse drug reactions were reported. Hence, for the first time, in a well designed study, supraphysiological testosterone did appear to increase muscle strength. One other placebo-controlled study has used higher doses of anabolic steroids (methandrostenolone, 100 mg/day for six weeks). 8 Reported 20 years ago, it used a crossover design, with attempts to control for most variables. The active drug was found to be no better than placebo in increasing strength. However, some caveats should be considered in assessing Bhasin et al.'s data. A placebo response has not been completely eliminated. It was not stated that the placebo was identical to the active drug in terms of pH, viscosity and other factors that may have allowed the code to be broken by either the administrator or recipient of the drug. Indeed, in a controlled study of oral anabolic steroids, all subjects correctly identified the active drug when directly asked. 9 The importance of the placebo response was shown by Ariel and Saville, who found that strength increased considerably in subjects who received placebo, but who were told they were receiving anabolic steroids. 10 Bhasin et al.'s subjects were experienced weightlifters. Although they reported that they had not taken anabolic steroids, these medications are illicit, and thus self-reporting may not be reliable. As 38%-58% of bodybuilders and weightlifters have been reported to use anabolic steroids, 11,12 some of Bhasin et al.'s subjects may well have been able to identify the active drug. Before generalising these results to athletes who use anabolic-androgenic steroids in the community, it should be remembered that they receive and use their supplies in very different ways to the controlled circumstances of Bhasin et al.'s study. Street supplies are often veterinary or illegally manufactured preparations, often combined with other medications such as diuretics and stimulants. Doses and duration are often well in excess of those used in this study. Although no major side effects were reported, the well documented long-term adverse effects of anabolic-androgenic steroids on cardiovascular risk, gynaecomastia, carcinogenesis, prostate and sexual function would not have been evident in a study of this duration. 13 On considering the available evidence, it appears that anabolic steroids definitely increase muscle size, and probably strength, but the mechanism is unknown. Further studies, using a crossover design, including inexperienced as well as experienced weightlifters, and the same drug vehicle for both placebo and active drug, with confirmation of subject blinding, should probably be conducted to confirm these findings. In addition, whether androgen-induced muscle hypertrophy translates into improved performance in sports that require skill as well as strength remains to be determined. But such studies should not overshadow the need for significant research into the prevention of anabolic-androgenic steroid abuse. Michael C Kennedy Department of Clinical Pharmacology and Toxicology, St Vincent's Hospital; and Manly Hospital, Sydney, NSW. Anthony J O'Sullivan Departments of Medicine and Endocrinology, St George Hospital, Sydney, NSW. Wade N. Anabolic steroids: Doctors denounce them, but athletes aren't listening. Science 1972; 176: 1399-1403. Skolnick AA. Tougher drug tests for Centennial Olympic Games. JAMA 1996; 275: 348-349. Buckley WE, Yesalis CE, Friedl KE, et al. Estimated prevalence of anabolic steroid use among male high school seniors. JAMA 1988; 260: 3441-3445. Urban RJ, Bodenburg YH, Gilkison C, et al. Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis. Am J Physiol 1995; 269: E820-E826. Elashoff JD, Jacknow AD, Shain SG, Braunstein GD. Effects of anabolic-androgenic steroids on muscular strength. Ann Int Med 1991; 115: 387-393. Forbes GB, Porta CR, Herr BE, Griggs RC. Sequence of changes in body composition induced by testosterone and reversal of changes after drug is stopped. JAMA 1992; 267: 397-399. Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996; 335: 1-7. Hervey GR, Hutchinson I, Knibbs AV, et al. "Anabolic" effects of methandienone in men undergoing athletic training. Lancet 1976; 2: 699-702. Freed DLJ, Banks AJ, Longson D, Burley DM. Anabolic steroids in athletics: crossover double-blind trial on weightlifters. BMJ 1975; 2: 471-473. Ariel G, Saville W. Anabolic steroids: the physiological effects of placebos. Med Sci Sports 1972; 4: 124-126. Perry HM, Wright D, Littlepage BNC. Dying to be big: a review of anabolic steroid use. Br J Sports Med 1992; 26: 259-261. Delbeke FT, Desmet N, Debackere M. The abuse of doping agents in competing body builders in Flanders (1988-1993). Int J Sports Med 1995; 16: 66-70. Kennedy MC. Anabolic steroid abuse and toxicology. Aust N Z J Med 1992; 22: 374-381. Reprints: Dr M C Kennedy, Manly Non-Invasive Cardiac Laboratory, Level 4, 22 Darley Road, Manly, NSW 2095.
Michael C Kennedy · Anthony J O'Sullivan
Research
Prevalence of childhood sexual abuse in a community sample of Australian women
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". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Author's details Abstract Objective: To ascertain the prevalence of childhood sexual abuse (CSA) in a community sample of Australian women. Design: Retrospective study, done in 1994, of cross-sectional data on the prevalence of CSA, collected as part of a larger two-stage case-control study of the possible relationship between CSA and alcohol abuse. Data were appropriately weighted to adjust for the different selection probabilities of cases and controls. Participants: 710 Women randomly selected from Australian federal electoral rolls. Results: One hundred and forty-four women (20%) had experienced CSA. In 14 of these 144 women (10%), the abuse involved either vaginal or anal intercourse (i.e., 2% of the sample population experienced such abuse). The mean age at first episode of CSA was 10 years, and most (71%) of the women were aged under 12 years at the time. Perpetrators of the abuse were usually male (98%) and usually known to the child; 41% were relatives. The mean age of abusers was 34 years, with a median age difference of 24 years from that of the abused individual. Only 10% of CSA experiences were ever reported to the police, a doctor or a helping agency (e.g., community organisations, such as sexual assault services). Conclusion: The high rates of CSA (estimated to be 20% of all women) and low rates of reporting (10%) indicate the need for general practitioners and other health professionals to be aware that a history of such abuse may be common in women in the general population. MJA 1997; 166: 65-68 Introduction Community-based studies in North America, the United Kingdom and New Zealand have shown that, for women, the prevalence of at least one incident of sexual contact with an adult before age 18 years ranges from 6% to 62%. 1-8 In an Australian study examining the extent of childhood sexual abuse (CSA) among social science students, 28% of the female students and 9% of the male students reported at least one such incident before the age of 16 years. 9 Official figures on the incidence of child abuse (including physical and sexual abuse and neglect) show that, in 1992-93, 59 122 cases were reported and investigated throughout Australia. Of these cases, 27 196 (46%) were officially substantiated, and the number of child sexual abuse cases was 5979 (22%). 10 Because of the secrecy and shame surrounding sexual abuse, the criminal sanctions against it, and the young age and dependent status of the child, it is likely that official statistics seriously underestimate its true extent. 11 To determine the true extent of CSA, prevalence studies that rely on retrospective reports of adult subjects are needed; this study presents epidemiological data on the prevalence of CSA in a community sample of Australian women. Methods Participants recruited The current study was part of a larger two-stage case-control investigation (conducted in 1994) into the relationship between CSA and alcohol abuse in women. Stage 1 of the study involved a postal questionnaire sent to 6000 women randomly selected from Australian federal electoral rolls. Approval for the study was provided by the ethics committee of the Australian National University. A total of 3958 (66%) valid responses were received. Women who had an alcohol problem were identified as cases from their answers to this questionnaire. Stage 2 of the survey involved sending all women identified as having an alcohol problem ( n= 184) and a random selection of controls (i.e., women identified as not having an alcohol problem [ n= 910]) a second questionnaire, which explored childhood sexual experiences. This paper reports the results of analysis of the responses to this second questionnaire. Questionnaire The questions used to ascertain the prevalence of CSA were based on those developed by Wyatt 2 . In addition to the questions on sexual experiences shown, questions were also asked about other areas, including family background and physical abuse. Women who said they had had sexual experiences before age 16 were asked about the sexual experience, including information on the type of abuse; age at the time of abuse; relationship to the abuser; age of the abuser; frequency and period of the abuse (the period being obtained by subtracting the age at first episode from age when the abuse stopped); whether coercion was used; whether the abuse was disclosed to anyone; and the self-perceived short- and long-term effects of the abuse. The effects of the abuse are dealt with in Fleming et al. (unpublished data) and Fleming et al. 12 If the women had told anyone about the abuse, they were asked whom and when they had told. Definition of childhood sexual abuse CSA was defined as all experiences of sexual contact occurring before the age of 12 with a person five or more years older, irrespective of consent , and all experiences of sexual contact occurring between age 12 and 16 years with a person five or more years older that were not wanted or were distressing. Sexual contact was defined as: touching or fondling the child's body; attempts to have the child arouse the adult, or touch his/her body in a sexual way; the adult rubbing his/her genitals against the child's body in a sexual way; touching the child's genitals with the mouth, or having the child touch the adult's genitals with the mouth; attempts to have anal or vaginal intercourse with the child; and completed anal or vaginal intercourse. For each episode, there was a progressive range of possible experiences, such as touching of the genitals or breasts to intercourse. Sample and statistical analysis A response rate of 65% ( n = 710) was obtained, with the final sample comprising 124 of 184 women identified as cases (67%) and 586 of 910 women (64%) as controls. To estimate the underlying prevalence of CSA in the population, the data were weighted to account for the different probabilities of selection for cases and controls. The controls received higher weighting than the cases (who were more likely to be selected in the sample because of the original design). The HLOGIT and HREG procedures in STATA Release 4 for Windows 13 were used to perform logistic and ordinary regressions on the weighted data and to obtain Huber standard errors, which were then used to obtain Wald statistics and corresponding P values. The significance testing thus allowed for individuals in the sample having different probabilities of selection. Results Respondents to the survey showed a demographic distribution similar to that recorded in the Australian Bureau of Statistics (ABS) census data. 14 Childhood sexual experiences Two hundred and ninety four of the 710 women (41%) responded that they had had at least one of the sexual experiences at least once before the age of 16 years. For 45 (6%) of these women, the experiences were categorised as consensual sexual experiences with peers (a peer being defined as a person less than five years older than the subject). Accordingly, 249 (35%) women reported some sexual abuse or experience that was unwanted or distressing during childhood. The sexual experiences were divided into four categories: non-contact (exposure and masturbation) (n = 87, 12%), consensual with peers (n = 45, 6%), unwanted with peers (n = 18, 3%), and unwanted sexual experiences with an adult that involved at least genital contact (which is defined as CSA and is the group on which the analyses are based) (n = 144, 20.3%; 95% CI = 17.3%-23.5%). A total of 13 women (2%) did not answer any of the questions on childhood sexual experiences. There was no significant difference (t = 1.63; P = 0.11) in mean current age between women who stated that they hadexperienced CSA (38.6 years; 95% CI, 36.7-40.4; range, 18 to 74 years) and women who had had no experience of CSA (40.3 years; 95% CI, 39.2-41.5; range, 17 to 79 years). To gain a measure of severity of abuse in the women (n =144) with CSA, sexual experiences were classified according to the most invasive act perpetrated. As shown in Box 2, 10% of these 144 women stated that intercourse had occurred and a further 17% stated that the abuser had attempted intercourse. From the sample group of 710 women, this extrapolates to 2% of the total Australian population of women having experienced CSA involving intercourse. Frequency and period of CSA The Figure shows the number of abuse episodes and Box 3 shows the frequency in women abused more than once. The period of abuse was less than one year for 57% of episodes, less than two years for 14% of episodes, and more than two years for 29% of episodes. Characteristics of individuals who experienced CSA CSA was rarely stated to have occurred before age five years. Most abuse (102/144 [71%]) occurred up to age 12 years, with the mean age at first abuse being 10 years (SD, 3.5 years). No significant differences were found for age at first abuse and relationship to the abuser. The rate of CSA reported in this study was two to four times higher for women who worked part-time (OR, 2.15; 95% CI, 1.24-3.71) or were students (OR, 4.44; 95% CI, 1.56-12.44) than for women who were either unemployed or at home. Women who were separated or divorced were more likely to have experienced CSA than women who were not separated or divorced (OR, 2.27; 95% CI, 1.12-4.64). There was evidence for a quadratic relationship with age (chi-squared = 4.1, df=1, P = 0.04), with prevalence increasing to approximately age 38 and then decreasing. There was no significant relationship for country of birth (Australia versus other), highest qualification, whether or not they had children, or number of children. Characteristics of the abuser Men were by far the most frequent abusers -- women accounted for only two reports. The mean age of abusers was 33.5 years (95% CI, 31.0-36.0; range, 11-70 years). Almost two-thirds of the abusers (83/144 [58%]) were more than 20 years older than the abused individual at the time of the abuse. The median age difference between the abused and the abuser was 24 years (range, 5-64 years). Most respondents (120/144 [83%]) stated their relationship to the abuser. Only 8% (11/143) of abusers were strangers. ( Note: Discrepancies in total group numbers arise from missing data.) Forty-one per cent of abusers (58/143) were family members (biological relatives, such as fathers, grandparents, uncles, siblings, and cousins, as well as stepfathers and adoptive fathers). Although biological fathers were more often stated to be abusers than step fathers, more women grew up with a biological father. Children who grew up without any father were the most likely to have experienced CSA (OR, 3.8; 95% CI, 1.1-13.8), followed by children with stepfathers (OR, 1.9; 95% CI, 1.0-3.6) and children who grew up with their biological father (reference group). The frequency of CSA was significantly different in women abused by relatives and those abused by non-relatives. For the 55 women who were abused once, 37 (70%) were abused by someone outside the family. When the abuser was a relative, the abuse was significantly more likely to have occurred regularly (daily or weekly, 14/25 [56%], and fortnightly, monthly or annually, 27/40 [68%]) (chi-squared = 13.7, df = 2, P = 0.001). Those abused by a relative were significantly more likely to have been abused more often (two to five times, 15/27 [56%]; six to 10 times, 6/12 [50%]; more than 10 times, 21/24 [88%]) than those abused by non-relatives (chi-squared = 16.6, df = 3, P = 0.001). Coercion Most women (102/143 [72%]) stated that some form of coercion was used; most commonly, they were frightened into compliance. The data were re-coded to provide a measure of the severity of force used: 92/143 (64%) said there had been verbal threats and threats of violence; 10/143 (7%) said there had been actual violence; and 41/143 (29%) said no form of coercion was used. Disclosure More than half (75/144 [52%]) of the women had disclosed the abuse. A further five women had tried to disclose the abuse, but their attempts to do so were unsuccessful. Of these 80 women, almost one-third (23 [28%]) disclosed, or tried to disclose, at the time of the CSA, seven (9%) within the first year, and 14 (18%) between one and 10 years later; almost half (36 [45%]) did not disclose until at least 10 years after the first abuse episode. There were no significant differences between age at first abuse experience and whether or not the women disclosed the abuse (chi-squared = 1.0, df = 1, P = 0.3). However, there were significant differences in the timing of disclosure (within one year, one to 10 years, more than 10 years) by age at time of abuse. Girls aged under 12 years at the time of the abuse were less likely to tell someone within a year of the abuse than were girls aged over 12 years (chi-squared = 7.8, df = 2, P = 0.02). Mothers were the most frequently told (39/80 [49%]), followed by friends (25/80 [32%]), and siblings (23/80 [29%]). Fewer than 10% of women (7/80) reported or had the abuse reported to either the police, a doctor or a helping agency (e.g., community organisations, such as sexual abuse services). Twenty-three per cent (17/75) stated that disclosure had stopped the abuse, compared with 22% (16/75) who said it had not. ( Note: More than one answer was possible for the questions about who was told and the reasons for prevention of disclosure.) When the women were asked what prevented disclosure, by far the most common reason given was embarrassment or shame (47/80 [46%]), followed by the belief that the other person would not be able to help them (23/80 [23%]), or would somehow blame or punish them for the abuse (19/80 [18%]). No significant differences in disclosure rates were found by relationship to abuser. Rates of disclosing abuse, examined by current age of the women, showed a significant decrease with age (chi-squared = 6.9, df = 1, P = 0.008), with 10/12 (83%) of young women (aged 17-24 years) having disclosed the abuse, compared with 26/44 (59%) of women aged 25-35 years, 23/45 (51%) aged 35-44 and 16/42 (38%) aged 45 or more. The timing of disclosure after abuse (within compared with more than one year) was not significantly different between the current 10-year age groups (chi-squared = 0.9, df = 4, P = 0.9). Discussion Although Australians have become increasingly aware of the existence and frequency of CSA, its prevalence in the community is not known. This study, the first national survey of Australian women on the prevalence of CSA, demonstrates a high rate of CSA. A rate of 20% for sexual abuse by an adult involving at least genital contact closely parallels the levels in a New Zealand study that used a comparable method of ascertainment. 7 The figure of 35% for any sexual abuse or unwanted sexual experience during childhood found in the present study is comparable to other reports which suggest that more than 50% of women had experienced sexual abuse or an unwanted sexual experience during childhood, but nearer to 10% to 15% had experienced CSA involving genital contact or intercourse. 2,4,7,8,15,16 A consistent finding from studies of CSA is that most of the reported abuse occurs in prepubescent girls. In this study, the mean age at first abuse experience was 10 years. This is within the range of ages of greatest risk, 8-12 years, reported by other studies. 3,7,15,17,18 It is important to note that, although few of the respondents stated that they had experienced sexual abuse before the age of five, it may be that such victims cannot remember the abuse. Australian Institute of Health and Welfare figures for sexual abuse by age group show that the rate of sexual abuse per 1000 children is similar in the two- to five- and six- to 10-years age groups (2.7 and 2.6 per 1000 children). 10 This suggests that abuse in this survey may have been under-reported because abuse that occurred before the age of five was not remembered. Another finding in this study is that only 10% of abuse experiences were ever reported to authorities. This supports claims that official figures may seriously underestimate the extent of the problem. Relatively high rates of abuse and low rates of reporting suggest that general practitioners, teachers, police and health and welfare personnel need to be aware that sexual abuse may be behind a range of interpersonal, behavioural and psychological problems in children. 19 Children will rarely disclose the abuse, but may have other symptoms which should arouse suspicion. This study indicates that young girls aged eight to 10 years are most at risk. Because of the usual closeness of the perpetrator to the victim and the victim's fear of being blamed or not being believed, our community as a whole needs to be mindful of the possibility of childhood sexual abuse. Acknowledgements This paper is based on data gathered for a PhD dissertation. The results presented represent stage 2 of the project. I am especially grateful to all the women who responded to this survey. I would like to thank my supervisors, Dr Gabriele Bammer, Dr Bev Sibthorpe and Dr Aileen Plant, for their advice and assistance. I would also like to thank Professor Paul Mullen for his editorial comments and suggestions and for his ongoing advice in the area of CSA, and Ms Robyn Attewell for her statistical advice. Financial support for this project was provided by the National Campaign Against Drug Abuse and by the National Centre for Epidemiology and Population Health, Australian National University. References Russell D. The incidence and prevalence of intrafamilial and extrafamilial sexual abuse of female children. Child Abuse Negl 1983; 7: 133-146. Wyatt GE. The sexual abuse of Afro-American and White American women in childhood. Child Abuse Negl 1985; 9: 507-519. Baker AW, Duncan SP. Child sexual abuse: a study of prevalence in Great Britain. Child Abuse Negl 1985; 9: 457-467. Bagley C, Ramsay R. Sexual abuse in childhood: psychosocial outcomes and implications for social work practice. J Soc Work Hum Sexuality 1986; 4: 33-46. Finkelhor D, Hotaling G, Lewis IA, Smith C. Sexual abuse in a national survey of adult men and women: prevalence, characteristics and risk factors. Child Abuse Negl 1990; 14: 19-28. Leventhal JM. Epidemiology of child sexual abuse. In: Oates RK, editor. Understanding and managing child sexual abuse. Sydney: Harcourt Brace Jovanovich Group, 1990: 18-42. Anderson JC, Martin JL, Mullen PE, et al. The prevalence of childhood sexual abuse. Experiences in a community sample of women. J Am Acad Child Adolesc Psychiatry 1993; 32: 911-919. Mullen PE, Romans-Clarkson SE, Walton VA, Herbison GP. Impact of sexual and physical abuse on women's mental health. Lancet 1988; I: 841-845. Goldman RJ, Goldman JDG. The prevalence and nature of child sexual abuse in Australia. Aust J Sex Marriage Family 1988; 9: 94-106. Angus G, Wilkinson K, Zabar P. Child abuse and neglect. Australia 1992-1993. In: Australian Institute of Health and Welfare, Child Welfare Series, No. 9; 1995 Canberra: AGPS. Finkelhor D. The international epidemiology of child sexual abuse. Child Abuse Negl 1994; 18: 409-417. Fleming J, Mullen P, Bammer G. A study of potential risk-factors for sexual abuse in children. Child Abuse Negl 1997; 21: 49-58. Stata C. Stata Statistical Software: Release 4.0. Stata Corporation, 1995 (Station C, ed. TX). Australian Bureau of Statistics. 1991 Census of population and housing -- Australia profile. 1993; Canberra: AGPS. Seigel JM, Sorenson SB, Golding JM, et al. The prevalence of childhood sexual assault. The Los Angeles Epidemiologic Catchment Area Project. Am J Epidemiol 1987; 126: 1141-1153. Russell DEH, Schurman RA, Trocki K. The long-term effects of incestuous abuse. A comparison of Afro-American and White American victims. In: Wyatt GE, Powell GJ, editors. Lasting effects of child sexual assault. Newbury Park: Sage Publications, 1988: 119-134. Sedney MA, Brooks B. Factors associated with a history of childhood sexual experience in a nonclinical female population. J Am Acad Child Adolesc Psychiatry 1984; 23: 215-218. Briere J, Runtz M. Symptomatology associated with childhood sexual victimization in a nonclinical adult sample. Child Abuse Negl 1988; 12: 51-59. Mullen PE, Martin JL, Anderson JC, et al. The long-term impact of the physical, emotional and sexual abuse of children. A community study. Child Abuse Negl 1996; 20: 7-21. (Received 15 Jul, accepted 20 Sep 1996) Author's details National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT. Jillian M Fleming, BSc, PhD. Current position: Coordinator, ACT Alcohol and Drug Service, Canberra, ACT. No reprints will be available. Correspondence: Dr J M Fleming, ACT Community Care, GPO Box 825, Canberra, ACT 2601. E-mail: jmf868 AT nceph.anu.edu.au ©MJA 1997 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.
Jillian M Fleming
Notable cases
Plasmodium vivax malaria acquired in far north Queensland
In February 1996, vivax malaria was diagnosed in a man from a remote community in far north Queensland who had not visited a malarious area for the past 19 years. Microscopy and DNA studies of blood from other residents of the community did not identify a source of infection. It was suspected the infection was transmitted by mosquitoes from a neighbour who had been infected in Papua New Guinea, but whose blood was not available for DNA tests. 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". Introduction - Clinical record - Investigations - Discussion - Acknowledgements - References - Authors' details Introduction We report a case of Plasmodium vivax malaria that we conclude was acquired in far north Queensland in early 1996. There has been only one other report of malaria acquired in mainland Australia 1 since the country was declared malaria-free by the World Health Organization in 1981. Clinical record A 31-year-old white male presented to a Cairns general practitioner in early February 1996 with a two-day history of fever, headaches, generalised aches and pains, lethargy and loss of appetite. Two days later he was hospitalised with vomiting and dehydration; he was given intravenous fluids and discharged within 24 hours. He remained unwell and consulted his general practitioner again the following day. A full blood count showed: lymphocytopenia (lymphocytes, 0.71 x 10 9 /L; normal, 1.5-4.0 x 10 9 /L); neutropenia (neutrophils, 1.95 x 10 9 /L; normal, 2.0-7.5 x 10 9 /L); and thrombocytopenia (platelets, 33 x 10 9 /L; normal, 150-450 x 10 9 /L). Haemoglobin concentration was in the normal range. On review of the routine blood film, schizonts of P. vivax were noticed, and malaria was diagnosed six days after onset of symptoms. The patient was treated with standard doses of chloroquine and primaquine, 2 and has remained well since. The patient had never received a blood transfusion nor used intravenous drugs. He had travelled to Papua New Guinea (PNG) 19 years before presentation, and for most of 1995 had worked as a tradesperson in a remote Aboriginal community in far north Queensland. Over the 1995 Christmas-New Year period he spent seven days in Cairns, followed by 12 days south of Cairns, at Mission Beach. For the next 24 days before onset of symptoms, he worked at the community in far north Queensland. Investigations Because the average incubation period for P. vivax malaria is 15 days (range, 12-17 days), 3 we investigated the possibility that the patient acquired malaria via a mosquito bite while at the community. It lies about 15¡ south of the Equator, 40 km from the coast of the Gulf of Carpenteria and about 450 km northwest from the closest international airport, at Cairns. The climate early in the year is monsoonal -- hot and humid with intermittent, heavy rainfall. Most of the population of about 1200 is Aboriginal. Investigations of source: After diagnosis of the index case, blood films were collected from 20 residents of the community who were considered possible sources of infection. These comprised: A person who had been diagnosed with P. vivax malaria in June 1995 (this had been acquired in PNG, and the person had remained well after appropriate treatment); All 13 people who presented to the community health centre with an undiagnosed fever within three weeks of the diagnosis of the index case; and Six people who had recently travelled from PNG. Further blood samples for DNA amplification by polymerase chain reaction were collected from five of these six people (blood was not available from one woman who had visited PNG in December 1995). Malaria parasites were seen in the blood films of only one of these 20 people. This person was Melanesian, had arrived in Australia from PNG in November 1995 and had taken no malaria-prophylactic drugs. No parasites were found in thin peripheral blood films, but three early ring trophozoites were seen in thick films. Although definitive species identification could not be made on morphological grounds, DNA amplification detected only P. falciparum (A Baddeley, Centre for Public Health Sciences, Brisbane, and A Saul, Queensland Institute of Medical Research, Brisbane, personal communication). The person was treated accordingly. 2 No evidence of malaria was found by DNA amplification in the other four people tested. The woman whose blood was not available for DNA amplification was also Melanesian, from PNG; she had lived in Australia for about four years and was related to the person with P. falciparum parasitaemia (who was staying with her). Although her house was about 2 km away from the home of the index patient, the latter often spent the evening socialising nearby. Both homes are about 50 m from a creek that runs along the periphery of the community. Investigations of vector: Two days after diagnosis of the index case, surface waters at the community (such as puddles, wheel ruts, ditches, swamps and drains) were surveyed for mosquito larvae with a standard 350-mL dipper. Adult mosquitoes were collected in Centers for Disease Control (CDC) light traps, baited with carbon dioxide and 1-octen-3-ol. Traps were placed beside the creek, in the central built-up part of the community and near the homes of the index patient and of the person with P. falciparum parasitaemia and his relative. Larvae were stored in 70% ethanol and adult mosquitoes at -70oC before identification. 4 Results are shown in the Box. Most Anopheles larvae were collected from small puddles and wheel ruts near the creek. Most adult Anopheles mosquitoes were also collected near the creek, with fewer at the two houses, and very few from the central part of the community. A larvicide, ( S )-methoprene, was used to treat surface waters where Anopheles larvae were breeding, and a residual insecticide, deltamethrin, was used for the thickly vegetated zone along the creek (along the periphery of the community). Further CDC light traps were set a week after initial mosquito collections, in the same locations along the creek as previously. Many Anopheles mosquitoes (12%, An. farauti s.l.) were still present (see Box). Discussion We believe that this case represents local mosquitoborne transmission of P. vivax malaria at the community in far north Queensland, because: The index patient had not been to a malarious area for 19 years. Although very long incubation periods and late hypnozoite relapses of P. vivax malaria (caused by reactivation of the dormant hepatic stage of the parasite) have been reported from temperate zones, 4,5 P. vivax malaria acquired in tropical regions, such as the Western Pacific region (including PNG), typically has a short incubation period (12-17 days), and relapses quickly (average, six weeks later). The usual duration of untreated P. vivax malaria is 1.5-5 years.3 Therefore, we conclude that this episode is not a late hypnozoite relapse of P. vivax malaria acquired in PNG. The index patient was at the community during the usual incubation period for P. vivax malaria. A competent malaria vector was present. There is strong evidence that An. farauti s.l. is the most important potential malaria vector in Australia, 6 and we showed that breeding An. farauti s.l. were present at the community. Further, although the index patient's home was screened, he often slept outside on the verandah because of the oppressive climate, and therefore was accessible to An. farauti s.l. mosquitoes during their peak biting hours (sunset to midnight). 7 There was a possible source of infection at the community. Although we did not identify another individual with P. vivax malaria, we believe that the woman whose blood was not available for DNA studies was infected. She had recently travelled to PNG, where P. vivax malaria is endemic, and our concerns are strengthened by the finding of low-level P. falciparum parasitaemia in her asymptomatic relative, who had recently come from the same region. Although she reported taking chloroquine and doxycycline prophylaxis during her visit, chloroquine-resistant malaria is well described in PNG. In addition, this prophylaxis will not prevent hypnozoite relapses. 3 Malaria symptoms may be less obvious in those who have chronic malaria, and may be further reduced by self-medication, which is common among PNG nationals (unpublished observations). Therefore, although we have not been able to prove that there was a source of infection (i.e., an untreated imported case) at the community, we believe that she was a possible source. There was no evidence of modes of transmission other than via mosquitoes (e.g., via contaminated blood). When an isolated case of malaria cannot be epidemiologically linked with another case of malaria, it is defined as "cryptic". 8 However, for the above reasons, we believe that this was a case of "introduced" malaria (malaria transmitted by mosquitoes from an imported case in an area where malaria does not usually occur). 8 Two episodes of locally acquired malaria in mainland Australia in 15 years attest to the rarity of local transmission, 6 despite frequent importations, particularly into the malaria-receptive north of Australia. 9 Nevertheless, sensitive and timely surveillance must be maintained to ensure that locally acquired cases are promptly recognised and investigated. Intensive mosquito-control measures may be needed, and other cases should be sought and treated promptly. Treatment should include primaquine as a gametocidal agent for P. falciparum . 10 Acknowledgements We commend Heather Moseley for detecting malaria parasites in the index patient's blood film when malaria was not expected. We wish to thank Dr Bill Glavin and the health staff at the community for assistance with the investigation. References Walker J. The role of a diagnostic reference laboratory in malaria surveillance. Comm Dis Intell 1996; 20: 302-304. Antibiotic Guidelines Subcommittee, Victorian Drug Usage Advisory Committee. Antibiotic guidelines. 8th ed. Melbourne: Victorian Medical Postgraduate Foundation, 1994: 103-107. Gilles HM. The malaria parasites. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 12-34. Lee DJ, Woodhill AR. The Anopheline mosquitoes of the Australasian region. Sydney: Australian Medical Publishing Company, 1944. Department of Zoology, University of Sydney, monograph no. 2. Bradley D, Newbold CI, Warrell DA. Malaria. In: Weatherall DJ, Ledingham JGG, Warrell DA. Oxford textbook of medicine. 3rd ed. Oxford: Oxford University Press, 1995: 835-862. Bryan JH, Foley DH, Sutherst RW. Malaria transmission and climate change in Australia. Med J Aust 1996; 164: 345-347. Service MW. The Anopheles vector. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 96-123. Zucker JR. Changing patterns of autochthonous malaria transmission in the United States: a review of recent outbreaks. Emerg Infect Dis 1996; 2: 37-43. Longbottom H. Epidemiology of malaria in Australia 1991-1995. Comm Dis Intell 1996; 20: 84-87. Warrell DA. Treatment and prevention of malaria. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 164-195. Received 5 Aug, accepted 26 Nov 1996 Authors' details Tropical Public Health Unit, Cairns, QLD. Dianne L Brookes, RN, Public Health Nurse; Scott A Ritchie, PhD, Medical Entomologist; Andrew F van den Hurk, BAppSc, Vector Control Officer. Cairns Base Hospital, Cairns, QLD. Julie R Fielding, BAppSc, Supervising Scientist (Haematology); Mark R Loewenthal, DTM&H, FRACP, Infectious Diseases Physician. No reprints will be available. Correspondence: D L Brookes, RN, Tropical Public Health Unit, PO Box 1103, Cairns, QLD 4870. E-mail: troppub AT citec.qld.gov.au
Dianne L Brookes · Scott A Ritchie · Julie R Fielding · Mark R Loewenthal
Clinical practice
The role of the general practitioner in the treatment of schizophrenia: general principles
In light of the emphasis on community care for schizophrenia and the increasing role likely to be played by general practitioners, this paper describes some of the general principles involved in the treatment of this disorder and provides a set of practical guidelines to assist general practitioners. Vaughan J Carr Introduction - Understanding the disorder - Symptoms - Early detection of psychosis - Diagnosis - Establishing a working relationship - Practice issues - Liaison with mental health agencies - Involuntary admissions - Conclusion - Acknowledgements - References - Authors' details - - More articles on Psychiatry This is part one of a two-part series. The second article appears in the MJA 3 February 1997 issue. Introduction Awareness of the importance of the general practitioner (GP) in the treatment of schizophrenia1-3 is growing. Factors contributing to this include continuing deinstitutionalisation (begun in the 1950s); the discovery in the 1960s and 1970s that GPs were the major providers of community psychiatric care;4,5 and the development of innovative community mental health service models in the 1980s,6,7 with recent efforts to integrate GPs into them.1,8Psychiatry texts suitable for assisting GPs in treating schizophrenic patients9,10 do not provide comprehensive practical guidelines for primary care. The two papers* in this series are intended to help fill this gap until specific primary care research provides more knowledge. Understanding the disorder Schizophrenia can be viewed in terms of a "vulnerability-stress" model,11 within which it manifests as a result of interactions between a biopsychological predisposition and environmental stress (see Figure). Vulnerability to schizophrenia is determined by premorbid risk factors, while environmental stressors are destabilising factors.12,13 For a given vulnerability-stress interaction, moderating influences may alter the illness threshold, thereby determining the occurrence of episodes of illness. Protective factors raise this threshold and perpetuating factors lower it. Treatment for schizophrenia is multimodal: antipsychotic medication and learned palliative coping techniques act on the underlying vulnerability; social support and instrumental coping (coping behaviours in relation to external rather than internal or disease-related events) help in adaptation to potentially stressful life events; and family interventions and rehabilitation strategies can augment protective factors or counter perpetuating influences. Symptoms Symptoms of schizophrenia are currently considered in three groups.14 These are: psychotic, or positive, symptoms (delusions and hallucinations); negative symptoms, representing loss of normal functions (flat affect, alogia, apathy, anhedonia-asociality and inattentiveness); and disorganisation symptoms (bizarre or disorganised behaviour, disjointed speech or formal thought disorder, incongruous affect). Schizophrenic patients often have other, traditionally non-schizophrenic, symptoms such as depression, anxiety, somatisation, phobias, obsessions, compulsions, and post-traumatic stress symptoms. Early detection of psychosis The longer psychotic symptoms go untreated, the worse the outcome.15-17 Therefore, early detection and treatment with antipsychotic drugs is crucial.17 Many patients who experience incipient psychotic symptoms consult their GP for some reason, placing the GP in a prime position to identify the problem early and make a prompt referral. There are two main facets to early detection: identifying individuals with prodromal symptoms before the emergence of frank psychosis; and recognising early or incipient psychotic symptoms.18,19Prodromal assessment: Schizophrenia cannot be diagnosed on the basis of prodromal symptoms alone because these are non-specific.20,21 They include impaired concentration, anxiety, depression, irritability, rebelliousness, social withdrawal, loss of interest or motivation, impaired function at school or work, deteriorating self-care, somatic complaints, restlessness, self-injury or suicide attempts, alcohol and drug abuse, emotional lability, and uncharacteristic aggression or poor impulse control. Also, it is important to note that the odd ideas or perceptions and peculiarities of speech or behaviour occurring in the prodromal stages of schizophrenia may also occur in normal adolescents.21 In schizophrenia, such phenomena may be present for two years or more, although usually not longer than 6-12 months, before the onset of psychotic symptoms.15,22 If such non-specific problems occur in an adolescent or young adult, they should be taken seriously, the possibility of schizophrenia kept in reasonable perspective, and the patient referred for psychiatric assessment with a letter detailing the main findings. While such an assessment in the prodromal phase may be inconclusive, it can be useful because, firstly, a positive encounter with a psychiatrist or mental health team establishes an important contact that can be resumed in the future. Secondly, the GP can provide ongoing support to the patient and family while diagnostic uncertainty prevails by acknowledging the problems identified and helping to implement any recommendations made by specialist services. Dismissing the problem ignores and invalidates the family's experience and may foster denial and thereby delay reassessment and hence eventual diagnosis and treatment. Thus, a useful short term measure may be a supportive counselling approach incorporating simple problem-solving strategies. Thirdly, it is important to monitor progress carefully in repeated clinical assessments, enlisting the cooperation of both patient and family, so that significant clinical change can be detected swiftly. Early psychotic symptoms: GPs are generally better able to detect psychiatric problems if they have good rapport with their patients, an interest in psychosocial problems, the ability to convey interest and concern, and good interviewing skills.23-25 The latter include appropriate eye contact, empathic responsiveness to cues of emotional distress, attentive posture, listening with few interruptions, an unhurried style, and the capacity to ask directive questions of a psychosocial nature. If indicated, GPs should ask, matter-of-factly and without embarrassment, a set of questions designed to elicit psychotic phenomena. For example: Do you hear noises or voices when there is no-one speaking or nothing to explain what you are hearing? What do they say? How many are there? Do they seem to be having a conversation among themselves about you?; or Do you have experiences that no-one else thinks are true, such as feeling you are under the control of some person or force that you can't explain, believing that the radio or TV are referring to you, thinking that others can read your mind, suspecting that someone is trying to hurt you?; or Is there some interference with your thinking such as thoughts being put into your head which are not your own, feeling that your thoughts are broadcast aloud so that other people can hear what you are thinking, feeling that thoughts are being taken out of your head against your will?. Patients experiencing their first early psychotic symptoms may deny or conceal such experiences. However, if asked these questions in the context of a confiding relationship, they may be able to acknowledge them for the first time. More harm is probably done if such symptoms persist undetected and untreated than would occur by asking about them in their absence. Having detected a possible new case of schizophrenia, referral to a psychiatrist or mental health service is imperative. While prolonged delays in the referral process are unacceptable, time should be taken to discuss the reasons for and purpose of the referral with the patient and efforts made to identify a psychiatrist or clinical service team suitable for the individual concerned. Diagnosis The diagnosis of schizophrenia is a specialist task. The current emphasis on detecting the earliest phase of onset of persistent psychotic symptoms -- for which antipsychotic drugs are indicated -- means that treatment may be initiated before a firm diagnosis can be made. Waiting for a confident diagnosis risks a poorer outcome. In general, psychiatric diagnoses are provisional hypotheses that may need revision as new information comes to light. Schizophrenia is particularly difficult to diagnose as there are several conditions that may mimic it and the pattern of psychotic symptoms tends to be relatively unstable early in the course of the illness.26-28For all these reasons, GPs should remain wary of a diagnosis of schizophrenia, even when long "established". If response to treatment is poor or the patient seems particularly sensitive to the adverse effects of treatment, a reappraisal of the diagnosis, including specialist reassessment, should be considered. Establishing a working relationship The cornerstone of successful treatment of schizophrenia is a good working relationship with the patient that embodies the principle of personal continuity of care over time.29,30 This is rarely possible in public mental health services and is not adequately provided by multidisciplinary teams. The GP, by providing long-term personal continuity of care,31 can fill this important gap in the patient's treatment even while the patient remains under the care of a community mental health team. If there is no well developed relationship between patient and GP before the onset of psychosis, one can be developed during the several 10-15-minute consultations per year which these patients tend to have with their GPs for renewal of prescriptions and other medical matters;6,32 the interview skills referred to previously are required. A trusting atmosphere can thus develop and be used as a basis for supportive therapy. Patients should be treated as autonomous adults, capable of mature decision-making and able to adopt a rational approach to the illness and its treatment. Fostering a collaborative partnership between patient and doctor for the joint management of the illness helps to counter the low self-esteem and lack of confidence that usually follows the experience of psychosis. Practice issues General practices should have a register or system for identifying the records of patients with schizophrenia31 to ensure regular reviews of patient progress, just as with diabetes or other chronic physical diseases. This also assists in auditing quality of care and patient outcomes. Management protocols for common problems in treating schizophrenia can be developed based on the case register. For example, missed appointments by schizophrenic patients are likely to portend relapse, deterioration in functioning, depression, suicidal preoccupations or an episode of drug or alcohol abuse. The management protocol could include having receptionist staff first notify the GP of a missed appointment, followed by telephone contact, home visit, or notifying the patient's community mental health team. It would also serve the patient's interests if the management protocol had the flexibility to handle unscheduled appointments -- frontal lobe impairments can make it difficult for schizophrenic patients to plan ahead or to appreciate the need to make appointments, and they may simply turn up unexpectedly. Also, in group practices, one GP should be identified as the primary care provider for a particular patient to facilitate the personal continuity of care. A standard record-keeping format with a checklist of items individually tailored for each patient may help to ensure that important clinical matters are not overlooked. Liaison with mental health agencies Close liaison between GPs and mental health services is crucial for the successful community treatment of schizophrenia by GPs. Well established lines of communication with the patient's psychiatrist or case manager are essential. Versions of the "shared care" model can provide practical support for GPs and facilitate their integration with mental health services in caring for schizophrenic patients. Divisions of general practice could be further encouraged to develop patterns of providing mental health care using innovative models of this kind. Involuntary admissions For acutely psychotic schizophrenic patients for whom involuntary hospitalisation may be indicated under the relevant mental health act, a coordinated approach involving the GP and the local mental health outreach team is the preferred option. If such a service is not available, the GP will first need to determine whether the patient's behaviour represents an immediate and substantial danger to others (e.g., presence of a weapon, demonstrably violent actions). In dangerous situations, GPs should first protect themselves and other people. The police should be involved if physical containment of the patient (including whatever restraint can be humanely applied using a minimum of force) is necessary. Only when the situation has been rendered reasonably safe should the GP venture to speak to the patient. If there is no immediate danger, the GP should approach the patient in a calm, non-threatening manner, avoiding confrontation, and conduct an interview in a safe place with whatever privacy is feasible, but with adequate assistance at hand.33 This can be provided by ambulance officers, medical or paramedical personnel and other responsible individuals. In either case, having interviewed the patient long enough to confirm, using whatever additional information is available from others, that the patient's condition meets the criteria for involuntary admission, then the GP should arrange that promptly according to the relevant mental health act. The patient should be informed of this and the legal status of the order explained simply and directly. Patients should be taken to hospital by ambulance (rather than police car) under appropriate supervision; this is both safer for patients, especially if sedated, and also underlines the medical nature of the problem. Police officers should accompany the patient in the ambulance if continued restraint is necessary. Transport by police vehicle should be avoided as it is invariably traumatising for the patient and conveys an entirely wrong message to the patient as to the nature of the situation. Sedating an involuntary patient in the community before transport to the hospital should be avoided if possible, as it may interfere with subsequent diagnostic assessment. However, sedation is clinically indicated (although the legality varies from State to State) for patients thought to be at high immediate risk of injuring themselves or others, who require restraint to enable transportation, or if transportation is likely to be of long duration.34 The patient may need to be restrained first or, alternatively, may accept medication on being confronted by the persuasive presence of enough people. Sedation can often be achieved by giving chlorpromazine (100 mg) or diazepam (10-20 mg) orally; severely agitated psychotic patients may require diazepam (10-20 mg, orally) together with haloperidol (5-10 mg, orally). Suitable parenteral medications include intramuscular injection of droperidol or haloperidol (5-10 mg) and/or midazolam (2.5-5 mg).34 If a high potency antipsychotic drug is administered parenterally, it should be accompanied by benztropine (2 mg, intramuscularly) to avoid serious acute dystonic reactions like laryngeal dystonia. Intramuscular injection of chlorpromazine is always contraindicated as it can cause an injection abscess, while that of diazepam is unsuitable because rates of absorption vary. Conclusion Today's GPs are well positioned to play a major role in the early detection of schizophrenia. Given the importance of early detection in successful treatment, the alert GP can have a considerable impact on the course of this illness. This contribution continues beyond the initial stages of the illness as GPs can help to optimise treatment and improve clinical outcome by providing personal continuity of care, maintaining close liaison with other mental health agencies, and making specific provision for schizophrenic patients using clinical practice registers and management protocols, as well as confidently handling emergencies. Practical recommendations are summarised in the Box. More specific issues will be covered in a subsequent article in the Journal. Acknowledgements I am grateful to Associate Professor Patrick McGorry and Drs Peter Hopkins, Brian Masters, Steve Robinson and Tony Ryan for their comments on earlier drafts of this paper. References Falloon IRH, Shanahan W, Laporta M, Krekorian HAR. Integrated family, general practice and mental health care in the management of schizophrenia. J R Soc Med 1990; 83: 225-228. Wilkinson G. The role of primary care physicians in the treatment of patients with long-term mental disorders. Int Rev Psychiatry 1991; 3: 35-42. Kendrick T, Burns T, Freeling P, Sibbald B. Provision of care to general practice patients with disabling long-term mental illness: a survey in 16 practices. Br J Gen Pract 1994; 40: 301-305. Shepherd M, Cooper B, Brown AC, Kalton G. Psychiatric illness in general practice. London: Oxford University Press, 1966. Goldberg DP, Kay C, Thompson L. Psychiatric morbidity in general practice and the community. Psychol Med 1976; 6: 565-569. Stein LI, Test MA. Alternative to mental hospital treatment. I. Conceptual model, treatment program, and clinical evaluation. Arch Gen Psychiatry 1980; 37: 392-397. Hoult J. Community treatment of the acutely mentally ill. Br J Psychiatry 1986; 149: 137-144. Jackson G, Gater R, Goldberg D, et al. A new community mental health team based in primary care: a description of the service and its effect on service use in the first year. Br J Psychiatry 1993; 162: 375-384. Goldberg D, Benjamin S, Creed F. Psychiatry in medical practice. 2nd ed. London: Routledge, 1994. Pullen I, Wilkinson G, Wright A, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994. Zubin J, Spring B. Vulnerability: a new view of schizophrenia. J Abnorm Psychol 1977; 86: 103-126. McGlashan TH, Hoffman RE. Schizophrenia: psychodynamic to neurodynamic theories. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 957-968. Fenton WS, McGlashan TH. Schizophrenia: individual psychotherapy. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 1007-1018. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. Loebel AD, Lieberman JA, Alvir JMJ, et al. Duration of psychosis and outcome in first-episode schizophrenia. Am J Psychiatry 1992; 149: 1183-1188. Johnstone EC, Crow TJ, Johnson AL, MacMillan JF. The Northwick Park study of first episode schizophrenia: I. Presentation of the illness and problems relating to admission. Br J Psychiatry 1986; 148: 115-120. Wyatt RJ. Neuroleptics and the natural course of schizophrenia. Schizophr Bull 1991; 17: 325-351. McGorry P, Kulkarni J. Prevention and preventively oriented clinical care in psychotic disorders. Aust J Psychopharm 1994; 7: 62-69. McGorry P, Rosen A, Carr V, Pantelis C. Innovations in the treatment of psychosis. In: Andrews G, editor. Specialization in psychiatry. Proceedings of the 1993 Geigy Symposium. Sydney: CIBA-Geigy, 1994: 157-232. Jackson HJ, McGorry PD, Dudgeon P. Prodromal symptoms of schizophrenia in first-episode psychosis: prevalence and specificity. Compr Psychiatry 1995; 36: 241-250. McGorry PD, McFarlane C, Patton GC, et al. The prevalence of prodromal features of schizophrenia in adolescence: a preliminary survey. Acta Psychiatr Scand 1995; 92: 241-249. Beiser M, Erickson D, Fleming JAE, Iacono WG. Establishing the onset of psychotic illness. Am J Psychiatry 1993; 150: 1349-1354. Marks J, Goldberg D, Hillier V. Determinants of the ability of general practitioners to manage common mental disorders. Psychol Med 1979; 9: 337-353. Goldberg D, Steele JJ, Johnson A, Smith C. Ability of primary care physicians to make accurate ratings of psychiatric symptoms. Arch Gen Psychiatry 1982; 39: 829-833. Goldberg DP, Jenkins L, Millar T, Faragher EB. The ability of trainee general practitioners to identify psychological distress among their patients. Psychol Med 1993; 23: 185-193. McGorry PD. Paradigm failure in functional psychosis: review and implications. Aust N Z J Psychiatry 1991; 25: 43-55. McGorry PD, Copolov DL, Singh BS. Functional psychosis: the case for a loosening of associations. Schizophr Res 1990; 3: 221-234. Stanton MW, Joyce PR. Stability of psychiatric diagnosis in New Zealand psychiatric hospitals. Aust N Z J Psychiatry 1993; 27: 2-8. McGlashan T. Intensive individual psychotherapy of schizophrenia: a review of techniques. Arch Gen Psychiatry 1983; 40: 909-920. McGlashan T, Keats CJ. Schizophrenia: treatment process and outcome. Washington: American Psychiatric Press, 1989. Burns T, Kendrick T. Schizophrenia. In: Pullen I, Wilkinson G, Wright A, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994: 194-208. Melzer D, Hale AS, Burns T, et al. Community care for patients with schizophrenia one year after hospital discharge. BMJ 1991; 303: 1023-1026. Hyman SE. Manual of psychiatric emergencies. 2nd ed. Boston: Little Brown, 1988. Victorian Drug Usage Advisory Committee. Psychotropic drug guidelines. 3rd ed. Melbourne: Victorian Medical Postgraduate Foundation Therapeutics Committee, 1995. Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Newcastle, NSW. Vaughan J Carr, MD, FRANZCP, Professor of Psychiatry. Reprints: Professor V J Carr, Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Callaghan, NSW 2308. 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/> Vulnerability Premorbid risk factors Family history of schizophrenia Perinatal complications Attention deflicts Impaired arousal modulation impaired social competence coping deficits Moderating influences Protective factors Social support Family problem-solving skills Medication compliance Perpetuating factors Social impoverishment Critical or emotionally overinvolved family Unemployment Alcohol or drug abuse Stress Acute Life events Recent physical illness Psychoactive drugs Chronic Ongoing family conflict Poverty Academic or work pressures Vulnerability-stress model of schizophrenia. Back to text Practical recommendations for primary care management of schizophrenic patients Early detection of psychosis Be alert for: 1. Prodromal symptoms Refer patient for psychiatric assessment Monitor patient's progress Support and counsel patient and family 2. Incipient psychotic symptoms Ask psychological probe questions Refer promptly to a psychiatrist or mental health service Diagnosis Is a specialist task, but remains provisional. Therefore: Remain prepared to revise the diagnosis Consider specialist reassessment if there are problems with treatment Working relationship Is based on personal continuity of care. Therefore: Develop a trusting relationship with the patient Treat the patient as an autonomous adult Foster collaboration with the patient in managing the illness Practice issues As patients with schizophrenia have special needs: Maintain a patient register Develop management protocols for problems such as missed appointments, and include flexibility to allow for unexpected behaviour Liaison with mental health agencies Is essential for successful community treatment of schizophrenic patients. Therefore: Maintain communication with the patient's psychiatrist or case manager Involuntary admissions The medical nature of these circumstances needs to be emphasised. Therefore: Work with a mental health team if possible First ensure safety of self and others (involve police if necessary) Use a non-threatening, non-confrontational approach to the patient Determine whether criteria for involuntary admission are present Follow procedures of local mental health act Clearly explain and inform the patient of his or her legal status Ensure supervised transport to hospital (preferably by ambulance) Sedation may be clinically indicated Back to text
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