Volume 175 Issue 8

Public Health Gonorrhoea screening in general practice: perceived barriers and strategies to improve screening rates Basil Donovan, Vickie Knight, Anna M McNulty, Virginia Wynne-Markham and Michael R Kidd MJA 2001; 175: 412-414 Abstract - Methods - Results - Discussion - Acknowledgements - Competing interests - References - Authors' details - - More articles on Sexual health Abstract Objective: To investigate perceived barriers to gonorrhoea screening in general practice and suggest strategies to overcome them. Design: Questionnaire-based survey. Setting and participants: All 47 general practitioners (GPs) authorised to prescribe subsidised HIV drugs under the Pharmaceutical Benefits Scheme in inner, eastern and northern Sydney. Main outcome measures: Agreement on a five-point Likert scale with statements about attitudes and practices in relation to gonorrhoea screening of homosexually active men, and views on how testing rates could be increased. Results: 32 GPs responded (68%). Perceived barriers to gonorrhoea testing included structural measures imposed by the Federal Government to limit pathology testing by GPs (the Medicare "three-test rule") (17 respondents agreed or strongly agreed), pressure from the Health Insurance Commission (HIC) to minimise pathology testing (15), concerns about confidentiality of notification procedures (8), clinical time pressure (8), and concerns about recriminations against HIV patients with gonorrhoea (6). Suggested measures to increase testing were education of gay men to request testing (25), relaxation of the three-test rule (25), easier tests (23), anonymous notification procedures, review of HIC policy on screening, and training about testing (21 each). Conclusions: Sydney GPs with high HIV caseloads perceived structural barriers to gonorrhoea testing and supported a range of achievable strategies to overcome these. As the sustained epidemic of gonorrhoea in Sydney may be directly promoting HIV transmission, these strategies should be considered urgently. Sydney is currently in the fourth year of an epidemic of gonorrhoea among homosexually active men, with over 1000 cases reported annually in the inner city.1,2 This epidemic is of particular concern as gonorrhoea may be a marker of increased risk of HIV infection.3 Gonorrhoea also directly promotes HIV transmission,4 and treating gonorrhoea has been shown to reduce HIV levels in semen.5 Thus, these sustained high rates of gonococcal infection are likely to be leading to new, potentially preventable HIV infections. Factors that may be contributing to the epidemic are: increasing rates of unsafe sex among a subset of homosexually active men;6,7 gonorrhoea outbreaks among gay men in other industrialised cities7-9 that have links with Sydney;3 scaling down of the main public sexual health centre servicing the inner city;2,3 and limited gonorrhoea case-finding in the private sector.2 Most Australians diagnosed with sexually transmissible diseases (STDs) are managed in the private sector. Medicare, Australia's universal health insurance system, rebates or heavily subsidises patient services provided by the private sector. To minimise abuse of this system, Medicare imposes conditions, including: rebating only three pathology tests ordered by a general practitioner (GP) on any one patient on any one day (the "three-test rule"); discouraging "screening" (testing without symptoms) of patients through Health Insurance Commission (HIC) advisers, who monitor and counsel GPs about their use of pathology and radiology services; and not rebating STD testing of sex workers. While urethral gonorrhoea usually causes symptoms in men, prompting them to seek treatment, anorectal infections have variable, often subtle, symptoms,3,10 and pharyngeal gonorrhoea is asymptomatic.11 Consequently, detection of anorectal and pharyngeal gonorrhoea depends on screening according to sexual risk history, contact tracing, and maintaining a low threshold for testing. The relative infrequency of diagnosis of these infections in general practice2 suggests structural or cultural barriers to gonorrhoea screening of homosexually active men. Our study aimed to investigate these barriers and to seek solutions from a group of GPs with large numbers of patients at increased risk of gonorrhoea. Methods The study was conducted in October 1999. A one-page questionnaire was sent to all 47 GPs authorised to prescribe subsidised HIV drugs under the Pharmaceutical Benefits Scheme in inner, eastern and northern Sydney. This group was chosen because their practices were located at the centre of the gonorrhoea epidemic2 and were presumed to contain substantial numbers of homosexually active men, and because HIV-infected men are at increased risk of anorectal gonorrhoea.3The questionnaire comprised items enquiring about GPs' attitudes and practices in relation to screening homosexually active men for gonorrhoea, and their views on how STD testing rates could be increased. Questions were to be answered on a five-point Likert scale. All responses were kept anonymous. Most issues raised on the questionnaire were suggested at informal meetings with GPs with high HIV caseloads or during the pilot phase, when five such GPs were sent an earlier draft of the questionnaire for comment. Non-respondents were not prompted, as it was necessary to complete the study quickly, before commencement of a targeted community education program. Results Thirty-two of the 47 GPs (68%) returned the questionnaire. All disagreed that testing for gonorrhoea is "someone else's job", and 31 of the 32 disagreed with the suggestion that gonorrhoea is "trivial". Most respondents were aware that men at high risk of STDs who may have asymptomatic infections attended their practices and most felt competent to collect laboratory specimens. Other results are shown in the Box. Interestingly, no respondents said they treated gonorrhoea empirically without testing to avoid notification, and few were embarrassed about gonorrhoea testing or thought it would offend patients. Barriers to gonorrhoea testing perceived by respondents included Medicare's three-test rule (17 respondents agreed or strongly agreed), pressure from the HIC to minimise pathology testing (15), concerns about confidentiality of notification procedures (8), clinical time pressure (8), concerns about recriminations against HIV patients with gonorrhoea (6), and a need for the patient to raise the issue of testing (5). One respondent reported having been directly advised against STD screening by an HIC adviser, who allegedly stated that such screening was the role of public clinics. Respondents supported the following approaches to controlling gonorrhoea among homosexually active men: education to encourage gay men to ask for testing (25), relaxation of the three-test rule (25), easier gonorrhoea tests (23), anonymous STD notification procedures, review of the HIC policy on STD screening, and training about testing (21 each). Discussion The three-test pathology testing rule was the most common factor that respondents indicated was inhibiting their gonorrhoea screening: 25 of 32 respondents felt that reform was needed. A standard HIV monitoring visit includes determination of T-cell subsets, viral load and haematology and biochemistry profiles,12 which automatically exhausts any Medicare rebate for pathology providers. The cost of investigating any concurrent medical conditions, such as hepatitis C or HIV-related symptoms, must then be absorbed by the pathology service. Adding screening tests for bacterial STD (gonorrhoea, chlamydia and syphilis), particularly if required for several patients a day, inevitably strains the relationship between the ordering doctor and the pathology service. When preliminary results of this survey were presented to a general meeting of the Sydney HIV GP Study Group several GPs commented that they were distorting their clinical practice — and thus delaying necessary STD screening — to minimise the effect of the three-test rule. Clearly, policies intended to curb Medicare spending on pathology testing in general may have negative implications for STD control. The simplest solution might be to exempt testing for STDs from the three-test rule. As a precedent, an exemption has been justified for cervical cytology tests to promote screening. Clinical time pressure limiting gonorrhoea testing was an issue for a quarter of respondents. Possible solutions include moderating STD screening intervals according to level of risk, and developing screening guidelines according to results of recent research into risk factors.3 Respondents strongly supported development of easier tests for gonorrhoea. Swabbing the throat, urethra and anorectum for gonorrhoea generates three specimens. Testing the anorectum and urine for chlamydia — another emerging problem among homosexually active men8,13,14 — generates two more specimens. The reliability of gonorrhoea tests collected in general practice is unknown. There is considerable scope for research into streamlining and evaluating STD testing in general practice. Few respondents were concerned about disease notification procedures and possible repercussions for their HIV patients. However, notification might be a disincentive for some patients or their doctors, and anonymous STD notification procedures were supported by most respondents. Contact tracing was not seen as a major issue, perhaps because the identity of the source is very often not known to gay men with gonorrhoea. Nevertheless, general practice is not well structured for contact tracing, and support services could be enhanced. Acknowledgements This study was funded by the New South Wales Health Department, but the opinions expressed are not necessarily those of the Department. We thank Levinia Crooks (Australasian Society for HIV Medicine) for providing a list of authorised HIV drug prescribers, Paul Sweeney (Sydney Sexual Health Centre) for assistance with data handling, and the Sydney HIV GP Study Group for its involvement. Competing interests None declared. References New South Wales Health Department. Year in review: communicable disease surveillance, 1999. NSW Public Health Bull 2000; 11: 161-168. Donovan B, Bodsworth NJ, McNulty A, et al. Increasing gonorrhoea reports — not only in London [letter]. Lancet 2000; 355: 1908. Donovan B, Bodsworth NJ, Rohrsheim R, et al. Characteristics of homosexually active men with gonorrhoea during an epidemic. Int J STD AIDS 2001; 12: 437-443. Fleming DT, Wasserheit JN. From epidemiological synergy to public health policy and practice: the contribution of other sexually transmitted diseases to sexual transmission of HIV infection. Sex Transm Infect 1999; 73: 3-17. Cohen MS, Hoffman IF, Royce RA, et al. Reduction of concentration of HIV-1 in semen after treatment of urethritis: implications for prevention of sexual transmission of HIV-1. Lancet 1997; 349: 1868-1873. Van de Ven P, Prestage G, French J, et al. Increase in unprotected anal intercourse with casual partners among gay men in 1996-8. Aust N Z J Public Health 1998; 22: 814-818. Page-Shafer KA, McFarland W, Kohn R, et al. Increases in unsafe sex and rectal gonorrhoea among men who have sex with men — San Francisco, California, 1994-1997. MMWR Morb Mortal Wkly Rep 1999; 48: 45-48. Handsfield HH, Whittington WLH, Desmon S, et al. Resurgent bacterial sexually transmitted diseases among men who have sex with men — King County, Washington, 1997-1999. MMWR Morb Mortal Wkly Rep 1999; 48: 773-777. Hughes G, Simms I, Rogers PA, et al. New cases seen at genitourinary medicine clinics: England 1997. Comm Dis Rep 1998; 8: S1-S11. McNulty A. Anorectal gonorrhoea revisited. Venereology 1993; 4: 109-111. Weisner PJ, Tronca E, Bonin P, et al. Clinical spectrum of pharyngeal gonococcal infection. N Engl J Med 1973; 288: 181-185. Clinical Trials and Treatments Advisory Committee (CTTAC). Model of Care for HIV Infection in Adults. Canberra: Australian National Council on AIDS and Related Diseases, 1998. Debattista J, Dwyer J, Orth D, et al. Community screening for Neisseria gonorrhoeae and Chlamydia trachomatis among patrons of sex-on-premises venues: two years later. Venereology 2000; 13: 105-109. Bloch M, Delpech V, Austin D, et al. Screening for gonorrhoea and chlamydia in gay men in an inner city primary care practice. Presented at the Australasian Sexual Health Conference Jun 2000; Darwin, NT. (Received 2 May, accepted 26 Jul 2001) Authors' details Sydney Sexual Health Centre, Sydney Hospital, Sydney, NSW. Basil Donovan, MD, FACSHP, Director, and Clinical Professor, Department of Public Health and Community Medicine, University of Sydney, NSW; Vickie Knight, RN, MHScEd, Clinical Nurse Consultant; Anna M McNulty, MM, FACSHP, Clinical Senior Manager, and Nurse Consultant, School of Community Medicine, University of New South Wales, Sydney, NSW; Virginia Wynne-Markham, Administrative Officer. Department of General Practice, University of Sydney, Sydney, NSW. Michael R Kidd, MD, FRACGP, Professor, and Head. Reprints will not be available from the authors. Correspondence: Professor B Donovan, Sydney Sexual Health Centre, Sydney Hospital, GPO Box 1614, Sydney, NSW 2001. donovanbATsesahs.nsw.gov.au Make a comment Responses of 32 general practitioners with high HIV caseloads to a questionnaire about gonorrhoea screening (in order of frequency of responses) Questionnaire item Strongly agree/ agree No opinion Strongly disagree/ disagree (Please tick the box you feel is most appropriate) Please comment on the following potential influences on your screening of homosexually active men for gonorrhoea The 3-test pathology testing rule impedes my testing for gonorrhoea and other STDs 17 1 14 I feel pressure from the Health Insurance Commission about my pathology ordering practices 15 3 14 It is necessary to swab the throat, urethra and anus of every gay man who had sex >1 partner every 3 months* 9 5 16 I have concerns about the confidentiality of the notification procedure for gonorrhoea 8 5 19 Clinical time pressures prevent me from testing for gonorrhoea 8 1 23 I'm worried about recriminations against my HIV patients with gonorrhoea† 6 3 22 I rarely think of testing my patients for gonorrhoea 6 2 24 There are too many specimens to juggle 6 1 25 The patient needs to request gonorrhoea/STD testing 5 2 25 It would offend my patients if I suggested that they need testing† 3 2 26 I am too embarrassed to do anal swabs 1 2 29 I would usually know if my patients had gonorrhoea anyway 1 1 30 I treat gonorrhoea empirically without taking a swab to avoid confidentiality/notification issues 0 1 31 Which of the following do you believe would increase testing for gonorrhoea and other STDs Gay men need to be educated to ask for regular STD testing 25 4 3 Relaxing of the 3-test rule (eg, excluding STD and HIV tests from formula)* 25 2 5 Easier pathology tests† 23 1 7 Anonymous STD notification procedure† 21 7 3 Review of Health Insurance Commission policy on frequency of STD pathology tests 21 8 3 Training or an update on gonorrhoea and STD testing† 21 4 6 STD=sexually transmissible disease. *Two general practitioners did not respond to this question. †One general practitioner did not respond to this question. 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Basil Donovan · Vickie Knight · Anna M McNulty · Virginia Wynne-Markham · Michael R Kidd

Anaphylactoid reactions associated with menstruation have, to our knowledge, been reported only twice previously.1,2 The mechanism of these reactions is unclear. We report a further case of severe anaphylactoid reactions related to menstruation in a woman whose sister also had milder problems with menstruation-related urticaria. Our medical treatment of both women was successful. Clinical record Case 1 A 37-year-old nurse presented in 1997 on day 3 of her menstrual period with lower abdominal pain, hypotension, bradycardia, sweating, erythema, pruritus and facial swelling, but no respiratory distress. She had three children and had had a tubal ligation seven years previously. Her periods normally lasted 4-5 days, with a moderately heavy flow. She used tampons and sanitary towels interchangeably. She had no past history of known food allergy, allergic rhinitis, conjunctivitis, atopy, eczema or asthma. She did not take aspirin or non-steroidal anti-inflammatory drugs at the time of her periods. The day before her next period started, she had a similar, but milder, episode. The following three menstrual cycles were uneventful, but with the fourth she had a further episode of severe hypotension and generalised rash, necessitating acute admission to hospital. She was admitted electively two days before her next period was due. On day 3 of this period she developed lower abdominal pain, pruritus, a diffuse erythematous rash, oedema of the face and lips, hypotension and bradycardia. Full blood count, routine biochemical test results, erythrocyte sedimentation rate, and concentrations of C-reactive protein, C3, C4, IgE, mast-cell tryptase and urinary 5-hydroxyindolacetic acid were all normal during and after the attack, and there was no peripheral blood eosinophilia. At laparoscopy tubal ligation clips were found to be still in situ and there was no evidence of intraperitoneal bleeding. After treatment with intravenous fluids, intramuscular adrenaline and antihistamines, she recovered. Menstrual fluid was collected on sterile sanitary towels during her admission. The towels were rinsed in sterile saline and a skinprick test was performed with the eluted fluid and with other standard skin test antigens. She was found to be atopic, with positive reactions to house dust mite and cockroach antigens, but she did not react to her own menstrual fluid. She was treated with medroxyprogesterone 10 mg twice daily to suppress menstruation. Over the next four months she had minor itching and swelling associated with spotting at the time when her periods would be expected. Ibuprofen 400 mg three times daily was added to the treatment regimen. She remained well for one year, then had a further admission with facial swelling, urticaria and hypotension, though without vaginal blood loss. She responded rapidly to intravenous fluids and intramuscular adrenaline. This attack had been preceded by vigorous exertion (playing netball), but previous attacks had not, to her knowledge, been associated with exercise. The ibuprofen was replaced with the selective COX-2 inhibitor celecoxib (200 mg twice daily). Over the subsequent 18 months she has had no further menstrual loss and only three episodes of very minor itching, which responded to oral antihistamines. Case 2 This is the older sister of the woman described in Case 1. In 1999, when aged 48, she developed swelling and itching of the eyes on the first day of six out of eight successive periods. She had a past history of shellfish allergy that produced similar symptoms. She did not take aspirin or non-steroidal anti-inflammatory drugs and there were no other identifiable precipitants of her symptoms. Concentrations of IgE, C3, C4, C1 esterase inhibitor and mast-cell tryptase in blood taken during an attack were all normal. Radioallergosorbent testing (RAST) against common antigens was negative. The patient elected to have a trial of celecoxib 200 mg daily for three months: for each of the next three cycles, she started taking the drug three days before her period was due and took it for 10 days. Over the three months, she had no recurrence of facial swelling or itching, her menstrual loss diminished and her periods became irregular (although serum gonadotropin levels were low, suggesting that she was not menopausal). She then discontinued the celecoxib and symptoms recurred. Because of the irregularity of the periods, intermittent therapy became impractical and she elected to take celecoxib daily. She has had no further recurrence of symptoms. Discussion Exacerbations of chronic urticaria and asthma are well described in relation to the menstrual cycle, but the mechanism of these reactions is unclear.3-6 There have been only two reports of more severe reactions involving hypotensive episodes resembling anaphylactic shock — in both cases, treatment was by hysterectomy and bilateral salpingo-oophorectomy.1,2 Both the previously reported cases showed some similarities to our Case 1. In the first report,1 the patient was 38 years old at the onset of symptoms. The patient had previously suffered one attack of urticaria attributed to seafood. She was non-atopic and had negative skinprick tests to progesterone and oestrogens, but did produce a positive skin reaction to her own menstrual fluid. However, RAST testing showed no evidence of an IgE response to her menstrual fluid. Her serum IgE and complement levels were normal, but it is not clear from the report whether these were estimated during an attack. In the second report,2 the patient was a 35-year-old who had experienced previous attacks of urticaria for which no cause had been found. She too had normal complement levels during an attack and negative skinprick reactions to progestagens and oestrogens. She had a one-month trial of non-steroidal anti-inflammatory therapy with indomethacin but then elected to have a hysterectomy. Clinically, the episodes in our Case 1 resemble anaphylaxis caused by immune mechanisms, although the lack of eosinophilia and presence of bradycardia are unusual. We found no evidence of activation of the complement system in either case, and mast-cell tryptase concentrations were not elevated, although a normal concentration does not exclude mast-cell degranulation through IgE-mediated mechanisms. The positive skin test in one of the previous reports1 was interpreted as either an IgE-mediated response or an abnormal vasodilator response to prostaglandins in the menstrual fluid. This seemed to be an idiosyncratic response, as normal control subjects tested with the fluid did not respond. Such a reaction was not seen in our Case 1. The clinical features of Case 2 are more reminiscent of cyclical urticaria, which has been ascribed to an autoimmune reaction to progestagens7 or to oestrogen effects on mast-cell function.8 Hypersensitivity to progesterone has been suggested as a mechanism of recurrent anaphylaxis of uncertain cause,9 but it is difficult to understand why these attacks should occur at the time of menstruation, when progesterone concentrations are low. Progesterone has in fact been used to treat severe premenstrual exacerbations of asthma10 and was given to our Case 1 patient without any adverse effects. If progestagens are involved in these reactions, it seems more likely that they do so indirectly by modulating mast cell function and other immune reactions.11,12 Menstrual fluid is known to contain high levels of prostaglandins, particularly PGF2α, which has been shown to modulate mediator release in mast-cells.13 It was because of this observation that one of the patients in the previous reports2 had been treated with indomethacin and our Case 1 patient was treated initially with ibuprofen. However, as COX-2 is present in the endometrium, induction of COX-2 at the end of pregnancy seems to be important in the onset of labour,14,15 and, as selective COX-2inhibitors are effective in treating primary dysmenorrhea,16 we elected to trial the selective COX-2 inhibitor celecoxib. In Case 1, symptom control with celecoxib was better than with the non-selective inhibitor ibuprofen; in Case 2, complete control of the mild symptoms was obtained with celecoxib alone. This may reflect reduction in proinflammatory prostaglandins (such as PGF2α) by celecoxib without concurrent reduction in immunomodulatory prostaglandins (such as PGE2), as would occur with non-selective COX inhibition. We can not offer a complete explanation of this syndrome, but hypothesise that these severe anaphylactoid reactions are an extreme form of the better-known cyclical urticaria. The occurrence of these conditions in sisters suggests a genetic predisposition. On the basis of the response to treatment, it seems possible that altered production of prostaglandins in the uterus influences mast cell function and causes degranulation sufficient to produce severe reactions. Withdrawal of progesterone has been shown to upregulate COX-2 activity in the human endometrium.17 We have demonstrated that medical treatment of such patients, using a combination of suppression of cyclical hormonal changes and COX-2 inhibition, is possible without resorting to hysterectomy. We would also suggest that a detailed menstrual history be taken in women with apparently idiopathic anaphylaxis in case similar mechanisms are operating. References Basomba A, Guerro M, Campos A, et al. Grave anaphylactic-like reaction in the course of menstruation. Allergy 1987; 42: 477-479. Burstein M, Rubinow A, Shalit M. Cyclic anaphylaxis associated with menstruation. Ann Allergy 1991; 66: 36-38. Farah FS, Shbaklu A. Autoimmune progesterone urticaria. J Allergy Clin Immunol 1971; 48: 257-262. Leech SH, Kumar P. Cyclic urticaria. Ann Allergy 1981; 46: 201-203. Gibbs O, Couts II, Lock R, Finnegan OC, White RJ. Premenstrual exacerbations of asthma. Thorax 1984; 39: 833-836. Eliasson O, Scherzer HH, De Graff AC. Morbidity in asthma in relation to the menstrual cycle. J Allergy Clin Immunol 1986; 77: 87-94. Moghadam BK, Hersini S, Barker BF. Autoimmune progesterone dermatitis and stomatitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998; 85: 537-541. Slater JE, Raphael G, Cutler GB, et al. Recurrent anaphylaxis in menstruating women; treatment with a luteinising hormone-releasing hormone agonist — a preliminary report. Obstet Gynecol 1987; 70: 542-546. Leylek OA, Unlu S, Ozturkcan S, et al. Estrogen dermatitis. Eur J Obstet Gynecol Reprod Biol 1997; 72: 97-103. Meggs WJ, Pescovitz OH, Metcalfe D, et al. Progesterone sensitivity as a cause of recurrent anaphylaxis. N Engl J Med 1984; 311: 1236-1238. Wilkinson SM, Beck MH, Kingston TP. Progesterone-induced urticaria — need it be autoimmune? Br J Dermatol 1995; 133: 792-794. Mittman RJ, Bernstein DI, Steineberg DR, et al. Progesterone-responsive urticaria and eosinophilia. J Allergy Clin Immunol 1989; 84: 304-310. Kaliner M. Human lung tissue and anaphylaxis I. The role of cGMP as a modulator of the immunologically induced secretory process. J Allergy Clin Immunol 1977; 60: 204-211. Crankshaw DJ, Dyal R. Effects of some naturally occurring prostaconoids and some cyclo-oxygenase inhibitors on the contraction of the human uterine segment in vivo. Can J Physiol Pharmacol 1994; 72: 870-874. Slater D, Allport V, Bennett P. Changes in the expression of the type-2 but not the type-1 cyclo-oxygenase enzyme in chorion-decidua with the onset of labour. Br J Obstet Gynaecol 1998; 105: 745-748. Morrison BW, Daniels SE, Kotey P, et al. Rofecoxib, a specific cyclo-oxygenase-2 inhibitor, in primary dysmenorrhea: a randomized controlled trial. Obstet Gynecol 1999; 94: 504-508. Critchley HO, Jones RL, Lea RG, et al. Role of inflammatory mediators in human endometrium during progesterone withdrawal and early pregnancy. J Clin Endocrinol Metab 1999; 84: 240-248. (Received 30 Mar, accepted 26 Jun 2001) Authors' details Department of Thoracic Medicine, Cairns Base Hospital, Cairns, QLD. Graham Simpson, MD, FRACP, Director, and Clinical Associate Professor, James Cook University, Cairns; David Roomes, MB ChB, Registrar. Department of Obstetrics and Gynaecology, North Queensland School of Medicine, James Cook University, Cairns, QLD. Michael D Humphrey, FRANZCOG, FRCOG, Professor. Reprints will not be available from the authors. Correspondence: Associate Professor G Simpson, Department of Thoracic Medicine, Cairns Base Hospital, PO Box 902, Cairns, QLD. marjoATiig.com.au Make a comment

Graham Simpson · David Roomes · Michael D Humphrey

To benefit from the US experience of corporatisation, Australia must focus on the clinical advantages rather than the financial windfalls M Kevin Outterson MJA 2001; 175: 426-427 Clinical independence - Efficiency - Access to capital - The opportunity in Australia - References - Authors' details - - More articles on General practice and primary care From the annual reports of two publicly traded physician practice management corporations: . . . The Company enhances clinic operations by centralizing administrative functions and introducing management tools such as clinical guidelines, utilization review and outcomes measurement. The Company provides affiliated physicians with access to capital and advanced management information systems . . . The Company offers medical group practices and independent physicians a range of affiliation models. These affiliations are carried out by the acquisition of [practice] entities or practice assets, either for cash or through an equity exchange, or by affiliation on a contractual basis. In all instances, the Company enters into long-term practice management agreements that provide for the management of the affiliated physicians by the Company while assuring the clinical independence of the physicians. . . . As an integral element of these alliances, the Company utilizes sophisticated information systems to improve the operational efficiency of, and reduce the costs associated with, operating the Company's network and the practices of the affiliated physicians. . . .1 . . . [The Company] acquires and operates multi-specialty medical clinics . . . [Its] objective is to organize physicians into professionally managed networks that assist physicians in assuming increased responsibility for delivering cost-effective medical care, while attaining high-quality clinical outcomes and patient satisfaction. . . .2 As you may have guessed, these companies are not operating in Australia, although their plans may sound familiar. When these reports were written in 1997, the United States had 26 publicly traded physician practice management corporations.3 The two US public corporations described above employed 5650 physicians, with over 25 000 additional affiliated physicians. These two companies enjoyed peak stockmarket value in excess of US$6 billion. In the 10 months following December 1997, the 15 largest publicly traded physician practice management companies lost US$4.8 billion in stockmarket value.4 Today, MedPartners has utterly abandoned its physician division, while PhyCor is currently trading at less than 10 cents per share, down from a high of over US$37. Most other companies are either delisted or in bankruptcy. A few became dotcoms. Something went terribly wrong with corporatisation of physician practice management in the United States. Given the current developments in Australia,5 perhaps some lessons can be learned from the US experience. This article will briefly examine three claims that physician practice management corporations make to attract physicians to corporate practice: clinical independence, efficiency gains, and access to capital. Clinical independence Physicians selling to a corporate practice are promised clinical independence — that the allure of profits will not impair their clinical judgement. However, strong corporate pressures are brought to bear on referral patterns. If the practice owns a pathology or imaging centre, physicians are naturally inclined to use these facilities. For practices owned or affiliated with hospitals, the hospital benefits from inpatient admissions. Physicians owning equity in outpatient surgery centres likewise perform procedures in these centres. Primary care physicians employed by a multispecialty corporate practice may be encouraged to refer patients to specialists within the group. For example, one of MedPartners' large multispecialty clinics was the Summit Medical Group in New Jersey. After a concerted effort to redirect referrals, the use of outside specialists dropped from 30% to 18% of total referrals over a two-year period ending in 1996.6 Defenders of these practices make two points: (i) that existing independent practices are subject to the same financial pressures — a solo surgeon makes money by performing surgery, not by prescribing pharmaceuticals — and (ii) that quality is not compromised, even as referral patterns change.3 Given the poor quality of truly comparable data on outcomes of medical treatment in the United States, this quality assertion can not be proved.7 But, if one assumes that physicians were choosing high quality providers before, then why switch? If financial incentives under managed care can compromise quality,8 the same may be true under corporate ownership. The first argument is more difficult to counter. Physicians in independent practices have a direct financial incentive to see many patients and provide intensive and expensive treatments. This is a moral hazard for physicians, tempered by their ethical commitments to patients. The difference with corporations is the institutionalisation of ethical conflicts. Instead of answering to their own conscience, physicians in a large corporate practice must answer to a corporate superior, who will be analysing practice patterns. This could also be an advantage. If a corporate review using an evidence-based medicine system identifies physicians with inappropriate clinical practice patterns, then quality may improve in a corporate system.6 However, if the review is primarily with an eye to profitability, the opposite could result. Federal regulations in the United States discourage financial incentives for both referrals and some forms of cost cutting, unless the pool of physicians and patients involved is large enough to give the physician a negligible financial incentive with regard to any particular patient.9 The premise is that while a physician might subject a patient to unnecessary and potentially dangerous treatment for a $1000 financial reward, the same amount of money, spread over dozens of patients, will prove to be an inadequate incentive to overcome professional ethics. Efficiency Corporations were supposed to bring modern management practices to the cottage industry of physician practices. In retrospect, they added management layers as well as costs,4 where before there had been a single decision-maker. The cost of overheads was very difficult to control,10 particularly once corporate physicians became agitated and combative. Many corporate physicians chafed under what they called micromanagement. Nurse staffing levels, operating hours, and innumerable management details were modified to suit corporate objectives. Physician productivity also lagged behind expectations: the entrepreneurial energies of solo physicians were dissipated in the salaried corporate environment, particularly after receiving large payments for the sale of practices and goodwill.11 Some physicians who sold their practices to corporate entities in the late 1990s repurchased them at a fraction of the price a few years later. Others filed suit against their corporations, seeking damages for broken promises and a return to private practice.11 One article which is required reading for anyone considering involvement with a physician practice management corporation is The rise and fall of the physician practice management industry, by Professor Uwe E Reinhardt of Princeton University.4 He describes the "Ponzi schemes" and "pyramid scheme" (two fraudulent schemes which falsely lure an ever-increasing group of victims to invest money) which eventually characterised the US industry. The corporations chased unsustainable earnings per share growth, primarily through acquisitions, and neglected actual efficiency gains through "same store" growth (ie, increasing the size of each physician's practice).4 Optimists continue to point to the clinical efficiency of an integrated, multispecialty group practice, particularly if the practice maintains a single medical record. This practice model may offer the opportunity for quality and efficiency gains, but does not require corporate ownership. In the United States, many successful multispecialty group practices, such as the Mayo Clinic, are owned either by non-profit foundations or by physicians, without any equity investment of non-physicians. Access to capital Public companies by definition can access public capital markets that are closed to independent medical practices, and can deploy the capital to improve services. During the rapid growth phase of the American practice management sector, when company shares were trading at 40 times their earnings, promises of lavish clinical spending were easy to make and believe. When the bottom fell out of the market, the capital markets abandoned the sector quickly.11 Some clinics found their projects cancelled or delayed without warning. Capital spending decisions should be made for clinical reasons, with financial projections based on return on investment, not unrealistic multiples of projected earnings. The opportunity in Australia Australian corporations have the opportunity to improve quality and efficiency of care. Robust investment in clinical information systems and adoption of best business practices may be more likely in a corporate environment. However, so, too, will be ethical conflicts, short-term focus on profits, and opportunists who care little about healthcare. If Australia is to benefit from the US experience, then its focus must be on the long term and on the clinical advantages of consolidation rather than the US preoccupation with earnings growth and financial windfalls. References MedPartners, Inc. 1996 Annual report, Form 10-K, filed with the US Securities and Exchange Commission on 31 March, 1997. Available on Edgar at: <http://www.sec.gov/cgi-bin/srch-edgar> (accessed June 2001). Phycor, Inc. 1996 Annual report, Form 10-K, filed with the US Securities and Exchange Commission on 31 March, 1997. Available on Edgar at: <http://www.sec.gov/cgi-bin/srch-edgar> (accessed June 2001). Heller Financial. The physician practice management company. Alternative to the solo practice (winter 1998). Chicago: Heller Financial, 1998. Reinhardt UE. The rise and fall of the physician practice management industry. Health Affairs 2000; 19 (Jan/Feb): 42-55. Catchlove BR. GP corporatisation. The why and the wherefore. Med J Aust 2001; 175: 68-70. Robinson JC. Consolidation of medical groups into physician practice management organizations. JAMA 1998; 279: 144, 148. McGlynn EA. Six challenges in measuring the quality of health care. Health Affairs 1997; 16 (May/June): 7-21. Grumbach K, Osmond D, Vranizan K, et al. Primary care physicians' experience of financial incentives in managed-care systems. N Engl J Med 1998; 339: 1516-1521. Department of Health and Human Services, Health Care Financing Administration, Center for Health Plans and Providers, Medicare Managed Care Group. Physician Incentive Plan Regulations, 42 CFR. § 417.479 (2001). Baltimore, MD: DHHS, 2001. Moody's Investors Service. Not-for-profit health care: 1999. Outlook and medians. September 1999, pp 9-10. New York: Moody's Investors Service, 1999. Bank of America. Healthcare industry review and outlook: 1998 third quarter. October 1998, p 37, 34-40. New York: Bank of America, 1998. Authors' details Lauterpacht Research Centre for International Law, University of Cambridge, Cambridge, UK. M Kevin Outterson, BS, JD (Northwestern University), Visiting Scholar; and Partner, Baker, Donelson Bearman & Caldwell, Nashville, Tennessee, USA. Reprints will not be available from the author. Correspondence: Mr M Kevin Outterson, Lauterpacht Research Centre for International Law, University of Cambridge, 5 Cranmer Road, Cambridge, CB3 9BL, UK. kouttersonATbdbc.com Make a comment