944
COMMENTARIES
British Journal of Obstetrics and Gynaecology December 1992, Vol. 99, pp. 944-945
Pelvic inflammatory disease Microbial invasion of the female upper genital tract may result in pelvic inflammatory disease (PID). This is a complex condition and our understanding of the epidemiology, microbial aetiology and pathogenesis is limited. Furthermore, the disease process may be occult or overt, making clinical diagnosis far from straightforward. Optimal therapy that not only eradicates infecting micro-organisms but also preserves reproductive function and prevents long term sequelae has yet to be defined. For over 30 years, epidemiological data from industrialised countries has demonstrated an increasing incidence of PID. This has paralleled a rise in cases of sexually transmitted disease suggesting that a majority of cases of PID are caused by sexually transmitted micro-organisms. The available data to determine the basis for treatment and prevention regimens in the United Kingdom are limited. There are two sources of data: (1) returns to the Department of Health from genitourinary medicine (GUM) clinics (Department of Health 1991) and (2) Hospital Inpatient Enquiry data (Office of Population Censuses and Surveys 1989). Most cases of PID are diagnosed on clinical grounds alone with the inherent risk of over-diagnosis owing to the lack of specificity of symptoms and signs. Not included in the reported data are the cases treated by general practitioners (probably those with milder symptoms), and those treated as outpatients or in private practice. Women with atypical or silent PID who do not present, or are misdiagnosed, are also not included. Therefore, any assessment of incidence is inaccurate, probably underestimating the true number of cases. Notwithstanding these deficiencies, the trend for acute PID based on hospital discharge data continued to rise throughout the early 1980s with a 50% increase in cases occurring in young women age 20-24 years (Buchan & Vessey 1989). This contrasts with falling rates during the same period in both Sweden (Westrom 1988) and in America (Rolfs et al. 1992). There does not appear to have been a concomitant shift to outpatient diagnosis and treatment of PID in either of these countries. The 40% reduction in hospitalised cases seen in Sweden mirrored a dramatic fall in reported cases of uncomplicated genital tract infections. It is believed that this resulted from an active approach towards prevention, early diagnosis and treatment ofchlamydial infections and other sexually transmitted diseases. Educational campaigns directed at both young women and health professionals have led to a raised awareness of the potential risks associated with sexual activity. There has been an increase in demand from both women and doctors for laparoscopy to aid the accurate diagnosis of PID (Westrom 1988). Recognition on the part of gynaecologists of the need for identification and treatment of sexual partners has also helped to reduce both new and recurrent cases of PID.
In England and Wales between 1981 and 1990 there was a 37% increase in women attending as new cases to GUM clinics. Gonorrhoea in women halved during this decade, but chlamydia1 infections continued to rise (Catchpole 1992). Those involved in the care of women can support public health measures aimed at prevention of sexually transmitted diseases by routinely enquiring about sexual behaviour, by screening those women at risk and by arranging for examination and treatment of male partners where appropriate. Physicians working in GUM clinics have long been familiar with these ideas. However, Eynon-Lewis (1988) found that only 39% of general practitioners considered investigations or referral of the male partner in cases of PID. How many gynaecologists in the UK routinely arrange contact tracing after diagnosing PID? Numerous studies have established the polymicrobial aetiology of PID. Only two prospective studies employing laparoscopy have been reported from centres in the UK (Kinghorn et al. 1986; Stacey et al. 1992, see p. 992 of this issue). The total number of cases combined is less than 50, but the findings support those of the large Swedish and American studies. In the main, sexually active women with PID either had micro-organisms isolated or serological evidence of pathogens that are recognised to be sexually transmitted, e.g. Neisseria gonorrhoeae or Chlamydia trachomatis, suggesting a primary role in the acute infection. The role of Mycoplasma hominis remains unclear. It is a commensal of the genital tract in sexually active women and has yet to be isolated from the Fallopian tubes in asymptomatic women. Even in cases of PID it is rarely isolated from the Fallopian tubes. Serological evidence suggests that it may be involved in up to 30% of cases of PID (Westrom & Mirdh 1990). However, its role may be that of an opportunistic secondary pathogen, invading tissue that has already been compromised by a primary pathogen such as Ctrachomatis. The clinical manifestations of upper genital tract infections are in part determined by the characteristics of the invading micro-organism and in part by the hosts' immunological response to the microbial challenge. For any individual pathogen there may be a variable host response. Investigation of women with infertility lends some support to the concept of asymptomatic PID. Serological evidence of C.trachomatis has been found in up to 70% of women with tuba1 factor infertility and yet 50% of these women give no history of previous PID (Moore et al. 1982). Further elucidation of the immunological mechanisms operating within the female genital tract might help explain the varying presentation and severity of PID and in particular the phenomenon of silent PID. Clearly any reduction in the incidence of PID would lead to a reduction in the number of women suffering from the associated long term sequelae. Buchan et al. (1993 in press)
C 0 M M E NTA R 1E S
report on morbidity following an initial episode of PID using data from the Oxford Record Linkage study. They confirm that many women become recurrent outpatient attendees with chronic problems, culminating in a high rate of hysterectomy. Early accurate diagnosis allows instigation of appropriate antimicrobial therapy and this in turn might be expected to improve the clinical outcome. Failure to make a correct diagnosis may lead to late or no treatment with a potential for disease progresion, leading to an increased risk of sequelae. A mistaken diagnosis of PID and inappropriate antimicrobial therapy may delay the diagnosis of other serious intra abdominal pathology. Unfortunately, there is no simple diagnostic algorithm that is both sensitive and specific for PID. The sensitivity of clinical symptoms and signs alone is low when compared with laparoscopy (Jacobson & Westrom 1969). Early laparoscopy in conjunction with standardised clinical criteria (Hager et al. 1983) has much to recommend it. Diagnostic uncertainty is less likely, the severity of the disease canbe assessed and the prognosis for subsequent fertility stated. Although the use of laparoscopy in the diagnosis of PID has increased by 50% in the UK over the period from 1975 to 1985 (Buchan & Vessey 1989), its utilisation is still far from universal. Antimicrobial regimes must be effective against N.gonorrhoeae, C.trachomatis and Mhominis, and the facultative aerobic and anaerobic micro-organisms which, although normally commensals of the lower genital tract, can act as secondary invading pathogens in a compromised upper genital tract. Treatment regimes that offer maximum efficacy alongside optimal patient compliance should be used. It is therefore surprising to learn that antichlamydial therapy is still not routinely prescribed to all sexually active women with PID (Eynon-Lewis 1988; Rolfs e f al. 1992). Currently available antimicrobial agents, although producing clinical and microbiological cures, do not guarantee preservation of tubal function and have not been assessed for their efficacy at preventing long term gynaecological morbidity. Other therapeutic strategies, e.g. adjuvant treatment with non steroidal anti-inflammatory drugs, bed rest versus ambulant therapy and perhaps second look laparoscopy with early adhesiolysis need to be assessed prospectively. Continuing research is required to improve the specificity of clinical diagnosis, and to determine optimal therapy, but the major challenge is to reduce the incidence of PID. How the targets for reduction of sexually transmitted diseases outlined in the Sexual Health proposals of the Government’s recent white paper (HMSO 1992) are to be achieved, and what subsequent effect they will have on the incidence of PID in the UK, remains to be seen.
945
Colin Bevan Research Fellow, D e p a r t m e n t s of Obstetrics a n d G y n a e c o l o g y a n d Clinical Microbiology, University College Hospital, London
Geoffrey L. Ridgway Consultant Microbiologist,
University College Hospital, London References Buchanan H. & Vessey M. (1989)Epidemiology and trends in hospital discharges for pelvic inflammatory disease in England, 1975 to 1985. B r J Obstet Gynaecol96,1219-1223. Buchan H., Vessey M., Goldacre M. & Fairweather J. (1993) Morbidity following pelvic inflammatory disease: a record linkage study. B r J Obstet Gynaecol 100 (in press). Catchpole M. (1992) Sexually transmitted diseases in England and Wales: 1981-1990. C D R Review 2, RlLR7. Department of Health (1991) New cases seen at NHS genitourinary medicine clinics in England. KC 60 D H Statistics & Management Information (SM12B). Department of Health (1992) The Health of the Nation. A Strategy for Health in England. HMSO (CM 1986 ‘White Paper’). Eynon-Lewis A. (1988) Audit of the management of pelvic inflammatory disease in general practice. J R College Gen Pract 38, 492493. Hager W. D., Escenbach D. A,, Spence M. R. & Sweet R. L. (1983) Criteria for diagnosis and grading of salpingitis. Obstetrics & Gynaecology 61,113-1 14. Jacobson L. & Westrom L. (1969) Objectivised diagnosis of acute pelvic inflammatory disease. Am J Obstet Gynaecol 105, 1088-1098. Kinghorn G., Duerden B. & Hafiz S. (1986)Clinical and microbiological investigation of women with acute salpingitis and their consorts. Br J Obstet Gynaecol93,869-880. Moore D. E. et a/. (1982) Increased frequency of serum antibodies to Chlamydia truchomatis in infertility due to distal tubal disease. Lancet ii (8298), 574-577. Office of Population Censuses and Surveys (1989)Hospital Inpatient Enquiry: in-patient and day case trends 1979-1985. HMSO Series MB4 29, London. Rolfs R., Galaid E. & Zaida A. (1992) Pelvic inflammatory disease: trends in hospitalisations and office visits, 1979 through 1988. Am J Obstet Gynecoll66,983-990. Stacey C. M. etal. (1992)A longitudinal study of pelvic inflammatory disease. Br J Obstet Gynaecol99 (12), 992-997. Westrom L. (1988)Decrease in incidence of women treated for acutc salpingitis in hospital for acute salpingitis in Sweden. Genitourin Med 64,59-64. Westrom L. & MArdh P. (1990) In Sexually Transmitted Diseases. (K. K. Holmes, P. MArdh, I? E Sparling & P. J. Weisner eds) McGrawHill Inc., New York, p.596.
COMMENTARIES
British Journal of Obstetrics and Gynaecology December 1992, Vol. 99, pp. 944-945
Pelvic inflammatory disease Microbial invasion of the female upper genital tract may result in pelvic inflammatory disease (PID). This is a complex condition and our understanding of the epidemiology, microbial aetiology and pathogenesis is limited. Furthermore, the disease process may be occult or overt, making clinical diagnosis far from straightforward. Optimal therapy that not only eradicates infecting micro-organisms but also preserves reproductive function and prevents long term sequelae has yet to be defined. For over 30 years, epidemiological data from industrialised countries has demonstrated an increasing incidence of PID. This has paralleled a rise in cases of sexually transmitted disease suggesting that a majority of cases of PID are caused by sexually transmitted micro-organisms. The available data to determine the basis for treatment and prevention regimens in the United Kingdom are limited. There are two sources of data: (1) returns to the Department of Health from genitourinary medicine (GUM) clinics (Department of Health 1991) and (2) Hospital Inpatient Enquiry data (Office of Population Censuses and Surveys 1989). Most cases of PID are diagnosed on clinical grounds alone with the inherent risk of over-diagnosis owing to the lack of specificity of symptoms and signs. Not included in the reported data are the cases treated by general practitioners (probably those with milder symptoms), and those treated as outpatients or in private practice. Women with atypical or silent PID who do not present, or are misdiagnosed, are also not included. Therefore, any assessment of incidence is inaccurate, probably underestimating the true number of cases. Notwithstanding these deficiencies, the trend for acute PID based on hospital discharge data continued to rise throughout the early 1980s with a 50% increase in cases occurring in young women age 20-24 years (Buchan & Vessey 1989). This contrasts with falling rates during the same period in both Sweden (Westrom 1988) and in America (Rolfs et al. 1992). There does not appear to have been a concomitant shift to outpatient diagnosis and treatment of PID in either of these countries. The 40% reduction in hospitalised cases seen in Sweden mirrored a dramatic fall in reported cases of uncomplicated genital tract infections. It is believed that this resulted from an active approach towards prevention, early diagnosis and treatment ofchlamydial infections and other sexually transmitted diseases. Educational campaigns directed at both young women and health professionals have led to a raised awareness of the potential risks associated with sexual activity. There has been an increase in demand from both women and doctors for laparoscopy to aid the accurate diagnosis of PID (Westrom 1988). Recognition on the part of gynaecologists of the need for identification and treatment of sexual partners has also helped to reduce both new and recurrent cases of PID.
In England and Wales between 1981 and 1990 there was a 37% increase in women attending as new cases to GUM clinics. Gonorrhoea in women halved during this decade, but chlamydia1 infections continued to rise (Catchpole 1992). Those involved in the care of women can support public health measures aimed at prevention of sexually transmitted diseases by routinely enquiring about sexual behaviour, by screening those women at risk and by arranging for examination and treatment of male partners where appropriate. Physicians working in GUM clinics have long been familiar with these ideas. However, Eynon-Lewis (1988) found that only 39% of general practitioners considered investigations or referral of the male partner in cases of PID. How many gynaecologists in the UK routinely arrange contact tracing after diagnosing PID? Numerous studies have established the polymicrobial aetiology of PID. Only two prospective studies employing laparoscopy have been reported from centres in the UK (Kinghorn et al. 1986; Stacey et al. 1992, see p. 992 of this issue). The total number of cases combined is less than 50, but the findings support those of the large Swedish and American studies. In the main, sexually active women with PID either had micro-organisms isolated or serological evidence of pathogens that are recognised to be sexually transmitted, e.g. Neisseria gonorrhoeae or Chlamydia trachomatis, suggesting a primary role in the acute infection. The role of Mycoplasma hominis remains unclear. It is a commensal of the genital tract in sexually active women and has yet to be isolated from the Fallopian tubes in asymptomatic women. Even in cases of PID it is rarely isolated from the Fallopian tubes. Serological evidence suggests that it may be involved in up to 30% of cases of PID (Westrom & Mirdh 1990). However, its role may be that of an opportunistic secondary pathogen, invading tissue that has already been compromised by a primary pathogen such as Ctrachomatis. The clinical manifestations of upper genital tract infections are in part determined by the characteristics of the invading micro-organism and in part by the hosts' immunological response to the microbial challenge. For any individual pathogen there may be a variable host response. Investigation of women with infertility lends some support to the concept of asymptomatic PID. Serological evidence of C.trachomatis has been found in up to 70% of women with tuba1 factor infertility and yet 50% of these women give no history of previous PID (Moore et al. 1982). Further elucidation of the immunological mechanisms operating within the female genital tract might help explain the varying presentation and severity of PID and in particular the phenomenon of silent PID. Clearly any reduction in the incidence of PID would lead to a reduction in the number of women suffering from the associated long term sequelae. Buchan et al. (1993 in press)
C 0 M M E NTA R 1E S
report on morbidity following an initial episode of PID using data from the Oxford Record Linkage study. They confirm that many women become recurrent outpatient attendees with chronic problems, culminating in a high rate of hysterectomy. Early accurate diagnosis allows instigation of appropriate antimicrobial therapy and this in turn might be expected to improve the clinical outcome. Failure to make a correct diagnosis may lead to late or no treatment with a potential for disease progresion, leading to an increased risk of sequelae. A mistaken diagnosis of PID and inappropriate antimicrobial therapy may delay the diagnosis of other serious intra abdominal pathology. Unfortunately, there is no simple diagnostic algorithm that is both sensitive and specific for PID. The sensitivity of clinical symptoms and signs alone is low when compared with laparoscopy (Jacobson & Westrom 1969). Early laparoscopy in conjunction with standardised clinical criteria (Hager et al. 1983) has much to recommend it. Diagnostic uncertainty is less likely, the severity of the disease canbe assessed and the prognosis for subsequent fertility stated. Although the use of laparoscopy in the diagnosis of PID has increased by 50% in the UK over the period from 1975 to 1985 (Buchan & Vessey 1989), its utilisation is still far from universal. Antimicrobial regimes must be effective against N.gonorrhoeae, C.trachomatis and Mhominis, and the facultative aerobic and anaerobic micro-organisms which, although normally commensals of the lower genital tract, can act as secondary invading pathogens in a compromised upper genital tract. Treatment regimes that offer maximum efficacy alongside optimal patient compliance should be used. It is therefore surprising to learn that antichlamydial therapy is still not routinely prescribed to all sexually active women with PID (Eynon-Lewis 1988; Rolfs e f al. 1992). Currently available antimicrobial agents, although producing clinical and microbiological cures, do not guarantee preservation of tubal function and have not been assessed for their efficacy at preventing long term gynaecological morbidity. Other therapeutic strategies, e.g. adjuvant treatment with non steroidal anti-inflammatory drugs, bed rest versus ambulant therapy and perhaps second look laparoscopy with early adhesiolysis need to be assessed prospectively. Continuing research is required to improve the specificity of clinical diagnosis, and to determine optimal therapy, but the major challenge is to reduce the incidence of PID. How the targets for reduction of sexually transmitted diseases outlined in the Sexual Health proposals of the Government’s recent white paper (HMSO 1992) are to be achieved, and what subsequent effect they will have on the incidence of PID in the UK, remains to be seen.
945
Colin Bevan Research Fellow, D e p a r t m e n t s of Obstetrics a n d G y n a e c o l o g y a n d Clinical Microbiology, University College Hospital, London
Geoffrey L. Ridgway Consultant Microbiologist,
University College Hospital, London References Buchanan H. & Vessey M. (1989)Epidemiology and trends in hospital discharges for pelvic inflammatory disease in England, 1975 to 1985. B r J Obstet Gynaecol96,1219-1223. Buchan H., Vessey M., Goldacre M. & Fairweather J. (1993) Morbidity following pelvic inflammatory disease: a record linkage study. B r J Obstet Gynaecol 100 (in press). Catchpole M. (1992) Sexually transmitted diseases in England and Wales: 1981-1990. C D R Review 2, RlLR7. Department of Health (1991) New cases seen at NHS genitourinary medicine clinics in England. KC 60 D H Statistics & Management Information (SM12B). Department of Health (1992) The Health of the Nation. A Strategy for Health in England. HMSO (CM 1986 ‘White Paper’). Eynon-Lewis A. (1988) Audit of the management of pelvic inflammatory disease in general practice. J R College Gen Pract 38, 492493. Hager W. D., Escenbach D. A,, Spence M. R. & Sweet R. L. (1983) Criteria for diagnosis and grading of salpingitis. Obstetrics & Gynaecology 61,113-1 14. Jacobson L. & Westrom L. (1969) Objectivised diagnosis of acute pelvic inflammatory disease. Am J Obstet Gynaecol 105, 1088-1098. Kinghorn G., Duerden B. & Hafiz S. (1986)Clinical and microbiological investigation of women with acute salpingitis and their consorts. Br J Obstet Gynaecol93,869-880. Moore D. E. et a/. (1982) Increased frequency of serum antibodies to Chlamydia truchomatis in infertility due to distal tubal disease. Lancet ii (8298), 574-577. Office of Population Censuses and Surveys (1989)Hospital Inpatient Enquiry: in-patient and day case trends 1979-1985. HMSO Series MB4 29, London. Rolfs R., Galaid E. & Zaida A. (1992) Pelvic inflammatory disease: trends in hospitalisations and office visits, 1979 through 1988. Am J Obstet Gynecoll66,983-990. Stacey C. M. etal. (1992)A longitudinal study of pelvic inflammatory disease. Br J Obstet Gynaecol99 (12), 992-997. Westrom L. (1988)Decrease in incidence of women treated for acutc salpingitis in hospital for acute salpingitis in Sweden. Genitourin Med 64,59-64. Westrom L. & MArdh P. (1990) In Sexually Transmitted Diseases. (K. K. Holmes, P. MArdh, I? E Sparling & P. J. Weisner eds) McGrawHill Inc., New York, p.596.
