642
14. CDC: recommendations for prevention of HIV transmission in health care settings. MMWR 1987; 36 (suppl 25): 35-85. 15. Advisory Committee on Dangerous Pathogens. HIV-the causative agents of AIDS and related conditions. Second revision of guidelines. London: HM Stationery Office, 1990. 16. British Medical Association. A code of practice for the safe use and disposal of sharps. London: BMA, 1990. 17. Choudhury RP, Cleator SJ. Preventing needlestick injuries. BMJ 1991; 302: 1602. 18. Nixon AD, et al. Simple device to prevent accidental needle-prick injuries. Lancet 1986; i: 888-89. 19. Bessent RG, Donnet R, Shaw A. Device to permit recapping of syringes without risk of infection. BMJ 1987; 295: 307-08. 20. Krasinski K, LaCouture R, Holzman RS. Effect of changing needle disposal systems on needle puncture injuries. Infect Control 1987; 8: 59-62. 21. Haiduven DJ, De Maio TM, Stevens DA. A five-year study of needlestick injuries: significant reduction associated with communication, education and convenient placement of sharps containers. Infect Control Hosp Epidemiol 1992; 13: 265-71. 22. CDC: Statement on management of occupational exposure to HIV,
including considerations regarding zidovudine post-exposure MMWR 1990; 39: 1-14. 23. Jeffries DJ. Zidovudine after occupational exposure to HIV. 302: 1349-51.
use.
BMJ 1991;
Ocular complications of leprosy The introduction of multiple drug therapy (MDT, combination of rifampicin, dapsone, and a clofazimine) in 1982 by the World Health Organisation1 greatly improved the treatment of leprosy. Transmission of Mycobacterium leprae by infectious patients is interrupted by the rapid bactericidal action of MDT, and duration of treatment is reduced to 6 months for those with paucibacillary disease and 24 months for those with multibacillary disease. MDT in combination with extensive health education campaigns has encouraged patients to present with early lesions. Patients are released from treatment after completion of MDT, and advised to report immediately if any untoward event occurs.
The latest WHO figures show that there are 55 million leprosy patients world wide, with an incidence of about 1 million new patients per year.2About 250 000 leprosy patients are blind (visual acuity less than 3/60 in the better eye), this number being 2-2-5% of all present and former patients still alive.33 However, most of the data on blindness were based on reports dating from before or shortly after the introduction of MDT. The clinical impression, supported by some small studies,4’ is that MDT has a favourable influence on ocular lesions and that, at least in the short term, few new eye lesions appear after patients are released. The complications of leprosy, including eye complications, can be divided into two groups: (a) lesions due to immune processes-reversal reaction (RR) and erythema nodosum leprosum-and (b) late complications due to proliferation of M leprae and secondary atrophy of tissues. RR occurs in borderline leprosy and causes motor and sensory loss via damage to peripheral nerves. It tends to strike patients early in the disease, either before treatment, causing the patient to seek advice, or within the first 6 months of
antileprosy therapy, becoming increasingly less frequent thereafter.However, RR may still occur after release from treatment, especially in paucibacillary disease. RR in the facial nerve causes lagophthalmos (inability to close the eye fully). The resulting lid-gap can lead to exposure keratitis and progressive scarring over the lower half of the cornea, and finally blindness. Patients with large facial patches are at greatest risk.7 The lagophthalmos may become permanent, but the patch fades over time and disappears. Lagophthalmos due to RR is an early complication in leprosy and is commonly the way the disease presents in general clinics or eye departments ;8 in cases of recent onset lagophthalmos, the patch is usually still visible. Patients with severe RR in the face or lagophthalmos of less than 6 months’ duration are treated with systemic steroids, as is routine in RR with nerve damage, and good improvement of orbicularis function can be expected.9 Lagophthalmos of more than 6 months’ duration and a lid-gap on mild closure of 5 mm or less is treated conservatively with sunglasses for protection and blinking exercises to reinforce orbicularis function. With lagophthalmos of more than 6 months’ duration and a lid-gap on mild closure of more than 5 mm, lid surgery is indicated. Lagophthalmos will continue to occur despite improved antileprosy treatment, so health staff need to recognise patients at risk to institute early treatment. with Moreover, patients any or not have been whether they lagophthalmos, released from treatment, have a potentially sightthreatening lesion, which will need periodic surveillance. 10 RR may also affect the trigeminal nerve and cause corneal hypoaesthesia. It can occur in combination with lagophthalmos and results partly from exposure of the cornea. Corneal hypoaesthesia due to RR in otherwise normal eyes without lagophthalmos has not been documented, and there is no evidence on whether the hypoaesthesia can be influenced by prompt steroid treatment, as in sensory loss of the hands and feet due to RR. Damage to the long ciliary nerves by scleritis in erythema nodosum leprosum may likewise result in corneal hypoaesthesia.’1 Invasion and secondary atrophy of the corneal nerve endings, comparable to glove-and-stocking anaesthesia in longstanding multibacillary disease patients, may be another cause of corneal hypoaesthesia. Hypoaesthesia occurs mainly in patients with longstanding multibacillary leprosy and with severely affected eyes.12 Patients with advanced loss of corneal sensation are advised to use sunglasses for protection. Erythema nodosum leprosum is characterised clinically by an attack of fever with general malaise and painful subcutaneous nodules; ocular manifestations include acute iritis and episcleritis or a severe combined sclerouveitis. Most erythema nodosum reactions do not involve the eyes and the eye complications can occur without signs of systemic
643
nodosum. This reaction arises in both treated and untreated multibacillary disease, and repeated attacks are not unusual. General treatment is with steroids, clofazimine, and thalidomide. In the past the severe and often bilateral sclerouveitis could lead to blindness in a matter of weeks. This complication became less frequent13 soon after the introduction of dapsone and seems to have become even more rare with MDT. Acute iritis is treated with topical atropine and steroids. Systemic steroids are indicated only when there is a severe accompanying erythema nodosum reaction, as is common in sclerouveitis. Leprosy should be considered in the differential diagnosis of acute iritis and (epi)scleritis in patients in or from leprosy endemic countries. Acute iritis and scleritis may recur, many years after treatment has been stopped, as a severe and potentially
erythema
blinding eye complication. Late complications-notably, lepromas, corneal hypoaesthesia, and iris lesions-due to proliferation of M leprae and secondary atrophy occur only in multibacillary leprosy and should become less with earlier and more effective bactericidal MDT treatment. Ocular lepromas are painless nodules in the limbal area; they appear in multibacillary patients with longstanding and irregularly treated leprosy and may be an early sign of dapsone resistance. Treatment is by strictly supervised MDT, which should achieve slow resolution. The ciliary body is assumed to be the portal of entry to M leprae into the eye; from there the bacilli may invade the iris tissue via small autonomic nerves. Chronic iris breakdown, with slowly progressive miosis, poor dilatation with mydriatics, and thinning of the iris stroma, is typical of longstanding multibacillary leprosy. Invasion and late atrophy within the ciliary body leads to low production of aqueous fluid and low intraocular pressure. Once MDT is given, progression of all these lesions can be expected to slow and stop. For several reasons, the backlog in cataracts may be greater in leprosy patients than in the population at larger The stigma of leprosy is still strong in some societies and leprosy patients may well have problems in getting operated upon for simple senile cataract. Lengthy and repeated courses of prednisolone for reactions can cause cataract as a side-effect. Both acute iritis and invasion of the anterior uvea by M leprae can enhance cataract formation in multibacillary disease. common
Although surgery in multibacillary patients is hampered by poor dilatation of the pupil and fragility of the atrophic iris, the results can be good. 15 1. World Health
Organisation study group. Chemotherapy of leprosy for control programmes. WHO Tech Rep Ser 1982; 675. 2. Anon. Leprosy situation in the world and multidrug therapy coverage. Weekly Epidemiol Rec 1992; 67: 153-60. 3. Courtright P, Johnson GJ. Prevention of blindness in leprosy, rev ed. London: International Centre for Eye Health, 1991. 4. Rajan MA. Eye in multidrug therapy. Indian J Lepr 1990; 62: 33-38. 5. Hogeweg M, Faber WR. Progression of eye lesions in leprosy: ten-year follow-up study in the Netherlands. Int J Lepr 1991; 59: 393-97.
6. Naafs W, Wheate HW. The time interval between the start of anti-leprosy treatment and the development of reactions in borderline patients. Lepr Rev 1978; 49: 153-57. 7. Hogeweg M, Kiran KU, Suneetha S. The significance of facial patches and type I reaction for the development of facial nerve damage in leprosy: a retrospective study among 1226 paucibacillary leprosy patients. Lepr Rev 1991; 62: 143-49. 8. Bosher SK. Leprosy presenting as facial palsy. J Laryngol 1962; 76: 827-30. 9. Kiran KU, Hogeweg M, Suneetha S. Treatment of recent facial nerve damage with lagophthalmos, using a semistandardized steroid regimen. Lepr Rev 1991; 62: 150-54. 10. ffytche TJ. Residual sight-threatening lesions in leprosy patients completing multidrug therapy and sulphone monotherapy. Lepr Rev 1991; 62: 35-43. 11. Lyne AJ. Corneal sensitivity in scleritis and episcleritis. Br J Ophthalmol 1977; 61: 650-54 12. Karacorlu MA, Cakiner T, Saylan T. Corneal sensitivity and correlations between decreased sensitivity and anterior segment pathology in ocular leprosy. Br J Ophthalmol 1991; 75: 117-19. 13. Amendola FA. Ocular and otorhinolaryngological leprosy before and since sulfone therapy. Int J Lepr 1955; 23: 280-83. 14. Brandt F, Kampik A, Malla OK, Pokharel RP, Wos J. Blindness from cataract formation in leprosy. Dev Ophthalmol 1983; 7: 1-12. 15. ffytche TJ. Cataract surgery in the management of the late complications of lepromatous leprosy in South Korea. Br J Ophthalmol 1981; 65: 243-48.
Non-surgical
treatment of stress
incontinence incontinence is defmed by the International Continence Society as a condition in which the involuntary loss of urine is a social or hygienic problem and is objectively demonstrated.l It has been reported to occur in 8-5% of women,2 although this figure is probably an underestimate owing to the social stigma attached to the condition. About 50% of these women will have genuine stress incontinence (GSI),3 which is defined as sphincter incompetence in the absence of detrusor activity. Success rates of up to 95% have been reported4 for the surgical treatment of GSI, but surgery is not the first line of treatment indicated for all patients. Advanced age, previous incontinence surgery, and presence of detrusor instability are indicators of poor surgical outcome. In addition, alternatives to surgery as first-line treatment are appropriate in women who have not completed their childbearing and in whom stress incontinence is only slight or occasional. Increasing awareness of the prevalence of GSI, together with an understanding that surgery and its attendant risks are not indicated for all, has reawakened interest in conservative management. The mainstay of this approach continues to be physiotherapeutic interventions to improve the function of the pelvic floor musculature and thereby the urethral sphincter mechanism.5Kegel6 was among the first to introduce pelvic floor exercises as a method of treating GSI; he reported a subjective cure rate of 80% in a group of 500 patients. The most important factors influencing the successful use of this technique were the ability of the patient to identify correctly the muscles of the pelvic floor, and some form of biofeedback. During the past decade, objective studies have shown a cure rate for pelvic floor exercises of 27%with 60%8 of patients reporting a substantial
Urinary
14. CDC: recommendations for prevention of HIV transmission in health care settings. MMWR 1987; 36 (suppl 25): 35-85. 15. Advisory Committee on Dangerous Pathogens. HIV-the causative agents of AIDS and related conditions. Second revision of guidelines. London: HM Stationery Office, 1990. 16. British Medical Association. A code of practice for the safe use and disposal of sharps. London: BMA, 1990. 17. Choudhury RP, Cleator SJ. Preventing needlestick injuries. BMJ 1991; 302: 1602. 18. Nixon AD, et al. Simple device to prevent accidental needle-prick injuries. Lancet 1986; i: 888-89. 19. Bessent RG, Donnet R, Shaw A. Device to permit recapping of syringes without risk of infection. BMJ 1987; 295: 307-08. 20. Krasinski K, LaCouture R, Holzman RS. Effect of changing needle disposal systems on needle puncture injuries. Infect Control 1987; 8: 59-62. 21. Haiduven DJ, De Maio TM, Stevens DA. A five-year study of needlestick injuries: significant reduction associated with communication, education and convenient placement of sharps containers. Infect Control Hosp Epidemiol 1992; 13: 265-71. 22. CDC: Statement on management of occupational exposure to HIV,
including considerations regarding zidovudine post-exposure MMWR 1990; 39: 1-14. 23. Jeffries DJ. Zidovudine after occupational exposure to HIV. 302: 1349-51.
use.
BMJ 1991;
Ocular complications of leprosy The introduction of multiple drug therapy (MDT, combination of rifampicin, dapsone, and a clofazimine) in 1982 by the World Health Organisation1 greatly improved the treatment of leprosy. Transmission of Mycobacterium leprae by infectious patients is interrupted by the rapid bactericidal action of MDT, and duration of treatment is reduced to 6 months for those with paucibacillary disease and 24 months for those with multibacillary disease. MDT in combination with extensive health education campaigns has encouraged patients to present with early lesions. Patients are released from treatment after completion of MDT, and advised to report immediately if any untoward event occurs.
The latest WHO figures show that there are 55 million leprosy patients world wide, with an incidence of about 1 million new patients per year.2About 250 000 leprosy patients are blind (visual acuity less than 3/60 in the better eye), this number being 2-2-5% of all present and former patients still alive.33 However, most of the data on blindness were based on reports dating from before or shortly after the introduction of MDT. The clinical impression, supported by some small studies,4’ is that MDT has a favourable influence on ocular lesions and that, at least in the short term, few new eye lesions appear after patients are released. The complications of leprosy, including eye complications, can be divided into two groups: (a) lesions due to immune processes-reversal reaction (RR) and erythema nodosum leprosum-and (b) late complications due to proliferation of M leprae and secondary atrophy of tissues. RR occurs in borderline leprosy and causes motor and sensory loss via damage to peripheral nerves. It tends to strike patients early in the disease, either before treatment, causing the patient to seek advice, or within the first 6 months of
antileprosy therapy, becoming increasingly less frequent thereafter.However, RR may still occur after release from treatment, especially in paucibacillary disease. RR in the facial nerve causes lagophthalmos (inability to close the eye fully). The resulting lid-gap can lead to exposure keratitis and progressive scarring over the lower half of the cornea, and finally blindness. Patients with large facial patches are at greatest risk.7 The lagophthalmos may become permanent, but the patch fades over time and disappears. Lagophthalmos due to RR is an early complication in leprosy and is commonly the way the disease presents in general clinics or eye departments ;8 in cases of recent onset lagophthalmos, the patch is usually still visible. Patients with severe RR in the face or lagophthalmos of less than 6 months’ duration are treated with systemic steroids, as is routine in RR with nerve damage, and good improvement of orbicularis function can be expected.9 Lagophthalmos of more than 6 months’ duration and a lid-gap on mild closure of 5 mm or less is treated conservatively with sunglasses for protection and blinking exercises to reinforce orbicularis function. With lagophthalmos of more than 6 months’ duration and a lid-gap on mild closure of more than 5 mm, lid surgery is indicated. Lagophthalmos will continue to occur despite improved antileprosy treatment, so health staff need to recognise patients at risk to institute early treatment. with Moreover, patients any or not have been whether they lagophthalmos, released from treatment, have a potentially sightthreatening lesion, which will need periodic surveillance. 10 RR may also affect the trigeminal nerve and cause corneal hypoaesthesia. It can occur in combination with lagophthalmos and results partly from exposure of the cornea. Corneal hypoaesthesia due to RR in otherwise normal eyes without lagophthalmos has not been documented, and there is no evidence on whether the hypoaesthesia can be influenced by prompt steroid treatment, as in sensory loss of the hands and feet due to RR. Damage to the long ciliary nerves by scleritis in erythema nodosum leprosum may likewise result in corneal hypoaesthesia.’1 Invasion and secondary atrophy of the corneal nerve endings, comparable to glove-and-stocking anaesthesia in longstanding multibacillary disease patients, may be another cause of corneal hypoaesthesia. Hypoaesthesia occurs mainly in patients with longstanding multibacillary leprosy and with severely affected eyes.12 Patients with advanced loss of corneal sensation are advised to use sunglasses for protection. Erythema nodosum leprosum is characterised clinically by an attack of fever with general malaise and painful subcutaneous nodules; ocular manifestations include acute iritis and episcleritis or a severe combined sclerouveitis. Most erythema nodosum reactions do not involve the eyes and the eye complications can occur without signs of systemic
643
nodosum. This reaction arises in both treated and untreated multibacillary disease, and repeated attacks are not unusual. General treatment is with steroids, clofazimine, and thalidomide. In the past the severe and often bilateral sclerouveitis could lead to blindness in a matter of weeks. This complication became less frequent13 soon after the introduction of dapsone and seems to have become even more rare with MDT. Acute iritis is treated with topical atropine and steroids. Systemic steroids are indicated only when there is a severe accompanying erythema nodosum reaction, as is common in sclerouveitis. Leprosy should be considered in the differential diagnosis of acute iritis and (epi)scleritis in patients in or from leprosy endemic countries. Acute iritis and scleritis may recur, many years after treatment has been stopped, as a severe and potentially
erythema
blinding eye complication. Late complications-notably, lepromas, corneal hypoaesthesia, and iris lesions-due to proliferation of M leprae and secondary atrophy occur only in multibacillary leprosy and should become less with earlier and more effective bactericidal MDT treatment. Ocular lepromas are painless nodules in the limbal area; they appear in multibacillary patients with longstanding and irregularly treated leprosy and may be an early sign of dapsone resistance. Treatment is by strictly supervised MDT, which should achieve slow resolution. The ciliary body is assumed to be the portal of entry to M leprae into the eye; from there the bacilli may invade the iris tissue via small autonomic nerves. Chronic iris breakdown, with slowly progressive miosis, poor dilatation with mydriatics, and thinning of the iris stroma, is typical of longstanding multibacillary leprosy. Invasion and late atrophy within the ciliary body leads to low production of aqueous fluid and low intraocular pressure. Once MDT is given, progression of all these lesions can be expected to slow and stop. For several reasons, the backlog in cataracts may be greater in leprosy patients than in the population at larger The stigma of leprosy is still strong in some societies and leprosy patients may well have problems in getting operated upon for simple senile cataract. Lengthy and repeated courses of prednisolone for reactions can cause cataract as a side-effect. Both acute iritis and invasion of the anterior uvea by M leprae can enhance cataract formation in multibacillary disease. common
Although surgery in multibacillary patients is hampered by poor dilatation of the pupil and fragility of the atrophic iris, the results can be good. 15 1. World Health
Organisation study group. Chemotherapy of leprosy for control programmes. WHO Tech Rep Ser 1982; 675. 2. Anon. Leprosy situation in the world and multidrug therapy coverage. Weekly Epidemiol Rec 1992; 67: 153-60. 3. Courtright P, Johnson GJ. Prevention of blindness in leprosy, rev ed. London: International Centre for Eye Health, 1991. 4. Rajan MA. Eye in multidrug therapy. Indian J Lepr 1990; 62: 33-38. 5. Hogeweg M, Faber WR. Progression of eye lesions in leprosy: ten-year follow-up study in the Netherlands. Int J Lepr 1991; 59: 393-97.
6. Naafs W, Wheate HW. The time interval between the start of anti-leprosy treatment and the development of reactions in borderline patients. Lepr Rev 1978; 49: 153-57. 7. Hogeweg M, Kiran KU, Suneetha S. The significance of facial patches and type I reaction for the development of facial nerve damage in leprosy: a retrospective study among 1226 paucibacillary leprosy patients. Lepr Rev 1991; 62: 143-49. 8. Bosher SK. Leprosy presenting as facial palsy. J Laryngol 1962; 76: 827-30. 9. Kiran KU, Hogeweg M, Suneetha S. Treatment of recent facial nerve damage with lagophthalmos, using a semistandardized steroid regimen. Lepr Rev 1991; 62: 150-54. 10. ffytche TJ. Residual sight-threatening lesions in leprosy patients completing multidrug therapy and sulphone monotherapy. Lepr Rev 1991; 62: 35-43. 11. Lyne AJ. Corneal sensitivity in scleritis and episcleritis. Br J Ophthalmol 1977; 61: 650-54 12. Karacorlu MA, Cakiner T, Saylan T. Corneal sensitivity and correlations between decreased sensitivity and anterior segment pathology in ocular leprosy. Br J Ophthalmol 1991; 75: 117-19. 13. Amendola FA. Ocular and otorhinolaryngological leprosy before and since sulfone therapy. Int J Lepr 1955; 23: 280-83. 14. Brandt F, Kampik A, Malla OK, Pokharel RP, Wos J. Blindness from cataract formation in leprosy. Dev Ophthalmol 1983; 7: 1-12. 15. ffytche TJ. Cataract surgery in the management of the late complications of lepromatous leprosy in South Korea. Br J Ophthalmol 1981; 65: 243-48.
Non-surgical
treatment of stress
incontinence incontinence is defmed by the International Continence Society as a condition in which the involuntary loss of urine is a social or hygienic problem and is objectively demonstrated.l It has been reported to occur in 8-5% of women,2 although this figure is probably an underestimate owing to the social stigma attached to the condition. About 50% of these women will have genuine stress incontinence (GSI),3 which is defined as sphincter incompetence in the absence of detrusor activity. Success rates of up to 95% have been reported4 for the surgical treatment of GSI, but surgery is not the first line of treatment indicated for all patients. Advanced age, previous incontinence surgery, and presence of detrusor instability are indicators of poor surgical outcome. In addition, alternatives to surgery as first-line treatment are appropriate in women who have not completed their childbearing and in whom stress incontinence is only slight or occasional. Increasing awareness of the prevalence of GSI, together with an understanding that surgery and its attendant risks are not indicated for all, has reawakened interest in conservative management. The mainstay of this approach continues to be physiotherapeutic interventions to improve the function of the pelvic floor musculature and thereby the urethral sphincter mechanism.5Kegel6 was among the first to introduce pelvic floor exercises as a method of treating GSI; he reported a subjective cure rate of 80% in a group of 500 patients. The most important factors influencing the successful use of this technique were the ability of the patient to identify correctly the muscles of the pelvic floor, and some form of biofeedback. During the past decade, objective studies have shown a cure rate for pelvic floor exercises of 27%with 60%8 of patients reporting a substantial
Urinary
