640
need to be made about chickenpox: active immunisation is now feasible.19 The Oka strain of live attenuated varicella vaccine was originally developed in Japan for use in immunocompromised children at high risk of severe varicella.2O Reports from Japan and from the USA21.22 now suggest that 90% of healthy children can be completely protected by one dose of the vaccine and that immunity lasts as long as 10 years. The benefits are not difficult to assess: vaccination of infants at 15 months of age (at the same time as MMR vaccine) would prevent almost 80% of cases, would produce a 66% reduction in the total costs of varicella, and would have a benefit to cost ratio of 6,9:1.88 However, several concerns remain. One is the possibility that vaccine-induced immunity might wane in adults, who might then become exposed to wild-type virus (perhaps from cases of zoster) and get severe varicella. Although this hazard could probably be avoided by repeat vaccinations, this would necessitate greater public cooperation than has been seen with other vaccines. Of greater concern is the safety of a vaccine comprising a live DNA-virus that can establish latency in sensory ganglia, even though latency and reactivation to cause herpes zoster seem less likely to arise than with wild-type VZV.23 Although the Japanese have grasped the nettle and have licensed varicella vaccine for use in healthy children, elsewhere decisions still need to be made about whether and how to manage primary infection with this "not-so-benign virus" .10 Joseph CA, Noah ND. Epidemiology of chickenpox in England and Wales, 1967-85. BMJ 1988; 296: 673-76. 2. Dunkle LM, Arvin AM, Whitley RJ, et al. A controlled trial of acyclovir for chickenpox in normal children. N Engl J Med 1991; 325: 1539-44. 3. Balfour HH, Rotbart HA, Feldman S, et al. Acyclovir treatment of varicella in otherwise healthy adolescents. J Pediatr 1992; 120: 1.
627-33. 4. Balfour HH, Wood MJ. Acyclovir therapy is indicated for varicella in individuals with normal immunity. Rev Med Virol 1992; 2: 3-7. 5. Brunell PA. Chickenpox: examining our options. N Engl J Med 1991; 325: 1577-79. 6. Balfour HH, Kelly JM, Suarez CS, et al. Acyclovir treatment of varicella in otherwise healthy children. J Pediatr 1990; 116: 633-39. 7. Moore DA, Hopkins RS. Assessment of a school exclusion policy during a chickenpox outbreak. Am J Epidermiol 1991; 133: 1161-67. 8. Preblud SR. Varicella: complications and costs. Pediatrics 1986; 78 (suppl): 728-35. 9. Guess HA, Broughton DD, Melton LJ III, Kurland LT. Populationbased studies of varicella complications. Pediatrics 1986; 78 (suppl): 723-27. 10. Weller TH. Varicella and herpes zoster: changing concepts of the natural
history, control, and importance of a not-so-benign virus. N Engl J Med 1983; 309: 1362-68, 1434-40. 11.
Johnson RT.
Viral infections of the
nervous
system. New York:
Raven,
1982.
Englund JA, Arvin AM, Balfour HH. Acyclovir treatment for varicella does not lower gpI and IE-62 (p170) antibody responses to varicellazoster virus in normal children. J Clin Microbiol 1990; 38: 2327-30. 13. Bunnell PA. Acyclovir in chickenpox. N Engl J Med 1992; 326: 1226. 14. Boyd K, Walker E. Use of acyclovir to treat chickenpox in pregnancy. BMJ 1988; 296: 393-94. 15. van der Meer JWM, Thompson J, Tan WD, Versteeg J. Treatment of chickenpox pneumonia with acyclovir. Lancet 1980; ii: 473-74. 16. Weber DM, Pellechia JA. Varicella pneumonia: study of prevalence in adult men. JAMA 1965; 192: 572-73. 17. Feder HM. Treatment of adult chickenpox with oral acyclovir. Arch 12.
Intern Med 1990; 150: 2061-65. 18. Wallace M, Bowler W, Murray N, Brondine S, Oldfield E. Oral acyclovir in The treatment of adult varicella. Program and abstracts of the
19. 20.
21.
22.
23.
thirtieth Interscience Conference on Antimicrobial Agents and Chemotherapy, Atlanta, Georgia, Oct 21-24, 1990, abstr 727. Morag A, Gershon A. Live attenuated varicella vaccine. Infect Dis Clin Pract 1992; 1: 85-89. Takahashi M, Otsuka T, Okuno YT, et al. Live vaccine used to prevent the spread of varicella in children in hospital. Lancet 1974; ii: 1288-90. White CJ, Kuter BJ, Hilderbrand CS, et al. Varicella vaccine (VARIVAX) in healthy children and adolescents: results from clinical trials, 1987 to 1989. Pediatrics 1991; 87: 604-10. Gershon AA, LaRussa P, Steinberg S. Live attenuated varicella vaccine: current status and future uses. Semin Pediatr Infect Dis 1991; 2: 171-78. Hardy I, Gershon AA, Steinberg SP, LaRussa P, and the Varicella Vaccine Collaborative Study Group. The incidence of zoster after immunization with live attenuated varicella vaccine: a study in children with leukemia. N Engl J Med 1991; 325: 1545-50.
Needlesticks: preaching to the seroconverted? Needlestick accidents are everyone’s problem. Between 25 and 80% of medical students and junior doctors injure themselves during their first six months to one year in post,1-3 and the incidence is equally worrying in nursing and support staff;4,5 in one hospital 8 % of all employees sustained a needle injury in one year.6 Usually the injury is trivial, but the potential for infectious disease transmission causes much anxiety and consequent morbidity. Of the twenty or more pathogens that have been transmitted by needlestickthe principal causes for concern are human immunodeficiency virus (HIV), and hepatitis B virus (HBV). The risk of HIV transmission by definite inoculation from a known HIV antibodypositive source is around 04%8-ten times less than the lowest estimate for HBV (3-16%). Hepatitis B can potentially be controlled by vaccination of at-risk populations, including health-care staff who may be exposed during their work. After a needlestick accident the need is for a coordinated response whereby post-exposure prophylaxis is started quickly if the injured person has not been vaccinated or if the infectivity of the inoculum is high. HIV is a different problem. No vaccine is available and there is no post-exposure prophylaxis of proven efficacy In addition, the incubation period is long and variable, so even repeated testing cannot entirely relieve the victim’s anxiety. Small wonder that, since the recognition of AIDS as a blood-borne infectious disease, there has been renewed debate on the topic of needlestick injury, its causes, and possible strategies for prevention. Much debate has centred on the practice of re-capping needles after use, because as many as one-third of needlesticks occur during this procedure.7,11,12 Official guidelines in both the USA13,14 and the UK15,16 counsel against the resheathing of used needles, but those warnings were not based on studies of relative risk. It now seems that there may be little difference in injury rates between workers preferentially re-sheathing or not resheathing needles.12,17 Resolution of this question would require careful investigations with workers
641
highly motivated to change their technique. Jagger et aF note that various defects in device design and bedside disposal facilities would have to be overcome workers’ innate mistrust of nonresheathing methods. Other frequently encountered hazards include movement of operator or patient during a procedure, accidents during assembly or dismantling of equipment, and needles concealed in clinical waste. Once a procedure has been safely completed, the risk switches to a third party-often the junior nurse clearing used equipment, the domestic cleaning assistant, or a porter. For this innocent victim, the unsheathed needle is the obvious danger. Most of the work published on needlestick injury looks at invasive procedures, and events surrounding them, with a view to primary prevention. Improvements have been made in systems for safe re-capping of needles18.19 and for their disposal .2021 Jagger et aF argue that all needled devices should be scrutinised and redesigned for greater safety, and repeated calls have been made for improvements in staff training.1.4,8.21 Consistent use of infection-control precautions for every patient is the major defence against blood-borne disease. Secondary prevention issues have been less publicised. Optimum management of injuries and peace of mind, particularly in less medically informed staff, demand a hospital policy for action and an expert contact for advice. The policy should be easily understood, widely publicised, and applicable to all staff. It should be specifically taught to those responsible for implementing it: occupational health departments may provide this service, but the task may also fall to junior casualty staff. Important details include the specimens required from victim and source (if known), and the fact that informed consent is required, in the UK at least, for any test not directly related to diagnosis or treatment. The policy should state where and when specimens will be tested, and who should be notified to arrange this. The treatment options should be made known to the victim. With the advent of zidovudine as a potentia1,22.3 if unproven,l° postto
eliminate
some
prophylaxis against HIV, hospitals must decide in advance about availability of such treatment, and at-risk personnel must be told the decision. Counselling of the victim of a needlestick injury is important to prevent psychological morbidity. Every doctor likely to be involved should be acquainted with the relative risks of acquiring hepatitis and HIV. Full counselling can, and should, be left to an expert once HBV prophylaxis and, if appropriate, the initial dose(s) of zidovudine have been given. For coordination of action after needlesticks, a central agency is vital. Usually it will be the occupational health department, less commonly exposure
a
microbiology/virology
or
infectious
diseases
department. The agency will not only ensure that everything is done that can be done at the time of an incident, but also provide a focus for educational
activities and for
coordinating
the data necessary for
progress.
What of costs? In
of needlestick injure requiring follow-up beyond the initial HBV blooc tests, the financial loss to a health service will not bt high. If the victim becomes infected with HBV, th( figure will be multiplied greatly. As to infection ofa health-care worker with HIV, the expenses ofmedica treatment throughout the progressively debilitating illness must be added to those of lost years oi productivity for a young and possibly highly trainee member of staff. All this takes no account of litigation In treating patients and making informed decisions or cost/benefit ratios, the medical profession attache much importance to "quality of life". The cost o losing this "quality" for an infected, previously healthy, employee cannot be guessed at. Even fear o] potential infection after accidental inoculation ma3 lead to great psychological distress. Effective prevention is impossible without tht interest and commitment of both management anc clinical staff. 21 Well motivated, well rested, anc adequately supervised staff will make fewer mistakes Re-capping of needles is at best a temporary solution It would cease to be an issue if satisfactory disposa systems were always present at the point of use Needle users must take the lead in insisting or improved safety both of needled devices and o: disposal systems. Only sustained pressure from larg( consumer bodies will stimulate action by suppliers. Ir the interim, could greater care in use and disposa prevent 40% of these injuries?" More pricking oi professional consciences might reduce the number o innocent victims. cases
no
1.
Woolley PD, Palfreeman AJ, Patel R, Talbot MD, Samarasinghe PL. Blood-taking practices and needlestick injuries in house officers. Int J
STD AIDS 1991; 2: 46-48. 2. McGeer A, Simor AE, Low DE. Epidemiology of needlestick injuries in house officers. J Infect Dis 1990; 162: 961-64. 3. O’Neill TM, Abbott AV, Radecki SE. Risk of needlesticks and occupational exposures among residents and medical students. Arch Intern Med 1992; 152: 1451-56. 4. Hochreiter MC, Barton LL. Epidemiology of needlestick injury in emergency medical service personnel. J Emerg Med 1988; 6: 9-12. 5. Yassi A, McGill M. Determinants of blood and body fluid exposure in a large teaching hospital: hazards of the intermittent intravenous procedure. Am J Infect Control 1991; 19: 129-35. 6. Ribner BS, Landry MN, Gholson GL, Linden LA. Impact of a rigid, puncture resistant container system upon needlestick injuries. Infect Control 1987; 8: 63-66. 7. Jagger J, Hunt EH, Brand-Elnaggar J, Pearson RD. Rates of needle-stick injury caused by various devices in a university hospital. N Engl J Med 1988; 319: 284-88. 8. Gerberding JL. Risks to health care workers from exposure to hepatitis B virus, human immunodeficiency virus and cytomegalovirus. In: Moellering RC, Weber DJ, Rutala WA, eds. Nosocomial infections: new issues and strategies for prevention. Infect Dis Clin N Am 1989; 3: 735-45. 9. Kennedy DA. Needlestick injuries: mechanisms and control. J Hosp Infect 1988; 12: 315-22. 10. Jones PD. HIV transmission by stabbing despite zidovudine prophylaxis. Lancet 1991; 338: 884. 11. Wright GD, Farrer JA. Potential for the prevention of ’needlestick’ injuries in hospitals. Med J Austr 1990; 152: 111-12. 12. Gompertz S. Needlestick injuries in medical students. J Soc Occ Med 1990; 40: 19-20. 13. CDC acquired immune deficiency syndrome (AIDS) precautions for health care workers and allied professions. MMWR 1983; 32: 450-51.
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
need to be made about chickenpox: active immunisation is now feasible.19 The Oka strain of live attenuated varicella vaccine was originally developed in Japan for use in immunocompromised children at high risk of severe varicella.2O Reports from Japan and from the USA21.22 now suggest that 90% of healthy children can be completely protected by one dose of the vaccine and that immunity lasts as long as 10 years. The benefits are not difficult to assess: vaccination of infants at 15 months of age (at the same time as MMR vaccine) would prevent almost 80% of cases, would produce a 66% reduction in the total costs of varicella, and would have a benefit to cost ratio of 6,9:1.88 However, several concerns remain. One is the possibility that vaccine-induced immunity might wane in adults, who might then become exposed to wild-type virus (perhaps from cases of zoster) and get severe varicella. Although this hazard could probably be avoided by repeat vaccinations, this would necessitate greater public cooperation than has been seen with other vaccines. Of greater concern is the safety of a vaccine comprising a live DNA-virus that can establish latency in sensory ganglia, even though latency and reactivation to cause herpes zoster seem less likely to arise than with wild-type VZV.23 Although the Japanese have grasped the nettle and have licensed varicella vaccine for use in healthy children, elsewhere decisions still need to be made about whether and how to manage primary infection with this "not-so-benign virus" .10 Joseph CA, Noah ND. Epidemiology of chickenpox in England and Wales, 1967-85. BMJ 1988; 296: 673-76. 2. Dunkle LM, Arvin AM, Whitley RJ, et al. A controlled trial of acyclovir for chickenpox in normal children. N Engl J Med 1991; 325: 1539-44. 3. Balfour HH, Rotbart HA, Feldman S, et al. Acyclovir treatment of varicella in otherwise healthy adolescents. J Pediatr 1992; 120: 1.
627-33. 4. Balfour HH, Wood MJ. Acyclovir therapy is indicated for varicella in individuals with normal immunity. Rev Med Virol 1992; 2: 3-7. 5. Brunell PA. Chickenpox: examining our options. N Engl J Med 1991; 325: 1577-79. 6. Balfour HH, Kelly JM, Suarez CS, et al. Acyclovir treatment of varicella in otherwise healthy children. J Pediatr 1990; 116: 633-39. 7. Moore DA, Hopkins RS. Assessment of a school exclusion policy during a chickenpox outbreak. Am J Epidermiol 1991; 133: 1161-67. 8. Preblud SR. Varicella: complications and costs. Pediatrics 1986; 78 (suppl): 728-35. 9. Guess HA, Broughton DD, Melton LJ III, Kurland LT. Populationbased studies of varicella complications. Pediatrics 1986; 78 (suppl): 723-27. 10. Weller TH. Varicella and herpes zoster: changing concepts of the natural
history, control, and importance of a not-so-benign virus. N Engl J Med 1983; 309: 1362-68, 1434-40. 11.
Johnson RT.
Viral infections of the
nervous
system. New York:
Raven,
1982.
Englund JA, Arvin AM, Balfour HH. Acyclovir treatment for varicella does not lower gpI and IE-62 (p170) antibody responses to varicellazoster virus in normal children. J Clin Microbiol 1990; 38: 2327-30. 13. Bunnell PA. Acyclovir in chickenpox. N Engl J Med 1992; 326: 1226. 14. Boyd K, Walker E. Use of acyclovir to treat chickenpox in pregnancy. BMJ 1988; 296: 393-94. 15. van der Meer JWM, Thompson J, Tan WD, Versteeg J. Treatment of chickenpox pneumonia with acyclovir. Lancet 1980; ii: 473-74. 16. Weber DM, Pellechia JA. Varicella pneumonia: study of prevalence in adult men. JAMA 1965; 192: 572-73. 17. Feder HM. Treatment of adult chickenpox with oral acyclovir. Arch 12.
Intern Med 1990; 150: 2061-65. 18. Wallace M, Bowler W, Murray N, Brondine S, Oldfield E. Oral acyclovir in The treatment of adult varicella. Program and abstracts of the
19. 20.
21.
22.
23.
thirtieth Interscience Conference on Antimicrobial Agents and Chemotherapy, Atlanta, Georgia, Oct 21-24, 1990, abstr 727. Morag A, Gershon A. Live attenuated varicella vaccine. Infect Dis Clin Pract 1992; 1: 85-89. Takahashi M, Otsuka T, Okuno YT, et al. Live vaccine used to prevent the spread of varicella in children in hospital. Lancet 1974; ii: 1288-90. White CJ, Kuter BJ, Hilderbrand CS, et al. Varicella vaccine (VARIVAX) in healthy children and adolescents: results from clinical trials, 1987 to 1989. Pediatrics 1991; 87: 604-10. Gershon AA, LaRussa P, Steinberg S. Live attenuated varicella vaccine: current status and future uses. Semin Pediatr Infect Dis 1991; 2: 171-78. Hardy I, Gershon AA, Steinberg SP, LaRussa P, and the Varicella Vaccine Collaborative Study Group. The incidence of zoster after immunization with live attenuated varicella vaccine: a study in children with leukemia. N Engl J Med 1991; 325: 1545-50.
Needlesticks: preaching to the seroconverted? Needlestick accidents are everyone’s problem. Between 25 and 80% of medical students and junior doctors injure themselves during their first six months to one year in post,1-3 and the incidence is equally worrying in nursing and support staff;4,5 in one hospital 8 % of all employees sustained a needle injury in one year.6 Usually the injury is trivial, but the potential for infectious disease transmission causes much anxiety and consequent morbidity. Of the twenty or more pathogens that have been transmitted by needlestickthe principal causes for concern are human immunodeficiency virus (HIV), and hepatitis B virus (HBV). The risk of HIV transmission by definite inoculation from a known HIV antibodypositive source is around 04%8-ten times less than the lowest estimate for HBV (3-16%). Hepatitis B can potentially be controlled by vaccination of at-risk populations, including health-care staff who may be exposed during their work. After a needlestick accident the need is for a coordinated response whereby post-exposure prophylaxis is started quickly if the injured person has not been vaccinated or if the infectivity of the inoculum is high. HIV is a different problem. No vaccine is available and there is no post-exposure prophylaxis of proven efficacy In addition, the incubation period is long and variable, so even repeated testing cannot entirely relieve the victim’s anxiety. Small wonder that, since the recognition of AIDS as a blood-borne infectious disease, there has been renewed debate on the topic of needlestick injury, its causes, and possible strategies for prevention. Much debate has centred on the practice of re-capping needles after use, because as many as one-third of needlesticks occur during this procedure.7,11,12 Official guidelines in both the USA13,14 and the UK15,16 counsel against the resheathing of used needles, but those warnings were not based on studies of relative risk. It now seems that there may be little difference in injury rates between workers preferentially re-sheathing or not resheathing needles.12,17 Resolution of this question would require careful investigations with workers
641
highly motivated to change their technique. Jagger et aF note that various defects in device design and bedside disposal facilities would have to be overcome workers’ innate mistrust of nonresheathing methods. Other frequently encountered hazards include movement of operator or patient during a procedure, accidents during assembly or dismantling of equipment, and needles concealed in clinical waste. Once a procedure has been safely completed, the risk switches to a third party-often the junior nurse clearing used equipment, the domestic cleaning assistant, or a porter. For this innocent victim, the unsheathed needle is the obvious danger. Most of the work published on needlestick injury looks at invasive procedures, and events surrounding them, with a view to primary prevention. Improvements have been made in systems for safe re-capping of needles18.19 and for their disposal .2021 Jagger et aF argue that all needled devices should be scrutinised and redesigned for greater safety, and repeated calls have been made for improvements in staff training.1.4,8.21 Consistent use of infection-control precautions for every patient is the major defence against blood-borne disease. Secondary prevention issues have been less publicised. Optimum management of injuries and peace of mind, particularly in less medically informed staff, demand a hospital policy for action and an expert contact for advice. The policy should be easily understood, widely publicised, and applicable to all staff. It should be specifically taught to those responsible for implementing it: occupational health departments may provide this service, but the task may also fall to junior casualty staff. Important details include the specimens required from victim and source (if known), and the fact that informed consent is required, in the UK at least, for any test not directly related to diagnosis or treatment. The policy should state where and when specimens will be tested, and who should be notified to arrange this. The treatment options should be made known to the victim. With the advent of zidovudine as a potentia1,22.3 if unproven,l° postto
eliminate
some
prophylaxis against HIV, hospitals must decide in advance about availability of such treatment, and at-risk personnel must be told the decision. Counselling of the victim of a needlestick injury is important to prevent psychological morbidity. Every doctor likely to be involved should be acquainted with the relative risks of acquiring hepatitis and HIV. Full counselling can, and should, be left to an expert once HBV prophylaxis and, if appropriate, the initial dose(s) of zidovudine have been given. For coordination of action after needlesticks, a central agency is vital. Usually it will be the occupational health department, less commonly exposure
a
microbiology/virology
or
infectious
diseases
department. The agency will not only ensure that everything is done that can be done at the time of an incident, but also provide a focus for educational
activities and for
coordinating
the data necessary for
progress.
What of costs? In
of needlestick injure requiring follow-up beyond the initial HBV blooc tests, the financial loss to a health service will not bt high. If the victim becomes infected with HBV, th( figure will be multiplied greatly. As to infection ofa health-care worker with HIV, the expenses ofmedica treatment throughout the progressively debilitating illness must be added to those of lost years oi productivity for a young and possibly highly trainee member of staff. All this takes no account of litigation In treating patients and making informed decisions or cost/benefit ratios, the medical profession attache much importance to "quality of life". The cost o losing this "quality" for an infected, previously healthy, employee cannot be guessed at. Even fear o] potential infection after accidental inoculation ma3 lead to great psychological distress. Effective prevention is impossible without tht interest and commitment of both management anc clinical staff. 21 Well motivated, well rested, anc adequately supervised staff will make fewer mistakes Re-capping of needles is at best a temporary solution It would cease to be an issue if satisfactory disposa systems were always present at the point of use Needle users must take the lead in insisting or improved safety both of needled devices and o: disposal systems. Only sustained pressure from larg( consumer bodies will stimulate action by suppliers. Ir the interim, could greater care in use and disposa prevent 40% of these injuries?" More pricking oi professional consciences might reduce the number o innocent victims. cases
no
1.
Woolley PD, Palfreeman AJ, Patel R, Talbot MD, Samarasinghe PL. Blood-taking practices and needlestick injuries in house officers. Int J
STD AIDS 1991; 2: 46-48. 2. McGeer A, Simor AE, Low DE. Epidemiology of needlestick injuries in house officers. J Infect Dis 1990; 162: 961-64. 3. O’Neill TM, Abbott AV, Radecki SE. Risk of needlesticks and occupational exposures among residents and medical students. Arch Intern Med 1992; 152: 1451-56. 4. Hochreiter MC, Barton LL. Epidemiology of needlestick injury in emergency medical service personnel. J Emerg Med 1988; 6: 9-12. 5. Yassi A, McGill M. Determinants of blood and body fluid exposure in a large teaching hospital: hazards of the intermittent intravenous procedure. Am J Infect Control 1991; 19: 129-35. 6. Ribner BS, Landry MN, Gholson GL, Linden LA. Impact of a rigid, puncture resistant container system upon needlestick injuries. Infect Control 1987; 8: 63-66. 7. Jagger J, Hunt EH, Brand-Elnaggar J, Pearson RD. Rates of needle-stick injury caused by various devices in a university hospital. N Engl J Med 1988; 319: 284-88. 8. Gerberding JL. Risks to health care workers from exposure to hepatitis B virus, human immunodeficiency virus and cytomegalovirus. In: Moellering RC, Weber DJ, Rutala WA, eds. Nosocomial infections: new issues and strategies for prevention. Infect Dis Clin N Am 1989; 3: 735-45. 9. Kennedy DA. Needlestick injuries: mechanisms and control. J Hosp Infect 1988; 12: 315-22. 10. Jones PD. HIV transmission by stabbing despite zidovudine prophylaxis. Lancet 1991; 338: 884. 11. Wright GD, Farrer JA. Potential for the prevention of ’needlestick’ injuries in hospitals. Med J Austr 1990; 152: 111-12. 12. Gompertz S. Needlestick injuries in medical students. J Soc Occ Med 1990; 40: 19-20. 13. CDC acquired immune deficiency syndrome (AIDS) precautions for health care workers and allied professions. MMWR 1983; 32: 450-51.
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
