1302
is to remove the catheter.10 We need to know more about the treatment of catheter colonisation with antibiotics or antiseptics, and about changing (eg, over a guide wire) infected catheters, before these methods can be generally recommended. Removal is almost invariably required for tunnel infections,2 but local care can be effective for exit-site sepsis.16 Discussions about catheter sepsis are often hampered by problems of defining the condition. The most rigorous approach is to take blood simultaneously for quantitative culture from both the central venous catheter and a peripheral vein-higher colony counts’in the catheter sample would confirm the diagnosis of catheter sepsis.17 Since difficulties in obtaining a sample from either a peripheral vein or the catheter often hinder this approach, many researchers apply the principle that any unexplained signs of infection are catheter related. Such definitions encourage over-reporting of infections and can hinder comparisons. Tunnel and exit-site infections should be considered separately, because they are probably complications of insertion and fixation, respectively. For example2 -transparent plastic dressings are associated with higher rates of exit-site infection than are dry gauze dressings.18 Colonisation of the lumen probably results from lapses in techniques of catheter care and use: Puntis et apo showed that staff training, audit, and a strict protocol for catheter care can reduce
infection rates. Thrombosis may lead to occlusion of the catheter or to serious vascular complications.19 Routine screening of symptom-free patients is not rewarding,’9 but echocardiography can be helpful in patients with catheter malfunction, cardiopulmonary dysfunction, or sepsis.2° Catheter occlusion can be managed in most patients with thrombolytic agents,16,19 small volumes of dilute hydrochloric acid,21 or clearing with a guide wire;16 removal of the catheter may be necessary. Thrombi seldom require surgical remova119 although they seem to be especially troublesome in newborn babies.22 1. Essex-Cater A, Gilbert J, Robinson T, Littlewood JM. Totally implantable venous access systems in paediatric practice. Arch Dis Child 1989; 64: 119-23. 2. Ingram J, Weitzman S, Greenberg ML, Parkin P, Filler R. Complications of indwelling venous access lines in the pediatric hematology patient: a prospective comparison of external venous catheters and subcutaneous ports. Am J Pediatr Hematol Oncol 1991; 13: 130-36. 3. Ogata ES, Schulman S, Raffensberger J, Luck S, Rusnak M. Caval catheterisation in the intensive care nursery: a useful means for providing parenteral nutrition to the extremely low birth weight infant. J Pediatr Surg 1984; 19: 258-64. 4. Poole MA, Ross MN, Haase GM, Odom LF. Right atrial catheters in pediatric oncology: a patient/parent questionnaire study. Am J Pediatr Hematol Oncol 1991; 13: 152-55. 5. Halperin DL, Koren G, Attias D, Pellegrini E, Greenberg ML, Wyss M. Topical anesthesia for venous, subcutaneous drug reservoir and lumbar punctures in children. Pediatrics 1989; 84: 281-84. 6. Smith S, Dawson S, Hennessy R, Andrew M. Maintenance of the patency of indwelling central venous catheters: is heparin necessary? Am J Pediatr Hematol Oncol 1991; 13: 141-43. 7. Wiernowski JT, Elder-Thomley D, Dawson S, Rothney M, Smith S. Bacterial colonization of right atrial catheters in pediatric oncology: a
8.
comparison of sterile saline and bacteriostatic saline flush solutions. Am J Pediatr Hematol Oncol 1991; 13: 137-40. Puntis JWL. Percutaneous insertion of silastic central venous feeding
catheters. Intensive Ther Clin Monit 1987; 1: 7-10. 9. Goutail-Flaud MF, Sfez M, Berg A, Laguenie G, Couturier C, Barbotin-Larrieu F, Saint-Maurice C. Central venous catheter-related complications in newborns and infants: a 587 case survey. J Pediatr
Surg 1991; 26: 645-50. 10. Puntis JWL, Holden CE, Smallman S, Finkel Y, George RH, Booth IW. Staff training: a key factor in reducing intravascular catheter sepsis. Arch Dis Child 1991; 65: 335-37. 11. Wheeler RA, Griffiths DM, Burge DM. Retrograde tunnel: a method for the fixation of long-term paediatric central venous catheters. J Parent Enter Nutr 1991; 15: 114-15. 12. Grisoni ER, Mehta SK, Connors AF. Thrombosis and infection complicating central venous catheterization in neonates. J Pediatr Surg 1986; 21: 772-76. 13. King DR, Komer M, Hoffman J, Ginn-Pease ME, Stanley ME, Powell D, Harmel RP. Broviac catheter sepsis: the natural history of an iatrogenic infection. J Pediatr Surg 1985; 20: 728-33. 14. Olson
TA, Fischer GW, Lupo MC, Garcia VF, Maybee DA, Keiser J, Hartman KR. Antimicrobial therapy of Broviac catheter infections in pediatnc hematology oncology patients. J Pediatr Surg 1987; 22: 839-42. 15. Wiernowski JT, Rothney M, Dawson S, Andrew M. Evaluation of a home intravenous antibiotic program in pediatric oncology. Am J Pediatr Hematol Oncol 1991; 13: 144-47. 16. Dawson S, Pai MKR, Smith S, Rothney M, Ahmed K, Barr RD. Right atrial catheters in children with cancer: a decade of experience in the use of tunnelled, exteriorized devices at a single institution. Am J Pediatr Hematol Oncol 1991; 13: 126-29. 17. Balakrishnan G, Simpkins C, Greig M, Hallworth D. Catheter related sepsis. Prospective evaluation of catheter infection and catheter related sepsis in a paediatric intensive care unit. Br J Int Care 1991; 2: 17-23. 18. Conly JL, Grieves K, Peters B. A prospective randomised study comparing transparent and dry gauze dressings for central venous catheters. J Infect Dis 1989; 159: 310-19. 19. Ross P, Ehrenkrantz R, Kleinman CS, Seashore JH. Thrombus associated with central venous catheters in infants and children. J Pediatr Surg 1989; 24: 253-56. 20. O’Brodovich H, Adams M, Coates G, Way RC, Andrew M. Cardiopulmonary function during longterm central venous catheterization. Am J Pediatr Hematol Oncol 1991; 13: 148-51. 21. Duffy LF, Kerzner B, Gebus V, Dice J. Treatment of central venous catheter occlusion with hydrochloric acid. J Pediatr 1989; 114: 1002-04. 22. Berman W, Fripp RR, Yabek SM, Wernly J, Corlew S. Great vein and right atrial thrombus in critically ill patients and children with central venous lines. Chest 1991; 99: 963-67.
Colour
prejudice among pathologists
Important decisions based on colour perception are part of everyday life. Traffic signals outside the car and warning lights within have to be observed and interpreted correctly. It is not surprising that the transport industry in the UK has had legislation concerning the colour vision of its employees since the 1870s and that there is a legitimate community expectation that the highest standards of personal fitness and ability will be maintained in public transport or wherever an accident may have serious environmental consequences.1 By contrast, the colour perception of histopathologists, whose diagnostic decisions might have grave consequences, has received little or no scrutiny. Should the public be safeguarded from the colour-blind pathologist? Rigby and colleaguesz lately examined the colour perception of 30 histopathologists or cytopathologists by use of the Famsworth-Munsell 100-hue test. The basic ingredients of this test are 85 colour samples
1303
representing a complete hue circle in approximately equal steps. The samples are placed in four boxes and the subject is asked to arrange the colours in each box between two reference colours at each end, starting from a random sequence. Lighting conditions must be standardized,3a requirement not entirely satisfied in this study by seating the subjects at a north-facing window between 1100 and 1200 hours during the month of September at an unspecified location in
Bristol, England. The investigation found that
of the twentypathologists had serious defects in colour perception; this result accords with the known prevalence of colour defects in the general population. About 8% of caucasian males and 0-5% of females have a congenital colour defect affecting red-green discrimination, although other defects are rare.4 Rigby et al claim that the two pathologists with seriously defective colour vision might have been unable to interpret various stains, and that their findings imply that "among a group of people in whom the ability to discriminate colours is a vital part of their professional life there will be individuals with an unrecognised inability to do so". This study was prompted by the inability of one of the authors to distinguish the subtle differences in colour between colonic mucins stained by a technique familiar only to aficionados of mucin histochemistry. It seems unwarranted to extrapolate from this trifling shortcoming (albeit validated by his poor showing in the 100-hue test) to the recommendation of routine eye-tests for aspiring two
three male
histopathologists. routine staining method in diagnostic histopathology, and one applied almost universally, is haematoxylin and eosin, which yields a restricted range of colours from dark blue through purple to bright red. People with impaired colour vision do not generally confuse blue and red. Protans (individuals in whom the long-wave sensitive photopigment is either missing or abnormal) have diminished sensitivity to red light and may confuse red and black, while those individuals with defects in short-wave rare photopigment and a loss of sensitivity to blue light (tritans) may confuse blue and black.4Difficulties would be far more likely to arise if a red-yellow-green staining combination such as Masson trichrome was widely used for diagnosis. Structure and staining density from light to dark are much more important than colour differences in histological diagnosis; some of the most valuable handbooks in histopathology continue to have black and white illustrations. Colour differences largely provide redundant information and much histopathological diagnosis could be achieved in monochrome. Moreover, diagnosis is not simply a question of accurate observation: knowledge and judgment are essential. Thus colour deficiency is not a ground for concern in the selection and training of histopathologists. Greater benefit to the public would be achieved by checking that general practitioners can accurately
The
interpret the colour changes in dip-stick tests for glycosuria and proteinuria; others might argue that it is much more important that their dentist can match the subtle shade of yellow required for their prosthetic incisor.s By comparison, the colour perception of the person peering down a microscope at a biopsy specimen is an irrelevance. Vingrys AJ, Cole BL. Are colour vision standards justified for the transport industry? Ophthal Physiol Opt 1988; 8: 257-74. 2. Rigby HS, Warren BF, Diamond J, Carter C, Bradfield JWB. Colour perception in pathologists: the Famsworth-Munsell 100-hue test. J Clin Pathol 1991; 44: 745-48. 3. Birch J. Use of the Farnsworth-Munsell 100-hue test in the examination of congenital colour vision defects. Ophthal Physiol Opt 1989; 9: 1.
156-62. 4. Birch J. A practical guide for colour-vision examination: report of the standardization committee of the international research group on colour-vision deficiencies. Ophthal Physiol Opt 1985; 5: 265-85. 5. Davison
dental
SP, Myslinski NR. Shade selection by color vision-defective personnel. J Prosthet Dent 1990; 63: 97-101.
Who
cares
about homecare?
Europe is ageing rapidly, and none too well. Given the choice, many elderly or frail people would far prefer to live in their own homes than in institutions such as rest homes, nursing homes, or long-stay geriatric hospitals. Provision of services that enable them to remain at home for as long as possible should therefore improve their quality of life and reduce the need for institutional care. The UK Government is not alone (and later than some) in recognising the deficiencies in community care,l-4 and likewise it is not unique in failing to deliver homecare services efficiently, equitably, and according to need. How does the UK compare with other countries in the European Community? Age Care Research Europe, a project funded by the EC, have looked at the provision of homecare services in Belgium, Denmark, France, Greece, Germany, Ireland, Italy, the Netherlands, and the UK. They found that there was little awareness of the practices, and even the principles, that were pursued in other countries,5,6 and that national services had arisen out of local culture, ideology, history, and political expediency and not from any rational process of design or of intranational 6 or international comparison of efficacy.6 In many countries the starting point was parishbased support schemes. In Germany, for example, health insurance for working people was introduced in the 1880s, but such facilities were not extended to the elderly until 1941. Although homecare and home nursing were introduced in 1911 as a substitute for hospital treatment, homecare was not widely available with government support until social welfare legislation in the early 1960s. In France, private associations were set up to help mothers in the 1920s, but again only since the 1960s has there been large-scale government support for community services for the elderly. The Netherlands has had
is to remove the catheter.10 We need to know more about the treatment of catheter colonisation with antibiotics or antiseptics, and about changing (eg, over a guide wire) infected catheters, before these methods can be generally recommended. Removal is almost invariably required for tunnel infections,2 but local care can be effective for exit-site sepsis.16 Discussions about catheter sepsis are often hampered by problems of defining the condition. The most rigorous approach is to take blood simultaneously for quantitative culture from both the central venous catheter and a peripheral vein-higher colony counts’in the catheter sample would confirm the diagnosis of catheter sepsis.17 Since difficulties in obtaining a sample from either a peripheral vein or the catheter often hinder this approach, many researchers apply the principle that any unexplained signs of infection are catheter related. Such definitions encourage over-reporting of infections and can hinder comparisons. Tunnel and exit-site infections should be considered separately, because they are probably complications of insertion and fixation, respectively. For example2 -transparent plastic dressings are associated with higher rates of exit-site infection than are dry gauze dressings.18 Colonisation of the lumen probably results from lapses in techniques of catheter care and use: Puntis et apo showed that staff training, audit, and a strict protocol for catheter care can reduce
infection rates. Thrombosis may lead to occlusion of the catheter or to serious vascular complications.19 Routine screening of symptom-free patients is not rewarding,’9 but echocardiography can be helpful in patients with catheter malfunction, cardiopulmonary dysfunction, or sepsis.2° Catheter occlusion can be managed in most patients with thrombolytic agents,16,19 small volumes of dilute hydrochloric acid,21 or clearing with a guide wire;16 removal of the catheter may be necessary. Thrombi seldom require surgical remova119 although they seem to be especially troublesome in newborn babies.22 1. Essex-Cater A, Gilbert J, Robinson T, Littlewood JM. Totally implantable venous access systems in paediatric practice. Arch Dis Child 1989; 64: 119-23. 2. Ingram J, Weitzman S, Greenberg ML, Parkin P, Filler R. Complications of indwelling venous access lines in the pediatric hematology patient: a prospective comparison of external venous catheters and subcutaneous ports. Am J Pediatr Hematol Oncol 1991; 13: 130-36. 3. Ogata ES, Schulman S, Raffensberger J, Luck S, Rusnak M. Caval catheterisation in the intensive care nursery: a useful means for providing parenteral nutrition to the extremely low birth weight infant. J Pediatr Surg 1984; 19: 258-64. 4. Poole MA, Ross MN, Haase GM, Odom LF. Right atrial catheters in pediatric oncology: a patient/parent questionnaire study. Am J Pediatr Hematol Oncol 1991; 13: 152-55. 5. Halperin DL, Koren G, Attias D, Pellegrini E, Greenberg ML, Wyss M. Topical anesthesia for venous, subcutaneous drug reservoir and lumbar punctures in children. Pediatrics 1989; 84: 281-84. 6. Smith S, Dawson S, Hennessy R, Andrew M. Maintenance of the patency of indwelling central venous catheters: is heparin necessary? Am J Pediatr Hematol Oncol 1991; 13: 141-43. 7. Wiernowski JT, Elder-Thomley D, Dawson S, Rothney M, Smith S. Bacterial colonization of right atrial catheters in pediatric oncology: a
8.
comparison of sterile saline and bacteriostatic saline flush solutions. Am J Pediatr Hematol Oncol 1991; 13: 137-40. Puntis JWL. Percutaneous insertion of silastic central venous feeding
catheters. Intensive Ther Clin Monit 1987; 1: 7-10. 9. Goutail-Flaud MF, Sfez M, Berg A, Laguenie G, Couturier C, Barbotin-Larrieu F, Saint-Maurice C. Central venous catheter-related complications in newborns and infants: a 587 case survey. J Pediatr
Surg 1991; 26: 645-50. 10. Puntis JWL, Holden CE, Smallman S, Finkel Y, George RH, Booth IW. Staff training: a key factor in reducing intravascular catheter sepsis. Arch Dis Child 1991; 65: 335-37. 11. Wheeler RA, Griffiths DM, Burge DM. Retrograde tunnel: a method for the fixation of long-term paediatric central venous catheters. J Parent Enter Nutr 1991; 15: 114-15. 12. Grisoni ER, Mehta SK, Connors AF. Thrombosis and infection complicating central venous catheterization in neonates. J Pediatr Surg 1986; 21: 772-76. 13. King DR, Komer M, Hoffman J, Ginn-Pease ME, Stanley ME, Powell D, Harmel RP. Broviac catheter sepsis: the natural history of an iatrogenic infection. J Pediatr Surg 1985; 20: 728-33. 14. Olson
TA, Fischer GW, Lupo MC, Garcia VF, Maybee DA, Keiser J, Hartman KR. Antimicrobial therapy of Broviac catheter infections in pediatnc hematology oncology patients. J Pediatr Surg 1987; 22: 839-42. 15. Wiernowski JT, Rothney M, Dawson S, Andrew M. Evaluation of a home intravenous antibiotic program in pediatric oncology. Am J Pediatr Hematol Oncol 1991; 13: 144-47. 16. Dawson S, Pai MKR, Smith S, Rothney M, Ahmed K, Barr RD. Right atrial catheters in children with cancer: a decade of experience in the use of tunnelled, exteriorized devices at a single institution. Am J Pediatr Hematol Oncol 1991; 13: 126-29. 17. Balakrishnan G, Simpkins C, Greig M, Hallworth D. Catheter related sepsis. Prospective evaluation of catheter infection and catheter related sepsis in a paediatric intensive care unit. Br J Int Care 1991; 2: 17-23. 18. Conly JL, Grieves K, Peters B. A prospective randomised study comparing transparent and dry gauze dressings for central venous catheters. J Infect Dis 1989; 159: 310-19. 19. Ross P, Ehrenkrantz R, Kleinman CS, Seashore JH. Thrombus associated with central venous catheters in infants and children. J Pediatr Surg 1989; 24: 253-56. 20. O’Brodovich H, Adams M, Coates G, Way RC, Andrew M. Cardiopulmonary function during longterm central venous catheterization. Am J Pediatr Hematol Oncol 1991; 13: 148-51. 21. Duffy LF, Kerzner B, Gebus V, Dice J. Treatment of central venous catheter occlusion with hydrochloric acid. J Pediatr 1989; 114: 1002-04. 22. Berman W, Fripp RR, Yabek SM, Wernly J, Corlew S. Great vein and right atrial thrombus in critically ill patients and children with central venous lines. Chest 1991; 99: 963-67.
Colour
prejudice among pathologists
Important decisions based on colour perception are part of everyday life. Traffic signals outside the car and warning lights within have to be observed and interpreted correctly. It is not surprising that the transport industry in the UK has had legislation concerning the colour vision of its employees since the 1870s and that there is a legitimate community expectation that the highest standards of personal fitness and ability will be maintained in public transport or wherever an accident may have serious environmental consequences.1 By contrast, the colour perception of histopathologists, whose diagnostic decisions might have grave consequences, has received little or no scrutiny. Should the public be safeguarded from the colour-blind pathologist? Rigby and colleaguesz lately examined the colour perception of 30 histopathologists or cytopathologists by use of the Famsworth-Munsell 100-hue test. The basic ingredients of this test are 85 colour samples
1303
representing a complete hue circle in approximately equal steps. The samples are placed in four boxes and the subject is asked to arrange the colours in each box between two reference colours at each end, starting from a random sequence. Lighting conditions must be standardized,3a requirement not entirely satisfied in this study by seating the subjects at a north-facing window between 1100 and 1200 hours during the month of September at an unspecified location in
Bristol, England. The investigation found that
of the twentypathologists had serious defects in colour perception; this result accords with the known prevalence of colour defects in the general population. About 8% of caucasian males and 0-5% of females have a congenital colour defect affecting red-green discrimination, although other defects are rare.4 Rigby et al claim that the two pathologists with seriously defective colour vision might have been unable to interpret various stains, and that their findings imply that "among a group of people in whom the ability to discriminate colours is a vital part of their professional life there will be individuals with an unrecognised inability to do so". This study was prompted by the inability of one of the authors to distinguish the subtle differences in colour between colonic mucins stained by a technique familiar only to aficionados of mucin histochemistry. It seems unwarranted to extrapolate from this trifling shortcoming (albeit validated by his poor showing in the 100-hue test) to the recommendation of routine eye-tests for aspiring two
three male
histopathologists. routine staining method in diagnostic histopathology, and one applied almost universally, is haematoxylin and eosin, which yields a restricted range of colours from dark blue through purple to bright red. People with impaired colour vision do not generally confuse blue and red. Protans (individuals in whom the long-wave sensitive photopigment is either missing or abnormal) have diminished sensitivity to red light and may confuse red and black, while those individuals with defects in short-wave rare photopigment and a loss of sensitivity to blue light (tritans) may confuse blue and black.4Difficulties would be far more likely to arise if a red-yellow-green staining combination such as Masson trichrome was widely used for diagnosis. Structure and staining density from light to dark are much more important than colour differences in histological diagnosis; some of the most valuable handbooks in histopathology continue to have black and white illustrations. Colour differences largely provide redundant information and much histopathological diagnosis could be achieved in monochrome. Moreover, diagnosis is not simply a question of accurate observation: knowledge and judgment are essential. Thus colour deficiency is not a ground for concern in the selection and training of histopathologists. Greater benefit to the public would be achieved by checking that general practitioners can accurately
The
interpret the colour changes in dip-stick tests for glycosuria and proteinuria; others might argue that it is much more important that their dentist can match the subtle shade of yellow required for their prosthetic incisor.s By comparison, the colour perception of the person peering down a microscope at a biopsy specimen is an irrelevance. Vingrys AJ, Cole BL. Are colour vision standards justified for the transport industry? Ophthal Physiol Opt 1988; 8: 257-74. 2. Rigby HS, Warren BF, Diamond J, Carter C, Bradfield JWB. Colour perception in pathologists: the Famsworth-Munsell 100-hue test. J Clin Pathol 1991; 44: 745-48. 3. Birch J. Use of the Farnsworth-Munsell 100-hue test in the examination of congenital colour vision defects. Ophthal Physiol Opt 1989; 9: 1.
156-62. 4. Birch J. A practical guide for colour-vision examination: report of the standardization committee of the international research group on colour-vision deficiencies. Ophthal Physiol Opt 1985; 5: 265-85. 5. Davison
dental
SP, Myslinski NR. Shade selection by color vision-defective personnel. J Prosthet Dent 1990; 63: 97-101.
Who
cares
about homecare?
Europe is ageing rapidly, and none too well. Given the choice, many elderly or frail people would far prefer to live in their own homes than in institutions such as rest homes, nursing homes, or long-stay geriatric hospitals. Provision of services that enable them to remain at home for as long as possible should therefore improve their quality of life and reduce the need for institutional care. The UK Government is not alone (and later than some) in recognising the deficiencies in community care,l-4 and likewise it is not unique in failing to deliver homecare services efficiently, equitably, and according to need. How does the UK compare with other countries in the European Community? Age Care Research Europe, a project funded by the EC, have looked at the provision of homecare services in Belgium, Denmark, France, Greece, Germany, Ireland, Italy, the Netherlands, and the UK. They found that there was little awareness of the practices, and even the principles, that were pursued in other countries,5,6 and that national services had arisen out of local culture, ideology, history, and political expediency and not from any rational process of design or of intranational 6 or international comparison of efficacy.6 In many countries the starting point was parishbased support schemes. In Germany, for example, health insurance for working people was introduced in the 1880s, but such facilities were not extended to the elderly until 1941. Although homecare and home nursing were introduced in 1911 as a substitute for hospital treatment, homecare was not widely available with government support until social welfare legislation in the early 1960s. In France, private associations were set up to help mothers in the 1920s, but again only since the 1960s has there been large-scale government support for community services for the elderly. The Netherlands has had
