807
Didanosine is available on a named-patient basis for treatment of HIV infection in patients who are unable to tolerate treatment with zidovudine. Since these patients are likely to have a more advanced stage of HIV disease, we may expect to see manifestations of cardiac dysfunction more commonly in this group. We have seen three cases in which treatment with ddI may have been a cofactor in the development of cardiac failure. A 28-year-old man with an AIDS-defining candida-oesophagitis in February, 1989, started treatment with ddI in September, 1990. In December, 1990, he presented with persistent bilateral pitting oedema of the ankles. Plasma protein and albumin were normal, and there was no proteinuria or haematuria. Liver and kidney function was normal. Although the oedema was satisfactorily controlled by diuretics, it disappeared without a need for diuretic therapy only when ddI was stopped, which was decided on 10 days after the patient presented with oedema. There have been no recurrences. A 47-year-old man with Pneumocystis carinii pneumonia (PCP) as an AIDS-defming illness in February, 1989, started treatment with ddI in September, 1990. He was admitted in November, 1990, for acute pericarditis with high temperatures, pleural and pericardial effusions, and oedema of the legs. Renal and hepatic functions were normal. Treatment with ddI was interrupted and since there was no response to antibiotic and antituberculous chemotherapy, a pericardiocentesis to prevent tamponade was done, which resulted in the removal of 500 ml clear fluid. Cultures of pericardial fluid were negative for bacteria. After the pericardiocentesis, the symptoms resolved and did not recur, despite resumption of treatment with ddl. A 37-year-old man with an AIDS-defining PCP in May, 1989, was started on treatment with ddI in September, 1990, and was admitted in November, 1990, with a 4-week history of dyspnoea, orthopnoea, nocturia, and progressive oedema of the legs. On admission, his temperature was 38.5OC. Liver and kidney function were normal. Echocardiography showed evidence of a constrictive pericarditis. Treatment with ddI was interrupted and the symptoms were satisfactorily controlled with diuretics. The temperature settled spontaneously. After this episode, treatment with ddI was reinstituted and the symptoms have not recurred. Although a contribution of ddI to the precipitation or aggravation of clinically evident cardiac failure in these patients is not proven, we feel that these cases reinforce the opinion of Willcocks and colleagues that careful monitoring is required in patients with known cardiac dysfunction who are using the current formulation of ddI. National AIDS Therapy Evaluation Centre, Academic Medical Centre, University of Amsterdam, 1105 AZ Amsterdam, Netherlands
Department of Internal Medicine, Section of Immunology and Infectious Diseases, University Hospital, Utrecht
MENNO D.
DE
JONG
JAN C. C. BORLEFFS
(abstr)
airborne bacteria
dressings and
into air
by
two
Wound was a 1% burn of the calf heavily colonised with Staphylococcus aureus and Pseudomonas aeruginosa. Air sample size 40 litres.
UK) makes such studies readily possible. We have been investigating the extent and duration of airborne contamination during the redressing of small colonised wounds such as bums covering up to 1% body surface area (up to 180 cm2 in a normal
Biotest
adult). Removing conventional tulle-gras plus absorbent cotton wool or gauze dressings from such wounds colonised with bacteria releases appreciable numbers of organisms into the air despite careful technique by experienced nurses. The subsequent decline in dispersed bacteria was slow (figure, line A). However, similar wounds treated with a hydrocolloid dressing (Granuflex; Convatec) liberated appreciably fewer bacteria during dressing removal (line B). Laboratory experiments with both types of dressing on a simulated wound showed that airbourne dispersal was greatest with moderately dry dressings; with wet dressings the absorbent cellulose materials still released significant numbers of organisms but the hydrocolloid released hardly any. Clinical appraisal is in progress; to date, seven patients have been investigated by using one type of dressing first and the other at the next dressing change. Airborne dispersal of bacteria was consistently less when the
hydrocolloid was used. These findings have a practical application in infection control. Small wounds are sometimes redressed in open wards, in clinic where other patients with open wounds are present, or in rooms reserved for dressings. If several patients in sequence are having dressings changed there is an appreciable cross-infective hazard from the air. Furthermore, bacteria will tend to accumulate in the environment of such areas. Although hydrocolloid dressings will not eliminate this hazard they help to reduce it. Hydrocolloids have other advantages over conventional materials because they are bacterially occlusive and free of the particles and fibres that are readily shed into wounds by most cellulose materials. Although fuller investigation is required (and is in progress) and the behaviour of other modem dressings has yet to be explored thought should be given to the possibility that, for small surface area wounds, traditional absorbent cottonwool and cotton gauze dressings should be abandoned in favour of more satisfactory modem alternatives.
areas
1. Cammarosano C, Lewis W. Cardiac lesions m acquired immune deficiency syndrome (AIDS). J Am Coll Cardiol 1985; 5: 703-06. 2 Fink L, Reichek N, St John Sutton MG. Cardiac abnormalities in acquired immune deficiency syndrome. Am J Cardiol 1984; 54: 1161-63. 3. Reitano J, King M, Cohen H, et al. Cardiac function in patients with acquired immune deficiency syndrome (AIDS) and AIDS prodrome. J Am Coll Cardiol 1984; 3: 525
Wound
Comparison of numbers of bacteria released different types of dressing.
dispersal
of
SiR,—The classic work of Colebrook and colleagues1.2 demonstrated that removing dressings from bacterially colonised bums shed large numbers of organisms into the air and that the subsequent decline of these airborne bacteria was slow. Provision of plenum ventilation rapidly removes airborne bacteria, hence the provision of such systems in operating theatres and bums unit dressing stations. As far as we can ascertain airborne dispersal has not been addressed in the context of small surface wounds although the potential hazard in handling contaminated dressings is recognised.3 The availability of small hand-held air samplers (eg, Biotest RCS;
Burns Research Group, Birmingham Accident Hospital, Birmingham B15 1NA, UK
J. C. LAWRENCE H. A. LILLY A. KIDSON
L, Bourdillon RB. Air hygiene m dressing rooms for burns wounds. Lancet 1946; i: 561-65. 2. Colebrook L, Bourdillon RB. Air hygiene in dressing rooms for burns wounds. Lancet 1946, i: 601-05. 3. Lowbury EJL, Ayliffe GAJ, Geddes AM, Williams JD Control of hospital 2nd ed. London: Chapman & Hall, 1981. 1. Colebrook
or
major
or
major
infection,
Didanosine is available on a named-patient basis for treatment of HIV infection in patients who are unable to tolerate treatment with zidovudine. Since these patients are likely to have a more advanced stage of HIV disease, we may expect to see manifestations of cardiac dysfunction more commonly in this group. We have seen three cases in which treatment with ddI may have been a cofactor in the development of cardiac failure. A 28-year-old man with an AIDS-defining candida-oesophagitis in February, 1989, started treatment with ddI in September, 1990. In December, 1990, he presented with persistent bilateral pitting oedema of the ankles. Plasma protein and albumin were normal, and there was no proteinuria or haematuria. Liver and kidney function was normal. Although the oedema was satisfactorily controlled by diuretics, it disappeared without a need for diuretic therapy only when ddI was stopped, which was decided on 10 days after the patient presented with oedema. There have been no recurrences. A 47-year-old man with Pneumocystis carinii pneumonia (PCP) as an AIDS-defming illness in February, 1989, started treatment with ddI in September, 1990. He was admitted in November, 1990, for acute pericarditis with high temperatures, pleural and pericardial effusions, and oedema of the legs. Renal and hepatic functions were normal. Treatment with ddI was interrupted and since there was no response to antibiotic and antituberculous chemotherapy, a pericardiocentesis to prevent tamponade was done, which resulted in the removal of 500 ml clear fluid. Cultures of pericardial fluid were negative for bacteria. After the pericardiocentesis, the symptoms resolved and did not recur, despite resumption of treatment with ddl. A 37-year-old man with an AIDS-defining PCP in May, 1989, was started on treatment with ddI in September, 1990, and was admitted in November, 1990, with a 4-week history of dyspnoea, orthopnoea, nocturia, and progressive oedema of the legs. On admission, his temperature was 38.5OC. Liver and kidney function were normal. Echocardiography showed evidence of a constrictive pericarditis. Treatment with ddI was interrupted and the symptoms were satisfactorily controlled with diuretics. The temperature settled spontaneously. After this episode, treatment with ddI was reinstituted and the symptoms have not recurred. Although a contribution of ddI to the precipitation or aggravation of clinically evident cardiac failure in these patients is not proven, we feel that these cases reinforce the opinion of Willcocks and colleagues that careful monitoring is required in patients with known cardiac dysfunction who are using the current formulation of ddI. National AIDS Therapy Evaluation Centre, Academic Medical Centre, University of Amsterdam, 1105 AZ Amsterdam, Netherlands
Department of Internal Medicine, Section of Immunology and Infectious Diseases, University Hospital, Utrecht
MENNO D.
DE
JONG
JAN C. C. BORLEFFS
(abstr)
airborne bacteria
dressings and
into air
by
two
Wound was a 1% burn of the calf heavily colonised with Staphylococcus aureus and Pseudomonas aeruginosa. Air sample size 40 litres.
UK) makes such studies readily possible. We have been investigating the extent and duration of airborne contamination during the redressing of small colonised wounds such as bums covering up to 1% body surface area (up to 180 cm2 in a normal
Biotest
adult). Removing conventional tulle-gras plus absorbent cotton wool or gauze dressings from such wounds colonised with bacteria releases appreciable numbers of organisms into the air despite careful technique by experienced nurses. The subsequent decline in dispersed bacteria was slow (figure, line A). However, similar wounds treated with a hydrocolloid dressing (Granuflex; Convatec) liberated appreciably fewer bacteria during dressing removal (line B). Laboratory experiments with both types of dressing on a simulated wound showed that airbourne dispersal was greatest with moderately dry dressings; with wet dressings the absorbent cellulose materials still released significant numbers of organisms but the hydrocolloid released hardly any. Clinical appraisal is in progress; to date, seven patients have been investigated by using one type of dressing first and the other at the next dressing change. Airborne dispersal of bacteria was consistently less when the
hydrocolloid was used. These findings have a practical application in infection control. Small wounds are sometimes redressed in open wards, in clinic where other patients with open wounds are present, or in rooms reserved for dressings. If several patients in sequence are having dressings changed there is an appreciable cross-infective hazard from the air. Furthermore, bacteria will tend to accumulate in the environment of such areas. Although hydrocolloid dressings will not eliminate this hazard they help to reduce it. Hydrocolloids have other advantages over conventional materials because they are bacterially occlusive and free of the particles and fibres that are readily shed into wounds by most cellulose materials. Although fuller investigation is required (and is in progress) and the behaviour of other modem dressings has yet to be explored thought should be given to the possibility that, for small surface area wounds, traditional absorbent cottonwool and cotton gauze dressings should be abandoned in favour of more satisfactory modem alternatives.
areas
1. Cammarosano C, Lewis W. Cardiac lesions m acquired immune deficiency syndrome (AIDS). J Am Coll Cardiol 1985; 5: 703-06. 2 Fink L, Reichek N, St John Sutton MG. Cardiac abnormalities in acquired immune deficiency syndrome. Am J Cardiol 1984; 54: 1161-63. 3. Reitano J, King M, Cohen H, et al. Cardiac function in patients with acquired immune deficiency syndrome (AIDS) and AIDS prodrome. J Am Coll Cardiol 1984; 3: 525
Wound
Comparison of numbers of bacteria released different types of dressing.
dispersal
of
SiR,—The classic work of Colebrook and colleagues1.2 demonstrated that removing dressings from bacterially colonised bums shed large numbers of organisms into the air and that the subsequent decline of these airborne bacteria was slow. Provision of plenum ventilation rapidly removes airborne bacteria, hence the provision of such systems in operating theatres and bums unit dressing stations. As far as we can ascertain airborne dispersal has not been addressed in the context of small surface wounds although the potential hazard in handling contaminated dressings is recognised.3 The availability of small hand-held air samplers (eg, Biotest RCS;
Burns Research Group, Birmingham Accident Hospital, Birmingham B15 1NA, UK
J. C. LAWRENCE H. A. LILLY A. KIDSON
L, Bourdillon RB. Air hygiene m dressing rooms for burns wounds. Lancet 1946; i: 561-65. 2. Colebrook L, Bourdillon RB. Air hygiene in dressing rooms for burns wounds. Lancet 1946, i: 601-05. 3. Lowbury EJL, Ayliffe GAJ, Geddes AM, Williams JD Control of hospital 2nd ed. London: Chapman & Hall, 1981. 1. Colebrook
or
major
or
major
infection,
