Journal
of Hospital
Infection
(1991)
17, 83-94
REVIEW
Wound
infection
ARTICLE
under
J. J. Hutchinson
occlusive
dressings
and J. C. Lawrence*
Wound Healing Research Institute, Newtech Square, Deeside Industrial Park, Deeside, Clwyd CH5 2NU and *The Burns Research Group, Birmingham Accident Hospital, Bath Row, Birmingham B15 1NA Accepted for publication
12 October 1990
Summary: It is often supposed that occlusive dressings potentiate wound infection. However, even though heavy colonization by skin and wound flora is often seen under certain types of occlusion, clinical infection is not a frequent occurrence. Commensal wound flora consists of a variety of Grampositive and Gram-negative organisms and fungi which do not appear to be detrimental to healing. Certain aspects of wound healing may in fact be promoted by bacterial colonization, although clinical infection can lead to wound breakdown and systemic infection. Wounds compromised by devitalized tissue, drains or sutures are more susceptible than clean wounds to clinical infection. Occlusive dressings may help prevent infection by presenting a barrier to potential pathogens, and hydrocolloid occlusive dressings have been shown to prevent dissemination of methicillin-resistant Staphylococcus aureus. The rate of clinical infection as deduced from published trials of dressings is lower under occlusion than when non-occlusive dressings are used, and this is likely to be a result of normal activity of the host defences under occlusive dressings. Keywords:
Wound
healing;
occlusive
dressings;
infection.
Introduction
It is generally assumed that covering wounds with occlusive dressings potentiates the risk of infection’s2 and the work of Evans3 appeared to substantiate this concern. However, it is important to realize that the presence of bacteria within a wound is not indicative of infection4 and diagnosis should be based on the classical clinical signs together with supportive microbiology. Improved healing in occluded wounds was first reported by Bull, Squire 8-zTopley,’ and Schilling, Roberts & Goodman,6 but the classical work of Winte.r7 which demonstrated that occluded wounds re-epithelialized faster than those left exposed eventually led to the introduction of a wide variety of Correspondence
to: J. J. Hutchinson.
0195-6701/91/020083
112 $03.00/O
0 1991 The Hospital
83
Infectmn
Society
J. J. Hutchinson
84
Table Dressing Hydrocolloids
Hydrogels
(HCD)
(HG)
Polyurethane
Films
(PUF)*
Foams
* PUF also called semi-occlusive ** ‘DuoDERM’
is also known
and J. C. Lawrence
I. Examples
of occlusive
Proprietary
name
dressings Manufacturers
‘DuoDERM’** ‘Comfeel’ ‘Restore’ ‘Vigilon’ ‘Geliperm’ ‘OpSite’ ‘Tegaderm’ ‘Omiderm’ ‘Synthaderm’ ‘Lyofoam’ ‘Silastic foam’ or vapour-permeable as ‘Granuflex’
membrane and ‘Varihesive’.
Squibb ConvaTec Coloplast Hollister Bard Geistlich Smith and Nephew 3M Health Care Omikron Scientific Derma-Lock Ultra Labs Inc. Dow Corning (VPM).
occlusive dressings. Occlusive dressings may be defined as those which prevent uninhibited passage of water vapour, and which therefore maintain wounds in a moist state. Healing which takes place under them is often referred to as ‘moist wound healing’. Dressings which induce such a state include simple plastic films, polyurethane-backed hydrocolloids, foams and hydrogels (Table I). In addition to the effects on reepithelialization,s,9 occluded wounds exhibit altered collagen metabolism,” enhanced granulation tissue formation” and enhanced neovascularization.‘2 Occlusive dressings have been applied to virtually all wound types including burns, donor sites, ulcers, abrasions, incisions and excisions. Varicjus authors’3,‘4 have described the properties of an ‘ideal’ dressing-the more important factors are shown in Table II. Many current occlusive dressings (Table I) fulfil most of these criteria; moreover, in clinical use they appear to be associated with lower wound infection rates than traditional dressings. This review considers the effects of occlusion on the microbiology of normal skin and wounds, the distinction between wound colonization and infection and the role of microorganisms in wound healing. General factors relevant to the likelihood of wound infection developing are discussed together with the effect occlusive dressings have on this possibility. By reviewing the numerous publications concerning the use of occlusive dressings on a variety of wounds, it can be demonstrated that wound infection rates are lower than with conventional dressings. The reasons for the lower infection rates associated with occlusive wound cover are considered. The
effects
of occlusion
on commensal
flora
of normal
skin
The normal resident commensal flora of intact human skin is composed mainly of Gram-positive organisms such as Staphylococcus epidermidis, Streptococcus spp. and Corynebacterium spp. Occasionally Candida spp. may be isolated. The precise nature of the flora, i.e. species and number is
Infection Table
under
occlusive
II. Some characteristics
dressings
of the ‘ideal’
85
wound dressing”,14
Handling of excess exudate Removal of toxic substances Maintenance of moist environment over the wound Permit gaseous exchange Present a barrier to microorganisms Provide thermal insulation Demonstrate freedom from particulate contaminants Removal without trauma to new tissue
dependent upon: body site and subject;” antagonism between microorganisms;16 skin lipids and desiccation;‘7,‘8 and the degree of hydration or maceration of the skin. 19v2’There is also considerable variation between individuals21 and transient bacteria may also be encountered. The degree of hydration of the skin can be altered by occlusion and such changes in the microbial flora are described by Marples,” Bibel & LeBrum,20 Aly et uZ.,~* Easmon23 and Lawrence & Lilly.24~25 Total occlusion, as for instance provided by Saran Wrap, polyvinylchloride (PVC) sheets and impervious plastic tapes, causes the normal flora to proliferate22-24 and the viable count may increase up to 50 000 fold.22 Changes in the proportion of species isolated can occur; Gram-negative bacilli and lipophilic diphtheroids may increase whilst non-lipophilic diphtheroids decline.22’26 Occlusion with hydrocolloid24 and polyurethane film dressings23 has not led to changes in the resident flora. Lawrence & Lilly24 compared the occlusive hydrocolloid dressing ‘DuoDERM’ (also known as ‘Granuflex’ and ‘Varihesive’), with a conventional tulle gras/absorbent gauze dressing, and found that the flora remained unaltered under both dressings. The
effects
of occlusion
on wound
flora
Irrespective of the dressing, the flora isolated from wounds is often similar to that of normal skin and may include S. epidermidis, S. aureus, P-haemolytic streptococci of Lancefield groups A, B and C, diphtheroids and Micrococcus. Gram-negative organisms are usually isolated, and may include Pseudomonas aeruginosa, Klebsiella spp. and other ‘coliform’ bacteria. Furthermore, anaerobes such as Clostridium welchii, Bacteroides spp. and anaerobic cocci are often seen. Fungi may be isolated in burns, but rarely from venous ulcers. Use of a dressing alters the wound environment resulting in a specific sub-dressing ecology.27,28 As with normal skin, the most pronounced effects occur under dressings that prevent desiccation.29 Early concerns that occlusive dressings would promote wound infection retarded their widespread use3,3632 despite the healing benefits seen in both acute* and chronic wounds.33 Early investigations using dressings that permit fluid to accumulate
86
J. J. Hutchinson
and J. C. Lawrence
(‘Silastic’) appeared to support the claim that their use predisposed to infection34z35 such that P. aeruginosa numbers increased and caused clinical infection. The subsequent development of more advanced occlusive dressings which are either water vapour permeable and/or capable of holding exudate has reduced the risk of infection. Studies of these advanced occlusive dressings (discussed fully under clinical trial results) show that the colonizing flora of wounds is similar to that noted with ‘conventional’ dressings. These studies also show that the presence of microorganisms is not necessarily indicative of infection. It is essential to distinguish between colonization and infection when interpreting results of clinical trials.
Colonization
or infection?
Because of similarities in the inflammatory response to wound healing and infection36 confusion can arise between colonization and infection.37,38 Some authorities diagnose infection if the bacterial count is greater than lo5 colony forming units (cfu) g-’ of tissue.39,40 However, in burns, healing can occur in the presence of much larger numbers4i although numbers greater than 1O’cfu g-’ may be associated with a higher risk of infection42 and impaired graft take.43 . The importance of microbiological findings in diagnosing infection must be evaluated in conjunction with clinical signs such as local pain, cellulitis, lymphangitis, heat, erythema, oedema and purulent exudate.30 Histologically, infection, as distinct from colonization, can be characterized by invasion of viable tissue by pathogens. 36,44Organisms present in wound exudate are not necessarily invading tissue thus their presence can only be indicative, but not diagnostic, of infection. The role
of microorganisms
in wound
healing
Although it is generally accepted that clinical infection impairs wound healing, the effect of any colonizing microorganisms on the healing process is yet to be determined. The effects that organisms may exert on wound healing range from detrimental to stimulatory. Numerous publications suggest that commensal organisms do not usually adversely influence wound healing.4~29~45~46The study of sterile wounds is not usually practical since contamination rapidly occurs from the normal surrounding skin; thus a definitive answer concerning the real influence of contamination on healing is difficult to obtain. However, some evidence suggests that a relationship exists between colonization and the rate and quality of healing. The effect of bacterial numbers on healing remains controversial.47,48 However, some authors have established links between necrotic non-healing ulceration and the presence of specific organisms such as Proteus mirabilis, P. aeruginosa and Bacteroides ~pp.~~ Topical application of chlorhexidine and gentamicin” was shown to reduce the carriage of
Infection
under
occlusive
dressings
87
microorganisms in ulcers prior to grafting, although the use and effects of topical or systemic antibacterial administration remain controversial.5~47~4s,5’ Work by Greenhalgh, Gamelli & Fosters2 suggests that killed cells of the immunomodulating organism Corynebacterium parvum injected intraperitoneally into mice impair wound healing in a dorsal incision wound. This contrasts with the stimulating effect of this organism on host defence against sepsis, and could be due to the activation of inhibitory macrophages. Wound healing has also been shown to be adversely affected by a wide range of bacterial metabolites including those from S. aureus, P. aeruginosa53-55 and Lancefield Group A P-haemolytic streptococci.s4 Bacteria in wounds are not necessarily detrimental to the healing process, and can aid desloughing34 and possibly enhance wound healing by stimulating inflammation.56-58 Very early observations suggested that wounds may heal faster if contaminated.59,60 In conclusion it appears likely that the bacterial species37 and change in number of organisms detected31 are more important in wound healing than the total bacterial count.
Factors
affecting
wound
infection
The consequences of a wound becoming clinically infected as distinct from simply colonized must be regarded as detrimental to the healing process. Healing may stop and, occasionally, regress; sutured wounds may dehisce. Systemic infection can be a consequence of infection in necrotic undebrided wounds; bacteraemia has been reported in 76% of patients with decubitus ulcers.61 Local wound factors which predispose to infection include: the presence of devitalized tissue, haematoma, foreign bodies and method of wound closure used. Foreign bodies, such as suture$j2 and drains63,64 are reported to increase wound infection. Sutures have also been shown to harbour a dense surface population of adherent organisms, particularly Staphylococcus epidermid@ and to increase the pus forming ability of S. azweus lo3 to 104-fold.‘j6 Wounds close d p rimarily show a lower wound strength than those allowed to heal by secondary intention over a prolonged period,67 and are more likely to become infected than open granulating wounds. Haematoma in a wound may also potentiate infection.68 Systemic factors also affect the likelihood of infection; these include age, diabetes, steroid therapy, gross obesity, malnutrition and infection of other body sites. Inhibition of wound healing, as measured by the breaking strength of incision wounds, has been shown in rats with transient bacteraemia resulting from a distal site of infection.69 Measures aimed at preventing wound infection should include debridement of all dead tissue7’ and meticulous wound cleansing. Foreign materials must be removed and the use of drains in uninfected wounds kept
88
J. J. Hutchinson
and J. C. Lawrence
Tape closures instead of sutures reduce infective to a minimum. develop, complications of surgical wounds. 70,71 Should wound infection systemic antibiotic treatment may be required together with debridement and topical antisepsis. Occlusive
dressings
in wound
healing
Currently available occlusive dressings include hydrocolloids (HCD), hydrogels (HG), foams and polyurethane films (PUF) (Table I). These dressings do not alter the wound flora such that endogenous infection is potentiated (vi& +a). They also provide a barrier to exogenous pathogens. Endogenous and exogenous infection is therefore minimized. Clinical trials show that wound infection rates using occlusive dressings are lower than those observed with conventional dressings. Occlusive dressings as bacterial barriers In-vitro studies of the polyurethane-backed HCDs, ‘DuoDERM’, ‘Comfeel Ulcus’ and ‘Dermiflex’ and the PUFs, ‘OpSite’ and ‘Tegaderm’ show that these dressings are bacteria-proof. By contrast, a non-woven fibre-backed HCD, ‘Biofilm’ is readily permeated by P. aeruginosa and S. aureus.25 Studies by Mertz, Marshall & Eaglstein,27 in which partial thickness wounds on pigs were challenged with 10’ S. aureus and P. aeruginosa, showed that no wound contamination was detected in wounds dressed with ‘DuoDERM’ even if repeatedly challenged. The in-vitro effectiveness of ‘OpSite’ was not confirmed. The authors suggest that as skin moves, channel formation occurs under ‘OpSite’ leading to bacterial contamination. The HG, ‘Vigilon’, also showed protection from S. aUYeUs in 50% of wounds but no protection from P. aeruginosa; however, no barrier function is claimed for this dressing. Preliminary work by Wilson, Burroughs & Dunn,72 using the HCDs ‘DuoDERM’ and ‘Dermiflex’, suggests that they are effective in preventing the spread of epidemic methicillin-resistant S. aUYeUs (MRSA). Seven patients with MRSA-contaminated ulcers were managed with these HCDs to prevent contamination of the wound environment. Distal sites of MRSA contamination were treated with antibacterial measures. Despite wound colonization with MRSA there was continued absence of this organism from the outer surface of the dressing. This important clinical finding has implications not only on the epidemiology of MRSA but also on the costs involved in barrier nursing. Clinical trial results Collated data from 50 controlled trials on a variety of wounds yielded infection rates of 5.37% and 3.25% (P
of Hospital
Infection
(1991)
17, 83-94
REVIEW
Wound
infection
ARTICLE
under
J. J. Hutchinson
occlusive
dressings
and J. C. Lawrence*
Wound Healing Research Institute, Newtech Square, Deeside Industrial Park, Deeside, Clwyd CH5 2NU and *The Burns Research Group, Birmingham Accident Hospital, Bath Row, Birmingham B15 1NA Accepted for publication
12 October 1990
Summary: It is often supposed that occlusive dressings potentiate wound infection. However, even though heavy colonization by skin and wound flora is often seen under certain types of occlusion, clinical infection is not a frequent occurrence. Commensal wound flora consists of a variety of Grampositive and Gram-negative organisms and fungi which do not appear to be detrimental to healing. Certain aspects of wound healing may in fact be promoted by bacterial colonization, although clinical infection can lead to wound breakdown and systemic infection. Wounds compromised by devitalized tissue, drains or sutures are more susceptible than clean wounds to clinical infection. Occlusive dressings may help prevent infection by presenting a barrier to potential pathogens, and hydrocolloid occlusive dressings have been shown to prevent dissemination of methicillin-resistant Staphylococcus aureus. The rate of clinical infection as deduced from published trials of dressings is lower under occlusion than when non-occlusive dressings are used, and this is likely to be a result of normal activity of the host defences under occlusive dressings. Keywords:
Wound
healing;
occlusive
dressings;
infection.
Introduction
It is generally assumed that covering wounds with occlusive dressings potentiates the risk of infection’s2 and the work of Evans3 appeared to substantiate this concern. However, it is important to realize that the presence of bacteria within a wound is not indicative of infection4 and diagnosis should be based on the classical clinical signs together with supportive microbiology. Improved healing in occluded wounds was first reported by Bull, Squire 8-zTopley,’ and Schilling, Roberts & Goodman,6 but the classical work of Winte.r7 which demonstrated that occluded wounds re-epithelialized faster than those left exposed eventually led to the introduction of a wide variety of Correspondence
to: J. J. Hutchinson.
0195-6701/91/020083
112 $03.00/O
0 1991 The Hospital
83
Infectmn
Society
J. J. Hutchinson
84
Table Dressing Hydrocolloids
Hydrogels
(HCD)
(HG)
Polyurethane
Films
(PUF)*
Foams
* PUF also called semi-occlusive ** ‘DuoDERM’
is also known
and J. C. Lawrence
I. Examples
of occlusive
Proprietary
name
dressings Manufacturers
‘DuoDERM’** ‘Comfeel’ ‘Restore’ ‘Vigilon’ ‘Geliperm’ ‘OpSite’ ‘Tegaderm’ ‘Omiderm’ ‘Synthaderm’ ‘Lyofoam’ ‘Silastic foam’ or vapour-permeable as ‘Granuflex’
membrane and ‘Varihesive’.
Squibb ConvaTec Coloplast Hollister Bard Geistlich Smith and Nephew 3M Health Care Omikron Scientific Derma-Lock Ultra Labs Inc. Dow Corning (VPM).
occlusive dressings. Occlusive dressings may be defined as those which prevent uninhibited passage of water vapour, and which therefore maintain wounds in a moist state. Healing which takes place under them is often referred to as ‘moist wound healing’. Dressings which induce such a state include simple plastic films, polyurethane-backed hydrocolloids, foams and hydrogels (Table I). In addition to the effects on reepithelialization,s,9 occluded wounds exhibit altered collagen metabolism,” enhanced granulation tissue formation” and enhanced neovascularization.‘2 Occlusive dressings have been applied to virtually all wound types including burns, donor sites, ulcers, abrasions, incisions and excisions. Varicjus authors’3,‘4 have described the properties of an ‘ideal’ dressing-the more important factors are shown in Table II. Many current occlusive dressings (Table I) fulfil most of these criteria; moreover, in clinical use they appear to be associated with lower wound infection rates than traditional dressings. This review considers the effects of occlusion on the microbiology of normal skin and wounds, the distinction between wound colonization and infection and the role of microorganisms in wound healing. General factors relevant to the likelihood of wound infection developing are discussed together with the effect occlusive dressings have on this possibility. By reviewing the numerous publications concerning the use of occlusive dressings on a variety of wounds, it can be demonstrated that wound infection rates are lower than with conventional dressings. The reasons for the lower infection rates associated with occlusive wound cover are considered. The
effects
of occlusion
on commensal
flora
of normal
skin
The normal resident commensal flora of intact human skin is composed mainly of Gram-positive organisms such as Staphylococcus epidermidis, Streptococcus spp. and Corynebacterium spp. Occasionally Candida spp. may be isolated. The precise nature of the flora, i.e. species and number is
Infection Table
under
occlusive
II. Some characteristics
dressings
of the ‘ideal’
85
wound dressing”,14
Handling of excess exudate Removal of toxic substances Maintenance of moist environment over the wound Permit gaseous exchange Present a barrier to microorganisms Provide thermal insulation Demonstrate freedom from particulate contaminants Removal without trauma to new tissue
dependent upon: body site and subject;” antagonism between microorganisms;16 skin lipids and desiccation;‘7,‘8 and the degree of hydration or maceration of the skin. 19v2’There is also considerable variation between individuals21 and transient bacteria may also be encountered. The degree of hydration of the skin can be altered by occlusion and such changes in the microbial flora are described by Marples,” Bibel & LeBrum,20 Aly et uZ.,~* Easmon23 and Lawrence & Lilly.24~25 Total occlusion, as for instance provided by Saran Wrap, polyvinylchloride (PVC) sheets and impervious plastic tapes, causes the normal flora to proliferate22-24 and the viable count may increase up to 50 000 fold.22 Changes in the proportion of species isolated can occur; Gram-negative bacilli and lipophilic diphtheroids may increase whilst non-lipophilic diphtheroids decline.22’26 Occlusion with hydrocolloid24 and polyurethane film dressings23 has not led to changes in the resident flora. Lawrence & Lilly24 compared the occlusive hydrocolloid dressing ‘DuoDERM’ (also known as ‘Granuflex’ and ‘Varihesive’), with a conventional tulle gras/absorbent gauze dressing, and found that the flora remained unaltered under both dressings. The
effects
of occlusion
on wound
flora
Irrespective of the dressing, the flora isolated from wounds is often similar to that of normal skin and may include S. epidermidis, S. aureus, P-haemolytic streptococci of Lancefield groups A, B and C, diphtheroids and Micrococcus. Gram-negative organisms are usually isolated, and may include Pseudomonas aeruginosa, Klebsiella spp. and other ‘coliform’ bacteria. Furthermore, anaerobes such as Clostridium welchii, Bacteroides spp. and anaerobic cocci are often seen. Fungi may be isolated in burns, but rarely from venous ulcers. Use of a dressing alters the wound environment resulting in a specific sub-dressing ecology.27,28 As with normal skin, the most pronounced effects occur under dressings that prevent desiccation.29 Early concerns that occlusive dressings would promote wound infection retarded their widespread use3,3632 despite the healing benefits seen in both acute* and chronic wounds.33 Early investigations using dressings that permit fluid to accumulate
86
J. J. Hutchinson
and J. C. Lawrence
(‘Silastic’) appeared to support the claim that their use predisposed to infection34z35 such that P. aeruginosa numbers increased and caused clinical infection. The subsequent development of more advanced occlusive dressings which are either water vapour permeable and/or capable of holding exudate has reduced the risk of infection. Studies of these advanced occlusive dressings (discussed fully under clinical trial results) show that the colonizing flora of wounds is similar to that noted with ‘conventional’ dressings. These studies also show that the presence of microorganisms is not necessarily indicative of infection. It is essential to distinguish between colonization and infection when interpreting results of clinical trials.
Colonization
or infection?
Because of similarities in the inflammatory response to wound healing and infection36 confusion can arise between colonization and infection.37,38 Some authorities diagnose infection if the bacterial count is greater than lo5 colony forming units (cfu) g-’ of tissue.39,40 However, in burns, healing can occur in the presence of much larger numbers4i although numbers greater than 1O’cfu g-’ may be associated with a higher risk of infection42 and impaired graft take.43 . The importance of microbiological findings in diagnosing infection must be evaluated in conjunction with clinical signs such as local pain, cellulitis, lymphangitis, heat, erythema, oedema and purulent exudate.30 Histologically, infection, as distinct from colonization, can be characterized by invasion of viable tissue by pathogens. 36,44Organisms present in wound exudate are not necessarily invading tissue thus their presence can only be indicative, but not diagnostic, of infection. The role
of microorganisms
in wound
healing
Although it is generally accepted that clinical infection impairs wound healing, the effect of any colonizing microorganisms on the healing process is yet to be determined. The effects that organisms may exert on wound healing range from detrimental to stimulatory. Numerous publications suggest that commensal organisms do not usually adversely influence wound healing.4~29~45~46The study of sterile wounds is not usually practical since contamination rapidly occurs from the normal surrounding skin; thus a definitive answer concerning the real influence of contamination on healing is difficult to obtain. However, some evidence suggests that a relationship exists between colonization and the rate and quality of healing. The effect of bacterial numbers on healing remains controversial.47,48 However, some authors have established links between necrotic non-healing ulceration and the presence of specific organisms such as Proteus mirabilis, P. aeruginosa and Bacteroides ~pp.~~ Topical application of chlorhexidine and gentamicin” was shown to reduce the carriage of
Infection
under
occlusive
dressings
87
microorganisms in ulcers prior to grafting, although the use and effects of topical or systemic antibacterial administration remain controversial.5~47~4s,5’ Work by Greenhalgh, Gamelli & Fosters2 suggests that killed cells of the immunomodulating organism Corynebacterium parvum injected intraperitoneally into mice impair wound healing in a dorsal incision wound. This contrasts with the stimulating effect of this organism on host defence against sepsis, and could be due to the activation of inhibitory macrophages. Wound healing has also been shown to be adversely affected by a wide range of bacterial metabolites including those from S. aureus, P. aeruginosa53-55 and Lancefield Group A P-haemolytic streptococci.s4 Bacteria in wounds are not necessarily detrimental to the healing process, and can aid desloughing34 and possibly enhance wound healing by stimulating inflammation.56-58 Very early observations suggested that wounds may heal faster if contaminated.59,60 In conclusion it appears likely that the bacterial species37 and change in number of organisms detected31 are more important in wound healing than the total bacterial count.
Factors
affecting
wound
infection
The consequences of a wound becoming clinically infected as distinct from simply colonized must be regarded as detrimental to the healing process. Healing may stop and, occasionally, regress; sutured wounds may dehisce. Systemic infection can be a consequence of infection in necrotic undebrided wounds; bacteraemia has been reported in 76% of patients with decubitus ulcers.61 Local wound factors which predispose to infection include: the presence of devitalized tissue, haematoma, foreign bodies and method of wound closure used. Foreign bodies, such as suture$j2 and drains63,64 are reported to increase wound infection. Sutures have also been shown to harbour a dense surface population of adherent organisms, particularly Staphylococcus epidermid@ and to increase the pus forming ability of S. azweus lo3 to 104-fold.‘j6 Wounds close d p rimarily show a lower wound strength than those allowed to heal by secondary intention over a prolonged period,67 and are more likely to become infected than open granulating wounds. Haematoma in a wound may also potentiate infection.68 Systemic factors also affect the likelihood of infection; these include age, diabetes, steroid therapy, gross obesity, malnutrition and infection of other body sites. Inhibition of wound healing, as measured by the breaking strength of incision wounds, has been shown in rats with transient bacteraemia resulting from a distal site of infection.69 Measures aimed at preventing wound infection should include debridement of all dead tissue7’ and meticulous wound cleansing. Foreign materials must be removed and the use of drains in uninfected wounds kept
88
J. J. Hutchinson
and J. C. Lawrence
Tape closures instead of sutures reduce infective to a minimum. develop, complications of surgical wounds. 70,71 Should wound infection systemic antibiotic treatment may be required together with debridement and topical antisepsis. Occlusive
dressings
in wound
healing
Currently available occlusive dressings include hydrocolloids (HCD), hydrogels (HG), foams and polyurethane films (PUF) (Table I). These dressings do not alter the wound flora such that endogenous infection is potentiated (vi& +a). They also provide a barrier to exogenous pathogens. Endogenous and exogenous infection is therefore minimized. Clinical trials show that wound infection rates using occlusive dressings are lower than those observed with conventional dressings. Occlusive dressings as bacterial barriers In-vitro studies of the polyurethane-backed HCDs, ‘DuoDERM’, ‘Comfeel Ulcus’ and ‘Dermiflex’ and the PUFs, ‘OpSite’ and ‘Tegaderm’ show that these dressings are bacteria-proof. By contrast, a non-woven fibre-backed HCD, ‘Biofilm’ is readily permeated by P. aeruginosa and S. aureus.25 Studies by Mertz, Marshall & Eaglstein,27 in which partial thickness wounds on pigs were challenged with 10’ S. aureus and P. aeruginosa, showed that no wound contamination was detected in wounds dressed with ‘DuoDERM’ even if repeatedly challenged. The in-vitro effectiveness of ‘OpSite’ was not confirmed. The authors suggest that as skin moves, channel formation occurs under ‘OpSite’ leading to bacterial contamination. The HG, ‘Vigilon’, also showed protection from S. aUYeUs in 50% of wounds but no protection from P. aeruginosa; however, no barrier function is claimed for this dressing. Preliminary work by Wilson, Burroughs & Dunn,72 using the HCDs ‘DuoDERM’ and ‘Dermiflex’, suggests that they are effective in preventing the spread of epidemic methicillin-resistant S. aUYeUs (MRSA). Seven patients with MRSA-contaminated ulcers were managed with these HCDs to prevent contamination of the wound environment. Distal sites of MRSA contamination were treated with antibacterial measures. Despite wound colonization with MRSA there was continued absence of this organism from the outer surface of the dressing. This important clinical finding has implications not only on the epidemiology of MRSA but also on the costs involved in barrier nursing. Clinical trial results Collated data from 50 controlled trials on a variety of wounds yielded infection rates of 5.37% and 3.25% (P
