Title
Modern exudate management: a review of wound treatments
Author(s)
Richard White
PhD
Senior Research Fellow, Tissue Viability, Grampian NHS Trust,
Aberdeen, Scotland, UK.
Email: Richard@medicalwriter.co.uk
Keith F. Cutting
RN, MN, MSc, PGCE
Principal lecturer, Buckinghamshire Chilterns University College,
Chalfont St Giles, Buckinghamshire, UK.
Keywords: wound exudate; exudate management.
Key Points
1. The appropriate management of wound exudate requires an understanding of
the underlying processes that lead to its production.
2. Exudate can present in a variety of forms, indicating the need to assess it by
volume, viscosity and colour.
3. The selection of management options should be based on the characteristics
of the wound and the needs of the patient.
4. Dressings may not always be the most appropriate option for exudate
management. Consideration should also be given to physical methods of
exudate control.
Heading 1
Abstract
Exudate must be effectively managed if the optimal moist environment necessary
for wound healing is to be created, and the surrounding skin protected from the
risks of maceration. To achieve these goals a detailed knowledge of dressing
materials and their performance is required. An understanding of the impact of
other treatments and co-morbidities on the production of exudate is also
necessary. Exudate management is relevant to patient quality-of-life issues as it
is often associated with leakage and malodour. It impacts on health economics
because failure to control exudate production will lead to increased management
costs and patient morbidity. This review considers exudate from the perspectives
of its nature, composition, assessment and the range of management strategies
available.
Heading 1
Introduction
The management of wound exudate requires the clinician to have an
understanding of what it is, why it is present and how to accurately monitor and
assess it.
The production of wound exudate occurs as a result of vasodilation during the
early inflammatory stage of healing under the influence of inflammatory
mediators such as histamine and bradykinin. It presents as serous fluid in the
wound bed and is part of normal wound healing in acute wounds.
However, when the wound becomes ‘chronic’ and non-healing with persistent,
abnormal inflammation or when infection becomes established, exudate takes on
a different guise and generates clinical challenges. In the chronic wound,
exudate contains proteolytic enzymes and other components not seen in acute
wounds (1). This type of exudate has justifiably been termed ‘a wounding agent
in its own right’ because it has the capacity to degrade growth factors and periwound skin and predispose to inflammation (2).
In order to develop an effective management approach, the clinician must be
able to accurately assess and understand the implications of the composition and
quantity of exudate present in the wound.
Heading 1
Exudate composition
Wound exudate was described by the Swiss physician Paracelsus (c1491-1541)
as nature’s balsam (3). It is derived from serum through the
inflammatory/extravasation process. Acute wound exudate contains molecules
and cells that are vital to support the healing process. It has a high protein
content (although lower than that found in serum), with a specific gravity greater
than 1.020. Its composition includes electrolytes, glucose, cytokines, leukocytes,
metalloproteinases, macrophages and micro-organisms (4). In the first 48 to 72
hours after wounding, platelets and fibrin may be present, but this reduces as
bleeding diminishes. See Table 1.
Table 1: Some constituents of exudate and their functions.
Component
Function
Fibrin
Clotting.
Platelets
Clotting.
Polymorphonuclearcytes (PMNs)
Immune defence, production of
growth factors.
Lymphocytes
Immune defence.
Macrophages
Immune defence, production of
growth factors.
Micro-organisms
Exogenous factor.
Plasma proteins, albumin, globulin,
Maintain osmotic pressure, immunity,
fibrinogen
transport of macromolecules.
Lactic acid
Product of cellular metabolism and
indicates biochemical hypoxia (5).
Glucose
Cellular energy source.
Inorganic salts
Buffering, pH hydrogen ion
concentration in a solution.
Growth factors
Proteins controlling factor-specific
healing activities.
Wound debris/dead cells
No function.
Proteolytic enzymes
Enzymes that degrade protein,
including serine, cysteine, aspartic
proteases and matrix
metalloproteinases (MMPs).
Tissue inhibitors of
Controlled inhibition of
metalloproteinases (TIMPS)
metalloproteinases.
As fluid passes through the inflamed vessel walls (extravasation) it may be seen
that wound exudate is in essence modified serum and will therefore contain
similar solutes. As it arrives at the wound surface, this fluid may be contaminated
with tissue debris and micro-organisms (4). Healing acute wounds produce
exudate containing active growth factors. These are not present in chronic
wounds (6).
Heading 1
Appearance of exudate
Modest amounts of thin, pale yellow or straw-coloured exudate in an acute
healing wound is considered normal. In chronic wounds, the colour, consistency
and amount of exudate may change as a result of various physiological
processes (4).
Table 2: Types of exudate, their appearance and significance (4).
Type
Colour
Consistency
Significance
Serous
Clear,
Thin, watery
Normal. Possibly a sign of infection. Some
straw-
bacteria produce fibrinolysins, which degrade
coloured
fibrin clots or coagulated plasma. Some strains of
Staphylococcus aureus, β-haemolytic group A
streptococci and Bacteroides fragilis, produce
fibrinolysins. Pseudomonas aeruginosa produces
a non-specific enzyme that degrades fibrin.
Fibrinous
Cloudy
Thin
Contains fibrin protein strands.
Serosanguinous
Clear,
Thin, watery
Normal.
pink
Sanguinous
Red
Thin, watery
Trauma to blood vessels.
Seropurulent
Murky,
Thicker,
Infection.
yellow,
creamy
creamcoffee
Purulent
Yellow,
Thick
grey,
Infection. Contains pyogenic organisms and
other inflammatory cells.
green
Haemopurulent
Dark,
Viscous,
Contains neutrophils, dead/dying bacteria and
blood-
sticky
inflammatory cells. This means an established
stained
infection is present. Consequent damage to
dermal capillaries leads to blood leakage.
Haemorrhagic
Red
Thick
Infection. Trauma. Capillaries are so friable they
readily break down and spontaneous bleeding
occurs. Not to be confused with bloody exudate
produced by over-enthusiastic debridement.
Footnote style
Adapted with permission from Cutting KF. Exudate: composition and functions. In: White RJ,
editor. Trends in Wound Care Volume III. London: Quay Books, 2004 (4).
Heading 1
Exudate volume
In chronic wounds the inflammatory response is altered owing to an uncontrolled
expression of inflammatory mediators with a concurrent increase in vascular
permeability and the amount of extravascular fluid. If the wound becomes
infected, an abrupt increase in exudate volume may be seen initially, followed by
further quantitative and qualitative changes. This has been attributed in part to
specific bacterial virulence mechanisms that result in vasodilation and
extravasation (7).
Gautam et al (2001) (8) have described a process whereby neutrophils attracted
to the site of injury trigger the release of heparin-binding protein (HBP). It has
also been shown that chronic leg ulcer exudate contains increased levels of HBP
when compared to acute wound fluid (9). It is likely that HBPs are implicated in
the production of increased exudate. Certain bacteria such as Pseudomonas
aeruginosa stimulate the release of HBP from neutrophils, thus aggravating
chronic inflammation by augmenting endothelial hyper-permeability (9).
Recent research has indicated that some bacteria actually express histamine and
thus, if present, produce an additional physiological source of histamine to the
wound environment. Morganella species, for example M. morganii Gramnegative rods have been found to express histamine (10). Bacteria isolated from
chronic wounds have been found to produce physiologically significant levels of
histamine (11) (12). It has yet to be determined if the production of this proinflammatory agent may be effectively managed through the application of
antihistamines.
The volume of exudate may be described using the terms shown in Table 3 (13).
Table 3: Exudate volumes and their effects (13).
Exudate
Effect
volume
None
Wound tissues dry.
Scant
Wound tissues moist.
Small
Wound tissues wet; moisture evenly distributed in wound; drainage
involves 25% of dressing.
Moderate
Wound tissues saturated; drainage may or may not be evenly
distributed in wound; drainage involves 25-75% of dressing.
Copious
Wound tissues bathed in fluid; drainage freely expressed.
Footnote style
Adapted with permission from Bates-Jensen BM. The Pressure Sore Status Tool a few thousand
assessments later. Adv Wound Care 1997; 10(5): 65-73 (13). AWAITING PERMISSION
Heading 1
Exudate assessment
Accurate assessment of the volume and viscosity of exudate will indicate
whether or not the healing is progressing normally (14).
Inspection of a dressing on removal may yield valuable information on the level
of exudate produced during dressing wear time. To assess the exudate volume
the healthcare practitioner should count the number of dressings used over a
time period, note the wear time for individual dressings, examine the dressing for
the presence of strikethrough (wet or dry), examine the peri-wound skin condition
and note any leakage (15).
Some of the subjectivity attached to exudate assessment can be reduced by
using a tool such as the exudate continuum (Figure 1) (16). This is integral to the
applied wound management approach described by Grey et al (16). This tool has
the potential to assist in the accurate assessment of exudate and lend support in
the decision-making process. It offers a method of generating a score relevant to
volume and viscosity.
For example, if a score of 4 is obtained using the exudate continuum (medium
volume 3, and low viscosity 1) and this increases to 8 (high volume 5, and
medium viscosity 3) over three days then the wound is likely to be deteriorating
and may be infected. If the intervention chosen is appropriate, for example an
absorbent antimicrobial dressing, then it is likely this will be reflected in a lower
score after a few days.
Figure 1: The wound exudate continuum (16). Chuck- this is being
redrawn
Footnote style
Reproduced with permission from Gray D, et al. Understanding applied wound management.
Wounds UK 2005 1(1): 62-8 (16). AWAITING PERMISSION
Heading 1.
Exudate management
Several wound management tools have been developed that include a focus on
exudate. One example is the wound bed preparation model (17) with the
development of the acronym TIME, in which ‘M’ represents the need to maintain
moisture balance (18).
An exudate management strategy has been devised by Vowden and Vowden
(2004) (19). This presents a strategy for assessing and evaluating the
management of exudate. See Table 4.
Table 4: An exudate management strategy (19).
Cause
Control
Components Containment Correction
Complications
●Systemic ●Whether ●Bacterial
●Dressing
●Modification
●Skin
(local
effective
load
seal
of bacterial
protection
wound
systemic
●Necrotic
Where?
load
●Protein loss
related).
or local
tissue
- at wound
●Debridement ●Pain
control is
● ‘Chemical’
surface
●Exudate
possible.
composition
- within
modification.
and pH
dressing
●Viscosity
- away from
and volume.
wound.
●Odour.
Footnote style
Reproduced with permission from Vowden K, Vowden P. The role of exudate in the healing
process: understanding exudate management. In: White RJ, editor. Trends in Wound Care
Volume III. London: Quay Books, 2004 (19).
The selection of management options should be based on the characteristics of
the wound and the needs of the patient. Successful management requires careful
attention and continuous evaluation throughout the lifetime of a wound (14). For
example, in the case of a leg ulcer, pressure ulcer or diabetic foot ulcer, exudate
levels in the non-infected wound are generally higher in the early stages of
healing and reduce as healing progresses. Dressing selection should therefore
be tailored to the condition of the wound. This might necessitate the use of an
absorbent moist dressing initially, changing to a moist dressing suitable for low
exudate levels at a later stage.
In wounds that become infected, exudate levels often increase and exudate can
become viscous. The focus here should be on managing the underlying cause of
infection.
Cavity wounds and other wounds left to heal by secondary intention that are
producing high levels of exudate may be suitable for treatment with topical
negative pressure. One method is vacuum-assisted closure (VAC), which can be
effective in removing viscous exudate (20) (21) (22).
Heading 1
Methods used to manage exudate
Heading 2
Dressings
If dressings are indicated, then prudent selection and careful determination of
wear time are imperative. This will help ensure an optimal moist environment is
maintained, while protecting the surrounding skin from maceration (23) (24).
Certain key performance characteristics are required for any such dressing: they
must absorb and retain exudate, keep harmful chronic wound exudate away from
the surrounding skin, perform efficiently when used under compression, be easy
to remove and be demonstrated as cost-effective.
Wound dressings exhibit various fluid-handling mechanisms: absorption, gelling,
retention and moisture vapour transmission. Information on a dressing’s fluidhandling mechanism is available from the manufacturers. This information may
not always be based on accepted, independent test methodologies, but rather on
in-house laboratory data, which is invariably favourable to manufacturers’ own
products. There are standard test methods, published as monographs in various
pharmacopoeias and in peer-reviewed journals that provide independent,
objective data on dressing fluid handling (25).
The basic dressing mechanisms are as follows:
Heading 3
Absorption Exudate is absorbed into the dressing matrix. In the case of some
foam dressings, this is a reversible mechanism; the fluid can be expressed from
the dressing under pressure. Not all foams behave in this fashion.
Heading 3
Gelling Following absorption, the exudate interacts with the dressing material to
form a gel (26). This is a typical attribute of alginates: these carbohydrate
polymers gel according to the proportion of uronic acid units in their composition
(27). However, with alginate gels, fluid may come into contact with the periwound skin (27). This can also occur with hydrocolloid gel, the degree being
dependent on polymer composition (28).
Heading 3
Fluid retention In dressings with this mechanism, fluid is absorbed by the
dressing and is no longer available to wet the skin. Such materials retain the
absorbed fluid directly above the wound, without sideways spread or ‘lateral
wicking’. An example of this technology is the hydrofibre. Such dressings have
been demonstrated to be clinically and cost-effective in exudate management,
even when used under compression (29) (30).
Heading 3
Moisture vapour transmission In recent years dressings have been designed
to absorb fluid and, via an intermediate ‘wicking’ layer, move fluid away from the
wound/skin interface towards a permeable backing layer. Here, some fluid is lost
to the atmosphere by evaporation, a process known as moisture vapour
transmission. This mechanism is intended to increase the fluid-handling capacity
of the dressing (31) (32). The success of this process depends upon the
proportion of absorbed fluid that is lost. Evaporation will be compromised by the
presence of occluding materials, such as compression bandages, which may
reduce evaporation rates. There are no clinical data to suggest that this works in
practice. Indeed, some clinicians are sceptical that it has any performanceenhancing value (33).
Heading 3
Antimicrobial properties Dressings with an antimicrobial component are
intended for the control of the wound bioburden in critical colonisation and local
infection (34). These dressings are useful, therefore, where raised exudate levels
are attributed to bacterial causes. There is also justification for their use in cases
of spreading infection where systemic antibiotics have been used and impaired
perfusion is suspected (35) (36). Typical antimicrobial dressings are those
containing silver, iodine or honey (12) (35) (37).
Heading 2
Physical therapies
Heading 3
Topical negative pressure therapy Suction drainage of wounds has been used
for many years (38), and a variety of systems exist, including vacuum-assisted
closure (VAC) therapy (39) (40) (41) (42). The VAC closed system is claimed to
improve perfusion, reduce oedema and promote granulation tissue formation and
is supported by evidence from many wound types, including trauma wounds,
pressure ulcers, leg ulcers and surgical wounds (43) (44). The removal of
exudate, particularly the more viscous forms, also removes bacteria and
protease enzymes – both barriers to healing. This technique does, however,
have disadvantages, and should not be used on wounds containing eschar or
necrotic tissue.
Heading 3
Compression In the healthy limb, the return of venous blood to the heart is
achieved through the combined actions of the calf muscle pump and the foot
pump, both of which require reasonable mobility and dorsiflexion of the ankle
(45). Where venous ulceration occurs, the patient needs assistance in achieving
venous blood return. Compression bandaging and intermittent pneumatic
compression therapy have both been found to be effective (46) (47).
Compression therapy has two main functions: to counteract venous hypertension
and to control oedema (48). In achieving these functions, exudate is reduced in
the non-infected venous leg ulcer (49) (50). In lymphoedema the application of
appropriate compression bandages or garments will result in a reduction both of
the limb oedema and of any exudate leakage (51) (52).
Intermittent pneumatic compression therapy is administered through a bootshaped device which, by means of a pump, is inflated and deflated to achieve
alternating, dynamic compression of the encased limb. IPC can be used as the
main method of compression or as an adjunct to orthodox compression
bandaging (53).
Heading 3
Elevation/exercise In venous leg ulceration, the patient is advised to elevate the
affected limb (with the ankle above the level of the heart) to achieve venous
blood return. While this may not always be practical, some degree of elevation
will aid venous return and, consequently, reduce exudate. In lymphoedema,
manual drainage (54) and exercise (54) (55) are central to the control of oedema
and leakage.
Heading 1
Conclusion
It is an unfortunate aspect of wound management that exudate is often regarded
as an issue only when it becomes a clinical challenge - when leakage occurs or
when peri-wound skin becomes macerated (56). However, such events are due
to a combination of inaccurate assessment, inappropriate dressing selection,
over-optimistic wear time or poor patient concordance. When dealing with
purulent exudate, clinicians sometimes resort to using absorbent pads, taped in
position and changed frequently. While dressings remain the mainstay of
treatment, not all are suitable or effective for exudate management.
Effective clinical management of exuding wounds depends on accurate
assessment of the volume and viscosity of exudate, an understanding of relevant
pathologies and the selection of an appropriate exudate management
mechanism. This is all too often left to a dressing, without due consideration for
other approaches.
A focus on this aspect of wound care has the potential to reduce morbidity and
costs, and is therefore justified.
References
Article
1. Vickery C. Exudate: what is it and what is its function? In: Cherry GW, Harding
K, editors. Management of wound exudate: Abstracts from the first combined
meeting of the European Tissue Repair Society and the European Wound
Management Association at Green College, University of Oxford. ETRS Bulletin
1997.
Article
2. Trengove NJ, Bielefeldt-Ohmann H, Stacey MC. Mitogenic activity and
cytokine levels in non-healing and healing chronic leg ulcers. Wound Rep Regen
2000; 8(1): 13-25.
Book
3. Haeger K. The Illustrated History of Surgery. London: Harold Starke, 1989.
Book
4. Cutting KF. Exudate: composition and functions. In: White RJ, editor. Trends in
Wound Care Volume III. London: Quay Books, 2004.
Article
5. Trengove NJ, Langton SR, Stacey MC. Biochemical analysis of wound fluid
from non-healing and healing chronic leg ulcers. Wound Rep Regen 1996; 4:
234-9.
Pubmed
6. Baker EA, Leaper DJ. Proteinases, their inhibitors and cytokine profiles in
acute wound fluid. Wound Repair Regen 2000; 8(5): 392-8.
Article
7. Wilson JW, Schurr MJ, LeBlanc CL, Ramamurthy P, Buchanan KL, Nickerson
CA. Mechanisms of bacterial pathogenicity. Postgrad Med J 2002; 78: 216-24.
Pubmed
8. Gautam N, Olofsson AM, Herwald H, Iversen LF, Lundgren-Akerlund E,
Hedqvist P, et al. Heparin-binding protein (HBP/CAP37): a missing link in
neutrophil-evoked alteration of vascular permeability. Nat Med 2001; 7(10): 11237.
Pubmed
9. Lundqvist K, Herwald H, Sonesson A, Schmidtchen A. Heparin binding protein
is increased in chronic leg ulcer fluid and released from granulocytes by secreted
products of Pseudomonas aeruginosa. Thromb Haemost 2004; 92(2): 281-7.
Pubmed
10. Kim SH, An H, Field KG, Wei CL, Velazquez JB, Ben-Gigirey B, et al.
Detection of Morganella morganii, a prolific histamine former, by the polymerase
chain reaction assay with 16S rDNA targeted primers. J Food Prot 2003; 66(8):
1385-92.
Pubmed
11. McDermott C, Mylotte JM. Morganella morganii: epidemiology of bacteraemic
disease. Infect Control 1984; 5(3): 131-7.
Article
12. Cooper RA, Morwood S, Burton N. Histamine production by bacteria isolated
from wounds. J Infect 2004; 49: 39.
Pubmed
13. Bates-Jensen BM. The Pressure Sore Status Tool a few thousand
assessments later. Adv Wound Care 1997; 10(5): 65-73.
Pubmed
14. Thomas S. Assessment and management of wound exudate. J Wound Care
1997; 6(7): 327-30.
Pubmed
15 Mulder GD. Quantifying wound fluids for the clinician and researcher. Ostomy
Wound Manage 1994; 40(8): 66-9.
Article
16. Gray D, White R, Cooper P, Kingsley A. Understanding applied wound
management. Wounds UK 2005; 1(1): 62-8.
Pubmed
17. Sibbald RG, Williamson D, Orsted HL, Campbell K, Keast D, Krasner D, et al.
Preparing the wound bed: debridement, bacterial balance, and moisture balance.
Ostomy Wound Manage 2000; 46(11): 14-35.
Book
18. Dowsett C, Ayello E. TIME: principles of chronic wound bed preparation and
treatment. In: Cutting KF, editor. Trends in Wound Care Volume IV. London:
Quay Books, 2005.
Book
19. Vowden K, Vowden P. The role of exudate in the healing process:
understanding exudate management. In: White RJ, editor. Trends in Wound Care
Volume III. London: Quay Books, 2004.
Pubmed
20. Armstrong DG, Lavery LA, Diabetic Foot Study Consortium. Negative
pressure wound therapy after partial diabetic foot amputation: a multicentre,
randomised controlled trial. Lancet 2005; 366(9498): 1704-10.
Pubmed
21. Lambert KV, Hayes P, McCarthy M. Vacuum-assisted closure: a review of
development and current applications. Eur J Vasc Endovasc Surg 2005; 29(3):
219-26.
Pubmed
22. Venturi ML, Attinger CE, Mesbahi AN, Hess CL, Graw KS. Mechanisms and
clinical applications of the vacuum-assisted closure (VAC) device: a review. Am J
Clin Dermatol 2005; 6(3); 185-94.
Pubmed
23. Bishop SM, Walker M, Rogers AA, Chen WY. Importance of moisture
balance at the wound-dressing interface. J Wound Care 2003; 12(4): 125-8.
Pubmed
24. Bolton LL, Monte K, Pirone LA. Moisture and healing: beyond the jargon.
Ostomy Wound Manage 2000; 46(1A Suppl): 51S-62S. Erratum in Ostomy
Wound Manage 2000; 46(3): 9.
Pubmed
25. Thomas S, Fram P. The development of a novel technique for predicting the
exudate handling properties of modern wound dressings. J Tissue Viability 2001;
11(4): 145-60.
Pubmed
26. Thomas S, Hay NP. Fluid handling properties of hydrogel dressings. Ostomy
Wound Manage 1995; 41(3): 54-9.
Article
27. Thomas S. Observations on the fluid handling properties of alginate
dressings. Pharm J 1992; 248: 850-1.
Article
28. Thomas S, Loveless P. A comparative study of the properties of six
hydrocolloid dressings. Pharm J 1991; 247: 672-5.
Pubmed
29. Armstrong SH, Ruckley CV. Use of a fibrous dressing in exuding leg ulcers. J
Wound Care 1997; 6(7): 322-4.
Pubmed
30. Guest JF, Ruiz FJ, Mihai A, Lehman A. Cost effectiveness of using
carboxymethylcellulose dressing compared with gauze in the management of
exuding leg ulcers in Germany and the USA. Curr Med Res Opin 2005; 21(1):
81-92.
Pubmed
31. Erasmus ME, Jonkman MF. Water vapour permeance: a meaningful
measure for water vapour permeability of wound coverings. Burns 1989; 15(6):
371-5.
Pubmed
32. Palamand S, Reed AM, Weimann LJ. Testing intelligent wound dressings. J
Biomater Appl 1992; 6(3): 198-215.
Article
33. Vowden K. Wound management: The considerations involved in dressing
selection. Nurs Prescr 2004; 2(4): 152-61.
Pubmed
34. Kingsley A. The wound infection continuum and its application to clinical
practice. Ostomy Wound Manage 2003; 49(7A Suppl): 1-7.
Article
35. White RJ, Cooper RA, Kingsley A (2001). Wound infection and microbiology:
the role of topical antimicrobials. Br J Nurs 10(9); 563-78.
Pubmed
36. Frank C, Bayoumi I, Westendorp C. Approach to infected skin ulcers. Can
Fam Physician 2005; 51: 1352-9.
Article
37. White RJ, Cutting KF, Cooper RA, Kingsley AR. The use of topical
antimicrobials to control wound bioburden. Ostomy Wound Manage 2006; in
press.
Pubmed
38. Maitland AI, Mathieson AJ. Suction drainage: a study in wound healing. Br J
Surg 1970; 57(3): 193-7.
Pubmed
39. Edlich RF, Haines PC, Pearce RS, Thacker JG, Rodeheaver G. Evaluation of
a new, improved surgical drainage system. Am J Surg 1985; 149(2): 295-8.
Pubmed
40. Smith SR, Gilmore OJ. Surgical drainage. Br J Hosp Med 1985; 33(6): 30815.
Pubmed
41. Ritter MA, Fechtman RW. Closed wound drainage systems: the Stryker
Constavac versus the Snyder Hemovac. Orthop Rev 1988; 17(5): 496-8.
Pubmed
42. Zerbe M, McArdle A, Goldrick B. Exposure risks to the management of three
wound drainage systems. Am J Infect Control 1996; 24(5): 346-52.
Pubmed
43. Banwell PE, Teot L. Topical negative pressure (TNP): the evolution of a novel
wound therapy. J Wound Care 2003; 12(1): 22-8.
Article
44. Moore K. VAC therapy: interactions in the healing process. Wounds UK
2005; 1(1): 86-90.
Article
45. Vowden K, Vowden P. Anatomy, physiology and venous ulceration. J Wound
Care 1988; 7(7 Suppl): S1-S7.
Pubmed
46. Douglas WS, Simpson N. Guidelines for the management of chronic venous
leg ulceration. Report of a multidisciplinary workshop. British Association of
Dermatologists and the Research Unit of the Royal College of Physicians. Br J
Dermatol 1995; 132(3): 446-52.
Article
47. NHS Centre for Review and Dissemination, University of York. Compression
therapy for venous leg ulcers. Effective Healthcare 1997; 3(4): 1-12.
Pubmed
48. Felty CL, Rooke TW. Compression therapy for chronic venous insufficiency.
Semin Vasc Surg 2005; 18(1): 36-40.
Pubmed
49. Burton CS. Venous ulcers. Am J Surg 1994; 167(1A): 37S-40S.
Pubmed
50. Brem H, Kirsner RS, Falanga V. Protocol for the successful treatment of
venous ulcers. Am J Surg 2004; 188(1A Suppl): S1-S8.
Pubmed
51. O’Brien JG, Chennubhotla SA, Chennubhotla RV. Treatment of edema. Am
Fam Physician 2005; 71(11): 2111-17.
Pubmed
52. Cheville AL, McGarvey CL, Petrek JA, Russo SA, Taylor ME, Thiadens SR.
Lymphedema management. Semin Radiat Oncol 2003; 13(3): 290-301.
Pubmed
53. Vowden K. The use of intermittent pneumatic compression in venous
ulceration. Br J Nurs 2001; 10(8); 491-509.
Pubmed
54. Szuba A. Literature watch. The addition of manual drainage to compression
therapy for breast cancer related lymphoedema: a randomized controlled trial.
Lymphat Res Biol 2005; 3(1): 36-41.
Pubmed
55. Badger C, Preston N, Seers K, Mortimer P. Physical therapies for reducing
and controlling lymphoedema of the limbs. Cochrane Database Syst Rev 2004;
18(4): CD003141.
Pubmed
56. Cutting KF, White RJ. Avoidance and management of peri-wound maceration
of the skin. Professional Nurse 2002; 18(1): 33-6.