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JOURNAL OF WOUND CARE VOL 11, NO 7, JULY 2002 275
References
1 Anderson, K.N. (Ed.)
Mosby’s Medical Nursing
and Allied Health
Dictionary. St. Louis,
Mosby-Year Book Inc, 1998.
2 Charcot, J.M. On
Diseases of the Nervous
System.Translated by
Sigerson, G. New Sydenham
Society 1877; 63: 126.
3 Falanga,V.Wound bed
preparation for optimal use
of advanced therapeutic
products. www.bu.edu/
woundbiotech/woundcare/
Woundbedpr.html; 2000,
accessed 24 April 2002.
4 Cocke,W.M.,White, R.R.,
Lynch, D.J. ,Verheyden, C.N.
Wound Care. New York:
Churchill Livingstone, 1984.
5 Harding, K.G., Hughes,
L.E., Marks, J.A guide to the
practical management of
granulating wounds. Cardiff:
Department of Surgery,
University of Wales, College
of Medicine/Dow Corning
Valbonne Cedex, 1986.
6 Jordan, M.M., Clark, M.
Report on Incidence of
Pressure Sore in the
Patient Community of the
Greater Glasgow Health
Board Area. Glasgow:
University of Strathclyde,
21 January 1977.
Maceration of the skin and wound
bed 1: its nature and causes
Maceration, caused by prolonged exposure to moisture, can complicate the healing
of wounds, especially chronic ones. This paper — the first of three reviewing the
literature on its aetiology and management — looks at how maceration occurs
healthy wounds; chronic wounds; exudate; transudate; transepidermal water loss; oedema
Keith F. Cutting, MN,
RGN, RMN, Dip N
(Lond), Cert Ed,
Principal Lecturer,
Buckinghamshire
Chilterns University
College, Newland Park,
Chalfont St Giles, UK
Email
kcuttin01@bsuc.ac.uk
Richard J White, PhD,
Clinical research
consultant, Medical
Communications,
Highbury,Whitstone, UK.
Email
info@medicalwriter.co.uk
▲
M
aceration (from the Latin maceratio —
to make wet/soften) is defined as the
softening and breaking down of skin
resulting from prolonged exposure to
moisture.
1
Originally described by
Charcot in 1877
2
it occurs typically in and around
the wound bed in acute and chronic wounds. Macer-
ation can complicate the healing of chronic wounds.
Healthy, non-macerated wound
Perversely, comprehensive descriptions of healthy
wounds are difficult to come by, as many focus on
features that identify an unhealthy state. Currently,
clinicians are concentrating on priming the
wounded tissue to provide optimal conditions
for healing — ‘wound bed preparation’,
3
although
the characteristics that hinder healing, necessitat-
ing removal from the wound i.e. infection,
necrotic/fibrous tissue and exudate, are addressed.
A definitive description of how a healthy wound
should appear once these impediments to healing
have been addressed is not included.
3
One is
tempted to ask: if you don’t know where you are
going how do you know you have got there?
Cocke et al
4
state that healthy granulation tissue
has a fine, granular surface and is red with a velvety
texture, a definition that many still accept as accu-
rate. Harding et al
5
offer a more comprehensive
description of a healthy wound: ‘A healthy wound
is neither inflamed nor inert in appearance, not
painful or tender to touch, has no excessive dis-
charge and does not bleed on light pressure; it heals
without interruption at a fairly predictable rate.
However, the process of repair in an open wound is
complex and individuals differ in the way their tis-
sues react to injury. The extent of normal variation
in wound appearance should be learnt to avoid
unnecessary anxiety or intervention.’
Causes of maceration
Maceration is caused by excessive amounts of aque-
ous fluid in contact with the skin or wound surface
for extended periods. This fluid may be produced by
the wound itself (exudate), or may be a result of uri-
nary incontinence
2
, excessive sweating, or water
lost through the skin by the process of transepider-
mal water loss (TEWL).
Excessive exposure to moisture causes deteriora-
tion of a wound and may lead to skin break-down.
A strong relationship exists between excessive skin
moisture, regardless of source and the development
of pressure ulcers.
6,7
Cochrane
8
states that ‘skin
should be kept clean and dry to prevent maceration.
Damp skin breaks down more easily under axial
pressure and shear forces.’
Composition of wound exudate
Transudates and exudates are serum derivatives.
9
A
transudate (an ultrafiltrate of blood) has a low pro-
tein content, with a specific gravity of less than
1.020. The presence of a transudate implies a non-
inflammatory source of the fluid, such as increased
hydrostatic pressure that exceeds oncotic pressure.
Exudates have a high protein content and a spe-
cific gravity greater than 1.020. They contain
inflammatory components, such as leukocytes, fib-
rinogen, fibrin, and will thus promote clotting.
10
Exudate varies in appearance and composition
according to the aetiology and condition of the
wound. It is normally a pale straw colour and
watery in appearance but may become discoloured
and viscous in the presence of infection. Different
types of exudate may be seen in Box 1.
11-13
Exudate (serous) is not per se a bad thing, as it pro-
vides essential nutrients for epithelial cells, facili-
tates the ingress of white cells and provides the
moist environment so important for healing. The
normal response to healing, inflammation, leads to
the development of local oedema. Histamine
released from damaged cells as a result of wounding
causes plasma leakage from blood vessels. As a con-
sequence oedema forms in the adjacent tissues.
This fluid, exudate, that seeps from the wound
surface is initially a clear, serous liquid. Later this
liquid may become more viscous and opaque due to
leukocytes and other constituents such as albumin,
macrophages and cellular debris. Although there is
limited understanding of exudate, Thomas
14
lists
7 Thyagarajan, C., Silver, J.R.
Aetiology of pressure sores
in patients with spinal cord
injury. BMJ 1984; 289:
1487-1490.
8 Cochrane, G. The
Severely Disabled. In: Bader,
D.L. (Ed.) Pressure Sores
— Clinical Practice and
Scientific Approach.
London: Macmillan, 1990.
9 Price, S.A.,Wilson, L.M.
Pathophysiology. 4th
Edition. St Louis, Mo:
Mosby, 1992.
10 Vickery, C. 1997.
Exudate — what is it and
what is its function in acute
and chronic wounds? In:
(Eds) Cherry, G., Harding,
K. Management of Wound
Exudate. Proceedings Joint
Meeting European Wound
Management Association
and European Tissue Repair
Society. London: Churchill
Communications, 1997.
11 Chen, J. Aquacel
hydrofibre dressing: the
next step in wound
dressing technology.
Monograph. London:
ConvaTec, 1998.
12 Harding, K. Is exudate a
clinical problem? In: (Eds)
Cherry, G., Harding, K.
Management of Wound
Exudate. Proceedings Joint
Meeting European Wound
Management Association
and European Tissue Repair
Society. London: Churchill
Communications, 1997.
13 Cooper, R.M. Personal
communication to the
authors: 25 April, 2002.
14 Thomas, S. 1997.
Exudate — Who Needs It?
Proceedings Joint Meeting,
European Wound
Management Association
and European Tissue
Repair Society.
Management of Wound
Exudate. London: Churchill
Communications, 1997.
15 Dale, J. 1995.The
anatomy and physiology of
the circulation of the leg.
In: (Eds.) Callum, M., Roe, B.
Leg Ulcers Nursing
Management. London:
Scutair Press, 1995.
16 Dale J. 1995.The
aetiology of leg ulceration.
In: (Eds.) Callum, M., Roe, B.
Leg Ulcers Nursing
Management. London:
Scutair Press, 1995.
17 Lamke, L. Nilsson, G.E.,
Reithner, H.L.The
evaporative water loss
from burns and water
permeability of grafts and
artificial membranes used
in the treatment of burns.
Burns 1997; 3: 159-165.
some of the factors that may influence its produc-
tion (Box 2), citing observations by others.
15-19
Acute wound exudate
Acute wound exudate has been shown to differ
from that produced by chronic wounds. Although
acute wound exudate contains metalloproteinases,
they are inactive (pro-enzyme stage) and chronic
wound fluid contains a greater variety of these
enzymes in higher concentrations.
20
Additionally,
in acute wounds α1-antitrypsin-degrading enzymes
are absent but present in chronic wounds. Likewise
polymorphonuclearcyte (PMN) elastase levels are
normal and fibronectin remains intact in acute
wounds but in chronic wounds PMN elastase levels
are high and fibronectin is degraded.
21
Chronic wound exudate
Qualitative differences have been identified
between exudates from acute and chronic
wounds.
22-26
Chronic wound exudate is predomi-
nantly blood serum with most platelets and ery-
throcytes removed: it is, however, enriched with
white blood cells.
14
These serve as a source of pro-
teases, particularly matrix metalloproteinases
(MMPs); enzymes which by definition break down
protein and may actively damage what may be oth-
erwise healthy tissue.
24
This has led to chronic
wound fluid being regarded as a ‘wounding agent’
in its own right.
11
MMPs and plasminogen activators are endoge-
nous extracellular matrix-degrading enzymes found
in exudate. Their purpose is to remove fibrin and
eschar from the wound.
20,23,27
In the normal,
healthy healing situation MMPs are regulated by
naturally occurring endogenous inhibitors known
as tissue inhibitors of metalloproteinases —
TIMPs.
28
This aspect of chronic wound pathophysi-
ology has led to a greater understanding of how
exudate can lead directly to wound enlargement, by
enzymatic degradation of exposed ‘healthy’ skin, if
not controlled adequately. Furthermore, it has
resulted in therapies that may be used to treat
chronic wounds.
29
Clinical implications
When a wound deteriorates, as is the case when
infected, it may exhibit an increase in level of exu-
date production (appearance/content continuum).
Clothes or bedclothes may become soiled, there
may be a change in odour and dressings may
require more frequent change, or may leak.
If a wound with moderate or higher levels of exu-
date is inappropriately dressed, then exudate-medi-
ated maceration is a likely outcome. Chronic
wounds such as leg ulcers, pressure ulcers and dia-
betic foot ulcers will exhibit this if the dressing can-
not cope with exudate output or if the dressing
wear time is too long. This maceration is generally
evident as an opaque or white ‘soggy’ area of peri-
ulcer skin that occurs when the wound is moder-
ately to heavily exuding. It is most evident where
there is thick calloused skin, as is typical around
plantar ulcers. Maceration of the wound bed does
occur occasionally, but after searching the litera-
ture, a definitive description to assist clinical identi-
fication could not be found. It would be reasonable
to presume that maceration of the wound bed is less
obvious to the eye than peri-wound skin or callus
maceration.
Increased levels of wound exudate are conducive
to bacterial wound colonisation.
30
The risk is proba-
bly increased in wounds that are not appropriately
managed. However, despite the possibility of non-
occlusive dressings becoming soaked with exudate
and thereby providing access for bacteria, there is
little evidence to support the theory that infection
risk is increased. When macerated tissue is present
and becomes infected it is most likely to be caused
by organisms that prefer an environment with high
water activity, e.g. Staph Aureus, and thereby thrive
in tissues with a high water content.
31
Water, skin and the permeability barrier
It has already been stated that maceration is not
always due to exudate; other aqueous liquids such
as water and urine also have this effect. The effect of
water is particularly evident in hand burns treated
with occlusive gloves.
32
The water is derived from
normal transepidermal water, lost by insensible
transpiration through the normal epidermis
(transepidermal water loss or TEWL). To understand
this concept better, it is necessary to look at the
water permeability barrier in the skin and its func-
276 JOURNAL OF WOUND CARE VOL 11, NO 7, JULY 2002
Box 1. Different types of exudate and
their contents
Serous: Clear, watery consistency. May be a sign of
infection as some bacteria produce fibrinolysins,
enzymes which degrade fibrin clots or coagulated
plasma. Some strains of S. aureus, b-haemolytic group
A streptococci, B. fragilis produce fibrinolysins and P.
aeruginosa produces a non-specific enzyme that
degrades fibrin
13
Fibrinous: Cloudy, contains fibrin protein strands.
Purulent: Pyogenic organisms and other
inflammatory cells.
Haemo-purulent: Contains neutrophils, dead/dying
bacteria and inflammatory cells i.e. established
infection is present. Consequent damage to dermal
capillaries leads to blood leakage.
Haemorrhagic: Capillaries have become so friable
that they easily break down and spontaneous, copious
bleeding occurs. Blood is the major component of this
type of exudate. Not to be confused with bloody
exudate as a result of over enthusiastic debridement.
education
education
tion. It is now accepted that the main functional
component of the barrier is the stratum compactum,
the lowermost layer of the stratum corneum.
33
The barrier serves to restrict the loss of water
through intact skin to a level commensurate with
functional needs and to reduce the ingress of
unwanted materials from the environment. The
region above (exterior) to the compactum is the
stratum disjunctum. It comprises porous, dead cells
in the process of desquamation. These cells contain
hygroscopic materials such as pyrrolidone car-
boxyic acid, sodium chloride, etc, that readily
absorb water. This maintains the plasticity/pliabil-
ity of a normal healthy stratum corneum.
The thickened disjunctum of palmar and plantar
surfaces will absorb water and thicken further, cre-
ating the characteristic wrinkling seen when a per-
son spends too long in the bath. This is the visible
evidence of early maceration. When normal,
healthy skin is occluded, as might be the case with
kitchen film, the TEWL fluid passes through the
epidermal barrier and causes swelling of the dis-
junctum (Fig 1). Removal of the occluding agent
rapidly reverses the excess hydration as evaporation
to the air occurs.
This is not evidence against occlusion; most mod-
ern dressings are not totally occlusive. Some, for
example the hydrocolloids, have sufficient capacity
to absorb and retain transepidermal water loss over
a wear time of seven days. It is the normal evapora-
tion of relatively small quantities of water through
intact skin, and not to be confused with sweating,
transudate or exudate.
Other dressings such as hydropolymer foams
have a high moisture vapour transmission rate
(MVTR); this is a novel physical mechanism for
dressing fluid handling. It involves the absorption
and evaporation of exudate by the dressing, rather
than absorption alone. Fluid is absorbed into the
hydropolymer and from there into a wicking layer.
From here it is able to pass into the air via the back-
ing polyurethane layer.
34
Maceration around the wound
When the skin around a wound is exposed to exu-
date the disjunctum initially absorbs fluid and
swells. Further fluid leads to saturation of the com-
pactum and reduced barrier function. Without bar-
rier protection, the living cells of the epidermis are
next to suffer from over-hydration, hence skin
breakdown follows untreated maceration.
Maceration is most likely to occur in chronic
wounds such as leg ulcers, pressure ulcers, diabetic
foot ulcers, fungating wounds and burns, particu-
Box 2. Factors that may influence exudate production
14
Biochemical changes, Histamine and vasoactive amines give rise to increased vascular permeability
eg with an effect on and extravasation in the inflammatory stage
capillary permeability
Gender An unsubstantiated observation that males produce more exudate than women
14
Hydrostatic pressure Posture,
15
Venous hypertension
16
Temperature Associated with capillary dilation
Type of dressing and Hygroscopic (Mesalt), debriding agents dressing providing
topical treatment back pressure, iodinated dressings
Wound depth and Generally, the deeper the wound the greater the production of exudate. However, in
surface area burns the exudate production remains more or less constant in relation to surface area
17
Wound infection Some bacteria induce vascular permeability. It is recognised that a sudden increase in
exudate may be a response to infection
18
Wound type Exudate production may vary with the type of wound and stage of healing
17,19
JOURNAL OF WOUND CARE VOL 11, NO 7, JULY 2002 277
18 Gilchrist, B.Wound
Infection. In: (Eds.) Miller,
M., Glover, D.Wound
Management Theory and
Practice London: Emap
Healthcare, 1999.
19 Thomas, S., Fear, M.,
Humphreys, J. et al.The
effect of dressings on the
production of exudate
from venous leg ulcers.
Wounds 1996; 8: 5, 145-150.
20 Wysocki,A.B.Wound
fluids and the pathogenesis
of chronic wounds.
JWOCN 1996; 23: 283-290.
21 Rao, C.N., Ladin, D.A.,
Liu,Y.Y. et al.Alpha1-
Antitrypsin is degraded and
non-functional in chronic
wounds but intact and
functional in acute wounds:
the inhibitor protects
fibronectin from
degradation by chronic
wound fluid enzymes. J
Investig Dermatol 1995;
105: 4, 572-578.
22 Chen,W.Y., Rogers,
A.A., Lydon, M.J.
Characterisation of biologic
properties of wound fluid
collected during early
stages of wound healing. J
Invest Dermatol 1992; 99:
5, 559-564.
23 Rogers,A. Burnett, S.,
Moore, J.C. et al.
Involvement of proteolytic
enzymes — plasminogen
activators — in the
pathophysiology of
pressure ulcers.Wound
Repair Regen 1995; 3: 3,
273-283.
24 Trengove, N., Langton,
S.R., Stacey, M.C.
Biochemical analysis of
wound fluid from non-
healing and healing chronic
leg ulcers.Wound Rep
Regen 1996; 4: 234-239.
25 Trengove, N.J., Stacey,
M.C., McAuley, S. et al.
Analysis of acute and
chronic wound
environments: the role of
proteases and their
inhibitors.Wound Repair
Regen 1999; 7: 6, 442-452.
26 Buchan, I.,Andrews, J.K.,
Lang, S.M. et al. Clinical and
laboratory investigations of
the composition and
properties of human skin
wound exudate under
semi-permeable dressings.
Burns 1980; 7: 326-334.
27 Ravanti, L., Matti-Kahari,
V. Matrix metalloproteinases
in wound repair (Review).
Int J Mol Med 2000;
6: 391-407.
▲
Fig 1. A cross-section of the skin
stratum disjunctum
stratum compactum
{
stratum corneum
education
28 Brew, K.,
Dinakarpandian, D., Nagase,
H.Tissue inhibitors of
metalloproteinases:
evolution, structure and
function. Biochim et
Biophys Acta 2000; 1477:
267-283.
29 Cullen, B, Smith, R.,
McCulloch, E. et al.The
mechanism of action of
Promogran, a proteinase
modulating matrix.Wound
Repair Regen 2002; 10: 1,
16-25.
30 Armstrong, S.H.,
Ruckley, C.V. Use of a
fibrous dressing in exuding
leg ulcers. J Wound Care
1997; 6: 7, 322-324.
31 Troller, J.A., Stinson, J.V.
Influence of water activity
on the production of
extracellular enzymes by
Staphylococcus aureus.
Appl Environ Microbiol
1978; 35: 3; 521-526.
32 Terrill, P.J., Kedwards,
S.M ., Lawrence, J.C. The
use of Gore-Tex bags for
hand burns. Burns 1991; 17:
2; 161-165.
33 Bowser, P.A.,White, R J.
Isolation, barrier properties
and lipid analysis of stratum
compactum, a discrete
region of the stratum
corneum. Brit J Dermatol
1985; 112: 1-14.
34 Schultze, H.-J., Lane, C.,
Charles, H. et al. Evaluating
a superabsorbent
hydropolymer dressing for
exuding venous leg ulcers. J
Wound Care 2001; 10: 1,
511-520.
35 Nelson,A. Is Exudate a
Clinical Problem. In: (Eds.)
Cherry, G., Harding, K.
Proceedings, Joint Meeting,
European Wound
Management Association
and European Tissue Repair
Society. Management of
Wound Exudate. London:
Churchill Communications
Europe, 1997.
36 Bolton, L.L., Monte, K.,
Pirone L.A. Moisture and
healing: beyond the jargon.
Ost Wound Man 2000; 46:
1A (Suppl), 51S-62S.
37 Scheuplein, R.J.
Mechanisms of percutaneous
absorption. 1 Routes of
penetration and the influence
of solubility. J Invest Dermatol
1965; 45: 334-346.
38 Blank, I.H.The effect of
hydration on the
permeability of the skin. In:
(Eds.) Bronaugh, R.L.,
Maibach, H.I. Percutaneous
Absorption — Mechanisms
— Methodology — Drug
Delivery. New York: Marcel
Dekker Inc, 1985.
larly where occlusive therapy is used inappropri-
ately. For example, patients who are bed-ridden and
are incontinent of urine are at risk of developing
lesions on the buttocks or sacrum; in obese individ-
uals lesions may occur between folds of skin, for
example sub mammary intertrigo. Nelson
35
has
indicated that when maceration occurs this may
lead to an increase in the overall size of the lesion
with excoriation and pain. Additional conse-
quences for the patient are: longer treatment time,
added discomfort, modified treatment regime and
uncertainty about wound progress. For the health
service provider increased costs result from longer
treatment time and additional material resources, as
well as possible increased staff costs.
In the healing wound, the advancing rim of new
epithelium often appears pale and slightly opaque.
The inexperienced practitioner may interpret this
as the effects of maceration
36
(Fig 2).
This delicate tissue, produced in a moist environ-
ment, may subsequently be exposed to inappropri-
ate measures in a futile attempt to reverse the
perceived maceration. The deleterious effects of des-
iccation generated by application of a dry dressing
will impede the healing process. If the observer
waits for a day or two the supposed ‘unhealthy’
white epithelium will be seen to change to a
healthy pink. This issue of ‘misunderstanding’
reminds us of the Harding et al
5
statement quoted
earlier, concerning the variations in normal wound
appearance, which have to be learnt to avoid
unnecessary intervention.
Bolton et al
36
also point out that maceration may
not be the cause but an effect of a slow to heal
wound. For example, in a venous leg ulcer this is
explained thus:
uncontrolled venous hypertension oedema
exudate maceration.
The underlying cause of oedema compressing
capillaries, leading to disruption of tissue blood
supply, needs to be addressed through effective
graduated compression bandaging.
Maceration — skin pathophysiology
As the stratum corneum (SC) becomes hydrated the
rate of diffusion of water through the SC
increases.
37
Hydration effectively reduces barrier
function in the skin.
It is also recognised that with an increase in
ambient relative humidity (as occurs when peri-
wound skin becomes macerated) there is a decrease
in transepidermal water loss. Additionally, as
hydration of the epidermis increases so does the
incursion or diffusion of materials into the skin.
38
Thus hydration and maceration reduce the skin’s
natural barrier function, permitting the growth
and ingress of pathogens and the inward diffusion
of toxins. Maceration is, therefore, best avoided at
all times.
Conclusion
This article has focused on the causes and effects of
maceration of the skin. It is important to consider
and to differentiate fluid involved in the wound
environment fluid arising from transepidermal
water loss. This should not be with wound exudates
and transudates, although both, to a degree, are
involved in maceration.
This can be mitigated by the careful choice of
dressings and wear times. Exudate from chronic
wounds is inherently different in composition from
acute wound exudate. These differences make
chronic wound fluid a wounding agent in its own
right and therefore potentially more deleterious.
In any exuding wound, particularly chronic
wounds, the possibility of maceration should be
borne in mind at all times. Maceration can delay
healing and indeed lead to enlargement of the
wound. When managing these wounds practition-
ers should consider the possibility of maceration. It
is preferable to avoid it than to treat it.
Future articles will deal with specific wound types
and the physical function of dressings in the con-
trol and reduction of maceration.
■
▼
▼
▼
Box 1. Summary of the main findings
Maceration can be a complication of any exuding
wound, but particularly chronic wounds
Maceration is caused by excessive amounts of
aqueous fluid — from a variety of sources including
water, urine and exudate — coming in contact with
the skin or wound surface for extended periods
Acute wound exudate differs from chronic wound
exudate. Chronic wound exudate’s properties have led
to it being seen as a wounding agent in its own right
It is important for practitioners to differentiate
between healthy and unhealthy wounds and between
when maceration is caused by water and when by
exudate, transudate or sweating.Transepidermal water
loss can often be controlled by appropriate dressings
278 JOURNAL OF WOUND CARE VOL 11, NO 7, JULY 2002
Fig 2.A healthy leg ulcer showing substantial
re-epithelialisation