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Clinical Practice Keywords Skin damage/Incontinence-

associated dermatitis/Continence
Review
Moisture-associated skin damage This article has been
double-blind peer reviewed

In this article...
● Definitions of moisture-associated skin damage and incontinence-associated dermatitis
● How urine and faeces damage the skin
● Risk factors for incontinence-associated dermatitis

Incontinence-associated dermatitis 1:
risk factors for skin damage
Key points
Author Ann Yates is director of continence services, Cardiff and Vale University
Moisture-associated Health Board.
skin damage
describes a group Abstract Moisture-associated skin damage has many causes including contact with
of skin conditions urine, faeces, perspiration and wound exudate. Incontinence-associated dermatitis
caused by contact occurs when there is contact between the skin and urine and/or faeces. This article,
between the skin part 1 of a three-part series, explores the reasons why urine and faeces cause skin
and excessive damage and outlines the risk factors for incontinence-associated dermatitis.
moisture
Citation Yates A (2020) Incontinence-associated dermatitis 1: risk factors for skin
Incontinence- damage. Nursing Times [online]; 116: 3, 46-50.
associated

M
dermatitis falls into
the overarching oisture-associated skin damage research is needed to establish how these fac-
category of (MASD) describes a group of tors combine to result in skin damage and to
moisture-associated skin conditions caused by inform prevention and treatment strategies.
skin damage contact between the skin and Incontinence-associated dermatitis (IAD)
excessive moisture including wound exu- has been described as a type of “irritant con-
Incontinence- date, perspiration, and urine and faeces. tact dermatitis” (Beeckman et al, 2015). It
associated Common types of MASD are: may be associated with infection and can
dermatitis is caused l I ncontinence-associated dermatitis occur on intact or damaged skin (Iblasi et al,
by prolonged – chemical irritation caused by contact 2019; Beeckman, 2017). IAD occurs in people
contact between between the skin and urine and/or who are incontinent of urine and/or faeces
the skin and urine faeces; (Beeckman et al, 2015) and is one of the most
and/or faeces l I ntertriginous dermatitis – skin common skin problems in this group (Iblasi
damage associated with sweat trapped et al, 2019; Van Damme et al, 2017; Van den
The precise in skin folds in areas with minimal air Bussche et al, 2017). IAD is also known as per-
pathophysiology circulation; ineal dermatitis, diaper rash, diaper/napkin/
of incontinence- l P eri-wound moisture-associated nappy dermatitis, napkin/nappy rash, irri-
associated dermatitis – skin maceration and tant dermatitis, moisture lesions, or per-
dermatitis is not breakdown caused by excessive wound ineal rash (Beeckman et al, 2015).
fully understood exudate;
l P eristomal moisture-associated Extent of the problem
Patients with dermatitis – inflammation and erosion Continence problems are the main cause of
suspected of skin caused by moisture at the IAD; NHS England (2018) estimates that:
incontinence- stoma/skin junction and extending l 1 4 million adults in the UK are affected
associated outward (Dowsett and Allen, 2013). by urinary incontinence;
dermatitis require The pathophysiology of MASD is not l > 6.5 million adults experience
a comprehensive fully understood but multiple factors problems with bowel control.
continence and including moisture, skin-care regimens, It also identified that one in ten of the UK
skin assessment changes in skin pH, presence of micro- population experience faecal incontinence,
organisms, and skin damage associated with with over half a million adults affected
pressure and friction all play a role. More (NHS England, 2018). Nearly two-thirds of

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Clinical Practice Funded by an unrestricted

Review educational grant from Essity

people with faecal incontinence also have
urinary incontinence – this is known as
‘double incontinence’ (National Institute
for Health and Care Excellence, 2007).
Faecal incontinence is closely associated
with age, and is more prevalent in residen-
tial or nursing homes: one in three individ-
uals in residential homes and two in three
in nursing homes are affected (NHS Eng-
land, 2007; NICE, 2015). However, these sta-
tistics are likely to be underestimates given
the stigma associated with the condition
and its consequent under-reporting
(Bedoya-Ronga and Currie, 2014).
Patients with a urinary catheter are not
classified as incontinent, but leakage and
the bypassing of urine can lead to them
experiencing the symptoms of IAD.
Exact figures of individuals who experi-
ence IAD are unknown but estimated preva-
lence rates range from around 6-50% across
different healthcare settings, patient popu-
lations and age ranges (Woo et al, 2017).
Beeckman (2017) estimated that 20-25% of
people with continence problems in hos-
pital will experience IAD, while Nix and
Haugen (2010) suggested that IAD affects as
many as 41% of adults in long-term care.
IAD can cause pain, considerable dis-
comfort and distress (Yates, 2018); it can be
difficult to diagnose, and time consuming
and expensive to treat.
Why does IAD occur?
The skin is the largest organ in the human
body and provides a semi-permeable barrier
that protects the body against mechanical
damage, harmful irritants, infectious
Fig 1. Structure of the skin
Sweat gland
Melanocytes
Sweat
Capillaries
Epidermis
Dermis
Fat layer
Nerve
pathogens and excessive fluids (Woo et al,
2017). Other functions of the skin are detailed
in Table 1. It is made up of three main layers:
the epidermis, dermis and hypodermis (sub-
cutaneous fatty tissue) (Fig 1). The outer layer
of the epidermis, the stratum corneum, con-
tains the protective building blocks often
described as the ‘bricks and mortar’ of the
skin. The bricks are protein-rich corneocytes,
held together by lipid-rich matrix (mortar)
and protein structures called desmosomes,
which act as rivets (Voegeli, 2016) (Fig 2). The
corneocytes are dead cells that start life as
keratinocytes. These cells are formed in the
basal epidermal layer of the skin; they
migrate through the epidermis and differen-
tiate before they degenerate and die.
Hair
Oil
Stratum corneum
(keratin)
Basement membrane
Sebaceous gland
Hair follicle
Blood vessels
The corneocytes keep the skin hydrated,
enhancing flexibility and elasticity. When
incontinence occurs, excess water from
urine and/or faeces is pulled into, and held
within, the corneocytes (Beeckman et al,
2015), causing the skin to become overhy-
drated, macerated and waterlogged.
At 4.6-5.5, the pH level of the skin is usu-
ally acidic (Voegeli, 2016); this creates an acid
mantle that helps to protect the body against
infection. Exposure to urine makes the skin
more alkaline. Urea, which is found in urine,
is converted by skin bacteria to ammonia –
this is alkaline breaking down the acid
mantle, making the skin more susceptible
to infection and/or IAD. Fig 3 outlines the
skin changes caused by incontinence.

Table 1. Functions of the skin

Function Explanation
Protection l Acts as a protective barrier, preventing internal tissues being damaged by trauma, ultraviolet
light, temperature changes, toxins, pathogenic microbes and chemical agents
Barrier to infection l Intact skin creates a physical barrier to infection
l The skin produces sebum, which is antibacterial and has an acidic pH of 4.6–5.5 (Voegeli, 2016);
this is known as the ‘acid mantle’
l Corneocytes found in the stratum corneum – the outer layer of the epidermis – contain
substances that actively attract and hold water; this keeps the skin hydrated so it can function as
a flexible barrier (Voegeli, 2016)
Production of vitamin D l This is produced by the skin in response to sunlight and is important for bone health
Maintenance of body l Heat is retained and lost from the body by vasoconstriction and vasodilation of blood vessels in
temperature the skin
Pain receptor l Nerve endings respond to painful stimuli and act as a protective mechanism to prompt the
individual to move away from pain or discomfort
Production of melanin l This is responsible for skin colouring and protects against radiation damage from sunlight
FRANCESCA CORRA

Communication l The physical appearance of the skin can give us information about a patient’s health and
wellbeing – for example, a yellow tinge can indicate jaundice
Source: Adapted from Yates (2018), Wounds UK (2012)

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Clinical Practice
Review

Patients with faecal incontinence are

Fig 2. Structure of corneocytes
more likely to develop IAD compared with
Intracellular lipid layers those who have urinary incontinence (Gray
between the corneocytes and Giuliano, 2018). This is because faeces
contain biolytic (lipid-digesting) and prote-
olytic (protein-digesting) enzymes that are
damaging to the skin. Liquid faeces contain
higher levels of digestive enzymes than
formed stools, so patients with diarrhoea
Desmosome and faecal overflow are at increased risk of
IAD (Beeckman et al, 2015). Those with
double incontinence are at greatest risk of
IAD (Gray and Giuliano, 2018); Fig 4 illus-
trates how urine/faeces affects the skin.

Associated risk factors

Corneocyte
Fig 3. Changes in the skin caused by incontinence
Fungal infection
Damp, warm skin associated with
incontinence is ideal for proliferation of
pathogenic fungi
Incontinence-associated
dermatitis
Breakdown of the skin due to
over exposure to urine and
faeces
Bacterial infection
Incontinence exposes the skin to
bacteria found in urine and faeces.
Cracks and fissures associated with dry
skin provides an ideal environment for
bacterial growth
Sources: Yates (2018), Beeckman et al (2015)
Exposure to caustic agents
Ammonia found in urine increases skin
pH causing irritation and provides a
nutritional source for bacteria
Maceration
Over-exposure to moisture
(waterlogged)
Once skin is macerated even gentle
rubbing with bed linen or washing can
cause damage
Although the key risk factor for IAD is
incontinence, the factors determining risk
of incontinence are multiple and complex.
These can include:
l I mmobility;
l C  ognitive impairment;
l A  ge.
The ageing process also affects the skin,
and bowel and bladder function. As the
skin ages, several physiological changes
make it more prone to damage (Table 2).
Age-associated changes to bladder func-
tion include decreased urinary flow as a
result of conditions such as prostate
enlargement, prolapse, poor detrusor con-
traction and recurrent urinary tract infec-
tions. Bowel function is affected by
increased susceptibility to diverticular dis-
ease or constipation with faecal impaction/
overflow. These risks, while associated with
ageing, are not exclusive to older people.
Continence issues can manifest at any
time of life making anyone who is inconti-
nent at risk of IAD (NHS England, 2018). The
risks factors associated with IAD are sum-
marised in Table 3.

Fig 4. How urine/faeces affects the skin Confusion between IAD and
pressure ulcers
Although the anatomical sites and general
Water from urine/faeces appearance of pressure ulcers and IAD are
is pulled in and held in similar, the aetiology and treatments are dif-
Causes disruption to the corneocytes Liquid faeces is more
the structure of the skin damaging than solid ferent. In practice, IAD is often misdiagnosed
leading to maceration This leads to stools as it has higher as pressure damage, which can lead to inap-
overhydration and levels of digestive
Irritants penetrate the damage to the acid propriate management (Iblasi et al, 2019) (see
stratum corneum emzymes
mantle of the skin, case study in Box 1). This year, NHS England
leading to inflammation which is usually Double incontinence is and NHS Improvement (2020) published
Skin becomes prone pH4.6-5.5 more damaging than
urine or faeces alone their patient safety CQUIN indicator for 2020-
to injury
2021, one of which addresses the assessment
Skin becomes more and documentation of pressure ulcer risk in
alkaline due to
formation of ammonia community hospitals and NHS-funded resi-
dents in care homes. It aims to ensure that
IAD
FRANCESCA CORRA

60% of residents have a pressure ulcer risk

assessment that meets NICE guidance with
evidence of actions being taken to address
Sources: Yates (2018); Voegeli (2016); Beeckman et al (2015) identified risks. To ensure correct reporting,

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Table 2. Effects of ageing on the skin

Physiological change
Thinning of epidermis and dermis
Decrease in production of sebum
20% decrease in volume of skin layer
Flattening of dermo-epidermal junction
between the epidermis and dermis
(Wounds UK, 2012; Voegeli, 2007)
Decrease in underlying fat
Source: Adapted from Yates (2018)
Effect on the patient
l Skin becomes more delicate/fragile and prone to damage from friction, moisture and
trauma (Wounds UK, 2012; Voegeli, 2007)
l Thinning of the dermis leads to a reduction of blood vessels, nerve endings and
collagen, which results in a decrease in sensation, rigidity and moisture retention, as well
as poor temperature control (Wounds UK, 2012)
l Skin becomes itchy and dry, with cracks and crevices (Watkins, 2011), and is more
susceptible to damage from washing, rubbing and drying
l Skin has a paper-thin appearance (Wounds UK, 2012). Damaged skin takes longer to
repair so healing time is increased
l A decrease in elasticity causes skin to stretch (Wounds UK, 2012; Voegeli, 2007). Sweat
and blood vessels respond less well to heat and individuals may become more susceptible
to cold/hypothermia (Wounds UK, 2012; Voegeli, 2007). The skin bruises easily
l Decreased protection against ultraviolet light

Table 3. Contributory risks factors for the development of incontinence-associated dermatitis

Incontinence
Frequent incontinence episodes
Prolonged exposure to urine
and faeces
Poor initial continence
assessment
Inappropriate assessment for
pad products
Inappropriate use of pad
products
Use of incorrect products on
skin
Frequent skin cleansing with
water and soap
Inability to perform personal
hygiene
Compromised mobility
Diminished cognitive
awareness
Medication
Poor nutritional status
Critical illness
Source: Adapted from Gray and Giulano (2018), Yates (2018) and Beeckman et al (2015)
l Urinary – incontinence or leakage from a device, such as an indwelling urinary catheter
l Faecal – diarrhoea/formed stool
l Double – faecal and urinary
Risks are higher in people who have faecal or double incontinence
This may be due to:
l Infrequent change of incontinence products
l Poor skin cleansing
l Ineffective equipment/appliance, such as an indwelling catheter or faecal-management system
that regularly leaks
This leads to:
l Mismanagement of symptoms
l Inappropriate interventions
l Over-reliance on containment products
Problems include selecting the wrong absorbency: absorbency that is too high can be just as
damaging as absorbency that is too low
This includes practices such as:
l Double padding
l Infrequent changes of pad products
Absorbent products or incontinence-containment devices (especially if plastic-backed) may
cause over-hydration by holding moisture against the skin surface
Thick, occlusive skin protectants (such as petroleum jelly and zinc oxide) may inhibit urine/
faeces uptake by absorbent incontinence products, causing over-hydration of the stratum
corneum
This damages the corneocytes, removing lipids, increasing dryness and creating friction, which
leads to damage in the skin barrier function
This is a particular issue if patients are reliant on carers to cleanse their skin and change pad
products after incontinence episodes
Patients who are immobile are significantly more likely to experience IAD than those who are
mobile (Iblasi et al, 2019)
Patients with dementia may no longer recognise the need to go to the toilet or be able to
identify the toilet, leading to a potential risk of continence problems
Antibiotics can cause diarrhoea, which can increase risk of IAD. Immunosuppressants and
steroids can cause skin fragility, skin thinning and increased risk of bruising
This has a negative effect on skin health, hydration and healing
This can lead to increased risk of incontinence and poor overall skin condition

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Box 1. Case study

Wendy Simmonds is community team leader, tissue viability
nurse, Cardiff and Vale University Health Board
Grace Simpson, aged 82, lives alone and is confined to a
wheelchair or bed as a result of spina bifida. She has a
urostomy, type 2 diabetes and has had an above-ankle
amputation. Management of her bowels comprises daily manual
evacuations and use of an anal plug to prevent faecal leakage.
Formation of a stoma is not possible due to Ms Simpson’s
condition and she was reluctant to have surgery. Poor mobility
and other comorbidities have also resulted in a history of
pressure ulcers to her labia and left ischial tuberosity.
Following a recent hospital admission, Ms Simpson’s bowel-
care regimen was changed: use of the anal plug was
discontinued and care reduced to alternate days as she had
developed an anal fissure. This resulted in an increase in faeces
leaking onto the surrounding skin, with subsequent moisture
damage, increased skin maceration and contamination of the
pressure ulcer on the left ischial tuberosity. The skin surrounding
the pressure ulcers, anal fissure and labia showed evidence of
moderate-to-severe moisture damage; the pressure ulcers
became clinically infected and leaked copious amounts of
exudate, which added to the moisture-associated skin damage.
Following our local pathway for incontinence-associated
dermatitis (IAD), the aim of treatment was to repair and restore
the integrity of the skin using a foam incontinence cleanser and
skin-protectant ointment after each episode of incontinence. We
protected the skin around the wounds with barrier film and, once
skin hydration was restored to normal, we aimed to maintain this
with a barrier cream or ointment, depending on further risks of
exposing the skin to moisture. Additional actions included:
l Treating the pressure ulcers with topical antimicrobial of
flamazine and hydrofibre dressing twice daily to manage the
exudate. Bed rest was advised, with frequent repositioning
and limited time sitting in a chair
l Reviewing the bowel-management regimen with the local
continence service, and reinstating daily bowel care and use
of an anal plug
l Reviewing pressure redistribution equipment and seating
l Arranging a referral to the nutrition and diabetic teams to
review Ms Simpson’s diet intake and diabetic management,
especially as her dietary intake had significantly reduced in
the community and her blood-glucose control was poor.
Reverting back to Ms Simpson’s daily manual evacuations
and use of the anal plug resulted in an improvement in her skin.
The moisture damage was resolved and her skin is now
managed with a skin cleanser and barrier film. The pressure
ulcers are still present but are no longer infected or at risk of
contamination from faeces.
*
The patient’s name has been changed
Points for reflection
l What was the direct cause of IAD in this case study?
l Using the information in Table 2 and Table 3 explain the
contributing factors for IAD
l What steps would you take to avoid this situation occurring?

staff must be able to distinguish between IAD
and pressure ulcer damage as part of a rou-
tine skin assessment and provide an appro-
priate individualised plan of care.
It is important to be aware that those who
experience IAD are also prone to pressure
damage, especially in the sacral and peri-
neum areas. This will be covered in detail in
part 3 of this series.
Conclusion
IAD is caused by continence problems but
many factors contribute to its development,
such as poor mobility and cognitive
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impairment. The nature of normal skin
ageing and the potential problems associ-
ated with that, along with additional risk
factors, means IAD is often misdiagnosed
and mismanaged as the underlying conti-
nence problem is often not addressed. Edu-
cation in the fields of IAD and continence is
lacking but needs to be improved. NT
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CLINICAL Incontinence-associated
SERIES
dermatitis series
Part 1: Risk factors Mar
Part 2: Prevention and treatment Apr
Part 3: Reporting skin damage May

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