Diaper Dermatitis: Current Concepts

(1)

Diaper

Dermatitis:

Current

Concepts

William L. Weston,

MD,

FAAP,

Alfred

T. Lane,

MD,

FAAP,

and Janet A. Weston,

MD

From the Departments of Dermatology and Pediatrics, University of Colorado Health Sciences Center, Denver

ABSTRACT.

Diaper dermatitis may result from

pro-longed skin contact with wetness and bacteria. Ammonia

plays no apparent role in the generation of diaper

der-matitis. Candida albicans frequently contaminates a

dia-per dermatitis and should be considered present in any

diaper dermatitis known to be present for longer than

three days. Topical fluorinated glucocorticosteroids, boric

acid, and mercury-containing preparations should be

avoided in the diaper area because of their toxicity.

Pediatrics 66:532-536, 1980.

The exact incidence of diaper dermatitis is

un-known, although the national survey of medicine

determined that dermatitis itself accounted for 97

doctor visits per year per 1,000 infants in the 0- to

2-year age group,’ and in Great Britain dermatitis

accounted for 28 consultant dermatology visits per

year per 1,000 infants.2 In Great Britain, overall,

diaper (napkin) dermatitis accounted for 20% of all

skin consultations in children aged 0 to 5 years.’ In

an examination of 1,349 babies during the first 7

days of life, up to 35% had perianal dermatitis but

none had dermatitis of other skin areas covered by

the diaper.4 Another study of 1,505 infants showed

a 7% incidence of perianal dermatitis.5 Thus,

der-matitis limited to the skin area covered by a diaper

is a frequent problem in pediatric practice.

It is the purpose of this report to re-examine

dermatitis limited to the diaper area with an

em-phasis on the recent findings regarding

pathogen-esis.

Received for publication Dec 18, 1979; accepted Feb 25, 1980. Reprint requests to (W.L.W.) Dept of Dermatology and Pedi-atrics, University of Colorado Health Sciences Center, Denver, CO 80262.

CLINICAL FEATURES

Forms of Dermatitis

to Wearing

a

Diaper

Four clinical forms of diaper dermatitis felt to be

related to diaper wear have been recognized. The

most frequently observed is chafing dermatitis.6

This form demonstrates mild redness and scaliness

seen over the buttocks, waist, and convex surface of

the thighs where the diaper contacts the skin,7 or

limited to the perianal area.4’8 Dermatitis limited to

the perianal area is seen in the neonatal period,9

and the more widespread form is seen after 3

months of age.8 The second, and also frequently

seen, form of dermatitis is a sharply demarcated

confluent erythema with involvement of the skin

folds with or without an accompanying whitish

exudate.9 The third form of dermatitis is

character-ized by discrete shallow ulcerations scattered

throughout the diaper area including the genitalia.8

In the fourth form, beefy red confluent erythema of

the entire perineum with prominent elevated

mar-gins, satellite oval lesions around the periphery of

the confluent area, and vesiculopustular lesions are

described. This form is seen when the dermatitis

becomes secondarily invaded with Candida

albi-cans.6’8 Diffuse involvement of the genitalia in the

inguinal folds is a regular feature of this form.68

Forms of

Dermatitis Unrelated to Wearing a

Diaper

Confluent erythema limited to the margins of the

diaper, the so-called tidemark dermatitis, is often

observed.89 Erythema, greasy scales, purpuric

pap-ules, or irregular deep erosions are rare features

seen with Letterer-Siwe disease in the diaper

re-gion.8 Bullous diaper area lesions are quite

uncom-mon and a variety of conditions have been found to

be responsible for the blister formation in the diaper

(2)

or inguinal creases are infrequently observed9 ‘ ‘ as

are red, thickened plaques with a thick scale that

mimic psoriasis.8”2

DIFFERENTIAL DIAGNOSIS

If the dermatitis is limited to the diaper area and

related to the use of a diaper, one may use the term

diaper dermatitis. It is, however, important to recall

that a variety of other skin conditions can begin on

or be more prominent in the diaper area. If skin

lesions are present in distal skin sites such as the

head and neck, or distal extremities, then one must

consider other conditions.8 A list of conditions

prominently noted in the diaper area and to be

considered in the differential diagnosis of diaper

dermatitis is found in the Table.

PATHOLOGY

There are no studies describing histopathologic

changes in the usual forms of diaper dermatitis

related to the wearing of a diaper. One may assume

that the dermatitis generated in relation to the

wearing of the diaper is not specific and would be

similar to that seen with any irritant contact

der-matitis. Biopsies of granulomatous nodules

appear-ing on the diaper area skin of infants with

long-standing diaper dermatitis demonstrate a

charac-teristic histopatholoy. Biopsy of these nodules show

edema of the epidermis and an inflammatory

infil-trate of lymphocytes, eosinophis, histiocytes, and

plasma cells within the dermis.’#{176} In addition,

in-creased blood vessel endothelial cell proliferation

that mimicked Kaposi’s sarcoma was seen.’#{176}

PATHOGENESIS

Only dermatitis related to the wearing of the

diaper will be considered in this discussion of

path-ogenesis. It is accepted by most authorities that

diaper dermatitis represents an irritant contact

der-matitis.89 The irritant properties result from

pro-longed contact of the skin with urine or feces or

both. Most authorities attribute perianal eruptions

to feces468 and involvement of thighs, waist, and

genitalia to urine.78 Which components of urine or

feces are responsible for the genesis of the

derma-titis remains controversial. Ammonia, bacteria and

bacterial products, urine pH, Candida albicans,

and water have each been implicated irritants,

a!-though few rigorous investigations are available to

substantiate any of these possibilities.

Ammonia

In 1921, Cooke first implicated ammonia in the

genesis of diaper dermatitis. He related that a

strong ammonia odor accompanied diaper

derma-TABLE. Differential Diagnosis of Diaper Dermatitis

Erythema with or without scaling Candidiasis

Atopic dermatitis Seborrheic dermatitis Allergic contact dermatitis Psoriasis

Letterer-Siwe disease Scabies

Granulomas Blisters or erosions

Bullous impetigo Papular urticaria

Acrodermatitis enteropathica Miiaria

Herpes simplex Varicella

Epidermolysis bullosa Bullous pemphigoid Dermatitis herpetiformis Burns

Child abuse

Congenital syphilis Bullous mastocytosis Incontinentia pigmenti

Chronic bullous dermatoses of childhood

this.7 In order to prove his thesis, he found a

gram-positive, nonmotile bacteria that grew from urine of

infants with diaper dermatitis but not from those

without. This bacteria liberated ammonia from urea

in culture and was called Bacillus ammoniagenes.7

Cooke’s theory of ammoniacal diaper dermatitis

was accepted by pediatric authorities and quoted in

a variety of textbooks.89” it has recently been

challenged by studies which demonstrated that

con-centration of ammonia (402 ppm) obtained from 26

infants with diaper dermatitis did not differ from

levels (465 ppm) obtained from 82 infants without

diaper dermatitis.’4 Even when ammonia was

lib-erated from infants urine with urease, the increased

urine ammonia levels (7,803 ppm and 7,566 ppm)

did not differ in the two groups.’4 Application of

16,320 ppm of ammonia (1.6%) to the skin of ten

infants for 24 hours did not produce erythema or

dermatitis.’4 Further, B ammoniagenes was not

recovered from infants urine who had diaper

der-matitis or diaper area candidiasis by using standard

microbiologic techniques.6 These findings cast

con-siderable doubt on the role of ammonia in diaper

dermatitis. In addition, the clinical observations

that most infants with diaper dermatitis do not

have a strong ammonia odor, and vice versa,

sug-gests that ammonia is not involved in the genesis of diaper dermatitis.

Bacteria

That bacteria may be involved in diaper

derma-titis derives from several observations. The studies

(3)

a dermatitis when applied to the skin of

3-month-old infants, but that urine allowed to stand 18 hours

at 37 C (the so-called “putrefied urine”) did produce

a dermatitis. Leyden and Kligman6 re-examined

bacteria obtained from the skin of infants with and

without the various forms of diaper dermatitis and

could detect no significant differences in the type

or quantity of microbial flora recovered. They did,

however, find that 50% of infants with chafing

der-matitis had Staphylococcus aureus recovered while

normal infants did not. The role of colonization

with S aureus was not clear from their study. The

density of bacteria per square centimeter skin

sur-face in infants with diaper dermatitis is higher in

the thigh and labial areas than those infants without

dermatitis but the same in the perianal, perineal,

and inguinal-fold areas. A mean number of

orga-nisms of 892,000/sq cm of skin surface area was

observed for the perineal area for example.

Bacterial overgrowth on the skin of infants with

diaper dermatitis may represent a secondary event.

Nonetheless, on moist skin with increasing time,

bacterial overgrowth is well described and the

pos-sibility that quantitative increases in bacteria and

bacterial products being involved in the genesis of

diaper dermatitis must stifi be considered. There is

no firm proof, however, that bacteria account for

the dermatitis.

Urine or Fecal pH

One explanation for production of a diaper

der-matitis from urine is the alkalinity of the urine.

Several studies demonstrate that at high pH (8.0 to

9.0) dermatitis can be induced by infants urine

when applied directly to skin but not at lower pH,

5, 6, or 76.15

A

study by Tanino et al5 failed to

support the theory of alkalinity of feces being

re-sponsible for the development of perianal

dermati-tis in 1,505 newborns.

The issue of alkalinity playing a role in diaper

dermatitis remains unresolved, although the skin

pH usually does not differ in those infants with and without dermatitis.’5

Candidiasis

Diaper dermatitis present for greater than 72

hours is likely to yield C albicans when cultured.’6

This is in contrast to the low yield in those infants

without diaper dermatitis. Leyden and Kligman6

recovered C albicans that reached a density

ac-counting for 2% to 4% of all microbial flora on infant

skin with diaper dermatitis but only 0.01% of the

microbial flora in infant skin without diaper

der-matitis. On the skin of normal infants, C albicans

may be recovered, but is found in only 1% to 3% in

several studies,6”7’9 yet up to 12% in one study.’6

Most authorities now agree that C albicans is a

frequent invader of the diaper area, recovered from

41% to 85% of infants who have active diaper

der-matitis.6”6”7 Thus, in most studies over half the

infants with diaper dermatitis will culture C

albi-cans, with a large quantity of organisms.6

Experimental models of C albicans infection

demonstrate that this organism itself, when applied

to the skin surface, has the ability to invade through

the epidermal barrier, perhaps by the role of

kera-tinases liberated by the C albicans.2#{176} The invading

yeast has been demonstrated to activate the

alter-native complement pathway producing

chemotrac-tants capable of attracting large numbers of

neutro-plus to tissue sites.2’ Biopsies of experimental C

albicans infections show neutrophiic microab-scesses within the epidermis.#{176}

Thus, C albicans need only to overgrow on the

skin surface to invade the skin without requiring

any additional factors to further compromise the

epidermal barrier. After 72 hours of a diaper

der-matitis, one may presume that most infants will be

secondarily infected with C albicans. It is of interest

that neither prior treatment with oral antibiotics,

nor treatment of the diaper area skin with topical

glucocorticosteroids increases the recovery rate of

C 18

The role of alimentary C albicans in persistent

or recurrent diaper dermatitis has been well

stud-,8 Although commonly recovered from the

rec-tum, British authorities have convincingly

demon-strated that alimentary C albicans does not play a

role in diaper candidiasis,’8”9 and concurrent

treat-ment with oral Nystatin had no influence on diaper

dermatitis when compared to placebo oral

ther-apy.’9

Water

Prolonged contact with urine is associated with

diaper dermatitis.’5 Studies that fresh urine

con-taming bacteria do not cause a dermatitis whereas

urine allowed to stand for 18 hours and “putrefy”

does produce a dermatitis.’5 This suggests that

wet-ness alone may not account for the genesis of the

dermatitis, but that water plus overgrowth of

bac-teria are required. Leyden and co-workers’4

dem-onstrated that skin that had been scarified with

cross strokes of a needle, produced an erosion with

the same ease whether water alone was applied or

water plus low or high concentrations of ammonia.

Water applied to the skin made it easier to produce

a skin erosion when compared to dry skin.’4

Wet-ness of the diaper area skin alone cannot account

for the generation of a dermatitis, but acts as a

(4)

TREATMENT

Frequent diaper change to avoid prolonged

con-tact with urine is the cornerstone of all successful

treatment protocols for diaper dermatitis. The exact

frequency of change required is not known since it

is not certain whether 4, 6, 8, 12, or 24 hours of

urine contact is required to generate a dermatitis.

Certainly, the infant who takes fluid just before

bedtime and sleeps ten to 12 hours at night is at

risk for prolonged contact with urine. A diaper

change at night in such infants may be a most

helpful therapeutic maneuver. Drying of the diaper

area skin by air exposure is recommended by most

authorities8’9”3 as is changing as soon as the diaper

is wet.

There are no convincing studies to demonstrate

the advantages of one type of diaper over another.

Undoubtedly, the volume of urine which can be

absorbed into the material is a major determinant

of a successful diaper. A thoroughly soaked diaper

of any composition may make the infant susceptible

to diaper dermatitis. Both cotton and

plastic-coy-ered paper diapers have been successfully

em-ployed.22 Air-tight occlusion from plastic or rubber

pants, or plastic covers on disposable paper diapers

inhibit the evaporation of water from the skin

sur-face and results in an increased hydration of diaper

area skin. Air-tight occlusion overnight can be

avoided by the use of three cotton diapers without

a diaper cover for increased absorbance. In a recent

retrospective study, cloth diapers alone accounted

for less diaper dermatitis than cloth diapers covered

with rubber pants or a commercial paper diaper

product.22 In addition, paper diapers were

associ-ated with more pustular eruptions than cloth

dia-pers.

After removal of a wet diaper, most authorities

suggest gentle rinsing of the skin with clear water.8’9

Excessive use of soap or alcohol for cleansing may

further damage the barrier properties of the skin

surface and make the infant more susceptible to

diaper dermatitis.8’9

Talc is soothing to the skin after cleansing, but

whether it adds to the overall dryness is unknown.

Cornstarch is contraindicated in diaper dermatitis

since it serves as a culture media for C albicans.23

Bacteriostatic agents, such as

methylbenzethon-ium chloride 1 : 1000, have been demonstrated in

several studies to reduce the frequency of diaper

dermatitis whether as a diaper rinse,24 ointment,25’26

or lotion.27 In a study of diaper dermatitis

prophy-laxis28 the combined use of methylbenzethomum

chloride diaper rinse plus powder reduced the

mci-dence of diaper dermatitis from 29% to 4%. Other

traditionally used preparations such as A & D

oint-ment or zinc oxide ointments have no evidence to

suggest efficacy other than skin lubrication.

Whether application of diaper area ointments

pro-vides a barrier to reduce irritation is unknown.

Boric acid29 and mercury preparations3#{176} have been

associated with systemic poisoning and should not

be used on infant’s skin. Oral agents used to

dimin-ish ammonia production have not been

demon-strated to be efficacious.

In diaper dermatitis over 72 hours old or with

clinical features of candidiasis, a topical antiyeast

agent should be used. Nystatin, Haloprogin,

Micon-azole, and Clotrimazole creams are equally effective

against C albicans.3’ Treatment protocols vary in

the frequency of application but most recommend

four times a day. Treatment protocols for every

other diaper change may also be valuable.

Recur-rences of C albicans diaper dermatitis are common

since C albicans may be found on the skin of normal

infants and is readily available to invade an area of

dermatitis.’8 Infants with recurrent diaper

derma-titis do not require an immunologic evaluation.

The use of topical steroids in diaper dermatitis is

frequently recommended.8’9”3 Absorption of topical

steroids in the diaper area is enhanced by increased

moisture of the skin and by air-tight occlusion by

plastic or rubber diaper covers.3236 Potent

fluori-nated glucocorticosteroids applied to the diaper

area have resulted in striae, epidermal atrophy,

suppression of the pituitary-adrenal axis, and

ces-sation of longitudinal growth and frank Cushing’s

syndrome.3236 Ifsteroids are to be used in the diaper

area, their use should be limited to low potency

preparations such as 1% hydrocortisone cream in

order to minimize side-effects. The popular use of

triamcinolone-containing preparations combined

with antiyeast and antibacterial agents is not

rec-ommended because of the fluorinated

glucocorti-costeroid in the preparation. One should limit use

of topical glucocorticosteroids to a period of one

week to avoid overuse of the steroid cream for its

lubricant value rather than for its antiinflammatory effects.

A

recommended approach to the therapy of

dia-per dermatitis is as follows: (1) Determine the

fre-quency of diaper change and suggest changing as

soon as the diaper is wet or at least at every two to

four hours including a change at night time; (2)

avoid overnight use of plastic pants, “triple diaper”

with cotton diapers, and use a rubber pad; (3)

expose diaper area to air as often as practical during

daytime; (4) if cotton diapers are used, an extra

rinse with diluted vinegar may reduce alkalinity of

the diaper; (5) if diaper dermatitis is present for

more than 72 hours assume it is contaminated with

(5)

four times a day or every other diaper change; (6)

severe inflammation may be reduced by the

appli-cation of 1% hydrocortisone twice a day for up to

one week; (7) recurrent diaper candidiasis should

be retreated in the same manner as initial therapy;

(8) one should not use topical fluorinated

glucocor-ticosteroids in the diaper area; (9) one should not

use boric acid or mercury-containing preparations

on infants’ skin.

We believe that adherence to these suggestions

wifi avoid side effects and provide a rational therapy

that can be used in the diaper area.

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Child 82:429, 1951

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6. Leyden JJ, Kligman AM: The role of microorganisms in diaper dermatitis. Arch Dermatol 1 14:56, 1978

7. Cooke JV: The etiology and treatment of ammonia derma-titis of the gluteal region of infants. Am J Dis Child 22:481, 1921

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1 1. Tappeiner J, Pfleger L: Granuloma gluteale infantum. Hau-tartz 22:383, 1971

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19. Dixon PN, Warm RP, English MP: Alimentary Candida albicans and napkin rashes. Br J Dermatol 86:458, 1972 20. Rebora A, Marples RR, Kligman AM: Experimental Candida

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in rodents. II. Role of the stratum corneum barrier and serum complement as a mediator of a protective inflamma-tory response. Arch Dermatol 1 14:539, 1978

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30. Lyons TJ, Christy CN, Larsen FS: Ammoniated mercury ointment and the nephrotic syndrome. Minn Med 58:383, 1975

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32. Scoggins RG, Kliman B: Percutaneous absorption of corti-costeroids. N Engl J Med 273:831, 1965

33. Keipert JA: The absorption of topical corticosteroids, with particular reference to percutaneous absorption in infancy and childhood. Med JAust 1:1021, 1971

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1980;66;532

Pediatrics

William L. Weston, Alfred T. Lane and Janet A. Weston