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NAPKIN AREA
Dr Sandeep Lal V
Napkin Dermatitis
Intact skin
In 1977, Leyden et al. proved that ammonia did not cause skin irritation
when patch tested on the skin of adults and children
The clinical features of cutaneous candidiasis in the napkin area were first
reported by Swift in 1956 as an exudative, erythematous plaque, with a
well - defined margin and often satellite lesions
History
Causative factors
Ideal napkin - able to contain water without preventing air flow, and also
inform the carer (colour change) as soon as the baby urinates
Prolonged contact with faeces - most irritant toxic factor on the skin as
single factor can cause napkin dermatitis
Diarrhoea prolonged contact of faeces with skin incr hydration of the skin
Irritant capacity of faeces ranging from acid stools burning the skin to
alkaline stools
Faecal proteases and lipases (?) 100oc heating destroyed enzymes but
not irritant potential
? Unidentified toxic substnaces ? Bile acids
Urine
Although history and correlating physical signs are often helpful, the
differential diagnosis is based primarily on the morphology and location
of the rash
Contact napkin dermatitis
Verrucous
Shortly after therapy is initiated, scaly psoriasiform papules and plaques rapidly
develop on the trunk, usually sparing the extremities Which last for days to
weeks. C. albicans cannot be cultured from these plaques
Macerated areas of erythema in the anogenital region; may also present with
papulopustules, widespread erosions or a burn - like dermatitis
The bullae rupture easily, leaving red, moist, denuded areas and honey -
coloured crusts
Multiple lesions involving the thighs, buttocks and lower abdomen, rapid
spread
Sites- fingerwebs, wrists, antecubital fossae, axilla, areolae and areas around the
umbilicus, lower abdomen, genitals and buttocks
In infant and young children, the palms, soles, head, neck and face may also be
affected. A high percentage of children with scabies may develop nodular
lesions
Hold up to 50 80 times its weight in liquid and form a gel when hydrated
Cloth napkins with several layers of the same fabric were less effective in
keeping the skin dry than cloth napkins that contained middle layers of different
non woven components
Treatment
Napkin dermatitis is self - limiting
Children will outgrow this disorder after successful potty training
Never give parents the incorrect impression that napkin dermatitis is the result
of improper or negligent baby care
Ingredients of the medication are:
(a) protective compounds
(b) antimicrobial agent (s)
(c) other additives
Basic preventive treatment
Increased frequency of napkin changes and cleansing the skin.
The skin is cleaned gently and nursed with lukewarm tap water without
rubbing.
If faecal material is still present, a mild soap is used.
The activating factors must be minimized
A barrier cream containing zinc - oxide, titanium dioxide or white soft paraffin,
or a water repellent substance such as dimethicone or other silicones, should
be applied.
The barrier agent selected should be non toxic and as cosmetically acceptable
as possible.
The baby can be bathed once or twice daily with bath oil preparations
Further treatment
For napkin dermatitis that is not controlled by improved hygiene and use of
emollients or barrier creams
for the more troublesome cases of napkin dermatitis, oral therapy (such as
Nystatin, fluconazole suspension) should be added
The rational for oral anticandidal therapy is that you need in addition to treat the
gut colonization, although the scientific proof for this approach is still lacking
HIV-infected patients with CD4 cell counts 200 cells/mL were 3.7 times
less likely to normalize CSFVenereal Disease Research Laboratory
(VDRL) test results than were those with CD4 cell counts 1200 cells/mL,
suggesting, that HIVassociated immunedysregulation may account for the
impaired clearance of organisms from the CNS
Certain studies recommend CSF examinations for HIV-infected patients
with a nontreponemal serum titer 1:32, regardless of the syphilis stage, or
for those with early-stage infection and a CD4 cell count !350 cells/mL,
regardless of titer But CDC guidelines say to follow clinical examination
and four fold rise in serology
Treatment
Persons with HIV infection who have early syphilis might be at increased risk
for neurologic complications and might have higher rates of serologic treatment
failure with recommended regimens. The magnitude of these risks is not
defined precisely, but is likely small. Although long-term (>1 year) comparative
data are lacking, no treatment regimens for syphilis have been demonstrated to
be more effective in preventing neurosyphilis in persons with HIV infection
than the syphilis regimens recommended for persons without HIV infection.
Careful follow-up after therapy is essential. The use of antiretroviral therapy as
per current guidelines might improve clinical outcomes in persons with HIV
infection and syphilis Unusual serologic responses have been reported in HIV-
infected persons with syphilis.
Persons with HIV infection and primary or secondary syphilis should be
evaluated clinically and serologically for treatment failure at 3, 6, 9, 12, and 24
months after therapy
Syphilis affecting HIV
Epidemiologic studies demonstrate that history of an STD, including syphilis, is
associated with an increased risk of HIV disease among both gay men and
heterosexuals because sexual behaviors that increase the risk of acquiring
STDs also increase the risk of acquiring HIV.
Furthermore, genital ulcerations and inflammation caused by STDs are
implicated as cofactors for acquiring or transmitting HIV infection.
Syphilitic ulcers disrupt epithelium and mucosa, thus aiding the passage of HIV.
HIV replication Oral routes being considered safe
Syphilis affecting HIV
CD4 count and syphilis
Syphilis, like many other acute infections, causes transient increases in the
viral load and decreases in the CD4 cell count that resolve after the
infection is treated
Syphilis infection, particularly the generalized stage of secondary syphilis,
may increase the immune activation of host cells, affect the secretion of
cytokines including TNF, and upregulate transcription factors such as
nuclear factor kappa beta to alter cell cycles, and thus enhance HIV
replication.
It is possible that these transient increases in viral load contribute to the
increased risk of HIV transmission among patients with concordant HIV
infection and syphilis