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in this lecture we will discuss a
variety of common pathologic rashes in
children let's start with seborrhoeic
dermatitis this is a chronic
inflammatory derma ptosis it happens
very commonly it's present in about 5%
of the general population and in
children often involves areas of high
density of sebaceous glands around the
nose in the ears wherever there are
sebaceous glands it causes inflammation
of the epidermis and it's not a disease
of the sebaceous glands themselves so
here is a very classic case of cradle
cap it's remarkably common and it occurs
in the first two months of life and then
again rears its ugly head during
adolescence cradle cap is an erythema
TISS scaly eruption found on the scalp
it's probably bothering the parents more
than it is the child later it can spread
to flexural areas like under the neck or
in the groin or under the armpits
unlike eczema this is not very itchy
so in infants it's usually asymptomatic
maybe slightly paretic and here's an
example of it under this child's neck
and then in adolescence it comes back
typically as dandruff patients can get
peri ocular redness and crusting as well
patience will have increased sebum
production in response to androgens also
a fungus with perhaps my favorite name
of any fungus malassezia furfur will
grow in that area in the infants we can
often treat this with simply mineral oil
or a little bit of combing in severe
cases or in adolescents we can simply
use a dandruff shampoo we generally
treat with emollients so four scales on
the scalp will give shampoo and combing
and maybe ketoconazole shampoo if it's
resistant for body wide eruptions we'll
treat with mild topical corticosteroids
and we may mix with an antifungal such
as ketoconazole to kill that malassezia
furfur
let's skip to another common childhood
inflammatory problem which is psoriasis
this is one of the chronic inflammatory
derma Tosi's and it is autoimmune in
nature it's pretty common though it
happens in one to two percent of the
general population with different forms
and different severity remember this is
an interaction between genes and the
environment so patients with HLA type c
particularly HLA cwo 6:02 are going to
have an increased risk of psoriasis and
homozygotes have an even further two and
a half times higher risk than
heterozygotes psoriasis is generally a
well demarcated Aerith ominous popular
lesion with plaques and it has a silvery
scale to it mainly on extensor surfaces
the clinical presentation is diagnostic
they will have itching they will
generally have a bilateral distribution
and you may see nail pitting on their
nail exams these are all findings of
psoriasis psoriasis is generally
triggered by some sort of problem a
patient has an underlying risk for it
and then they have flares I think
would be minor trauma upper respiratory
infections stress cold low sunlight
levels so sunlight helps and some
medications if you were to look
pathologically you would notice an
epidermal hyperplasia and peri chaotic
scale these patients have accumulation
of neutrophils within the superficial
epidermis when we see these patients we
recommend avoiding rubbing or scratching
because remember minor trauma makes it
worse and we give them emollients or
moisturizers sunlight exposure helps tar
preparations will help and we can put
them on topical steroids or vitamin D
analogues we'll move on to another
common infection in skin and this is
impetigo we see this a lot in children
this is a common superficial bacterial
infection of the skin and it's usually
caused by group a strep or
Staphylococcus it's highly contagious
and usually starts on the face and the
hands and then spreads patients
classically have a honey colored crusted
lesion moving on there's a more
significant bacterial infection than it
can encourage children which is bolus
impetigo bolus impetigo is also caused
by staph and group a strep we see it
more commonly in people with less
rigorous bathing it causes flaccid
thin-walled Bolle or tender shallow
lesions surrounded by the remains of the
blister roof that often pops this is
commonly implicated in staph scalded
skin syndrome patients with impetigo
have bacteria in their epidermis that
evoke innate humoral response they
suffer epidermal injury and they have
local serous exudate not posterior which
forms a scale or a crust these patients
will have accumulation of neutrophils
beneath their stratum corneum the
pathogenesis of blister formation is
somewhat interesting basically the
bacteria produce a toxin the toxin
Cleaves desmo glean one desmo glean one
is responsible for cell to cell adhesion
with that breakdown of cell to cell
adhesion these Bolle can now form in the
upper epidermal layers how do we treat
impetigo
well untreated lesions usually last two
to three weeks and then generally
resolve but we can gently remove the
crust to prevent spread and then we'll
provide topical antibiotics such as MU
Pearson which is very effective against
staff and group a strep we may in severe
cases also provide oral antibiotics such
as a first generation cephalosporin
cephalexin which can be given twice a
day in cellulitis or clindamycin if
we're suspecting mersa or there's
invasive disease
remember these lesions heal without
scarring and generally these patients do
well so that's a summary of a few common
infections or skin findings in children
thanks for your time
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you