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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_141_библиотеки_им_акад_М_И_Перельмана
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https://t.me/med1917
Fig. 54.13 Tinea manuum observed on the back of the hand appearing
in a ring shape like tinea corporis
54 Tinea Manus, Tinea Manuum
Hand, Foot, andMouth Disease (HFMD)
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55
I’m 24 years old, can I get hand, foot, and mouth disease?
The symptoms are exactly the same as my nephew who
was sick recently. (Figs.55.1 and 55.2).
24-year-old Ms. K came for treatment saying she had a
fever and blisters and rashes on her mouth, hands, and feet.
“I’m 24 years old, can I get hand, foot, and mouth disease?
The symptoms are exactly the same as my nephew who had
hand, foot, and mouth disease recently!” she said. Since
adults can also get hand, foot, and mouth disease, I took a
close look at Mr. K’s hands and feet using a magnifying glass
(Figs.55.3 and 55.4).
Hand, foot, and mouth disease (HFMD) is a highly conta-
gious viral disease that appears as small macules, papules, or
vesicles mainly on the palms and soles, sides of hands and
feet, and inside the mouth. In Korea, as of 2022, it is designated as a Class 4 infectious disease (sample surveillance
infectious disease) that requires sample surveillance activities to investigate the prevalence in addition to Class 1–3
infectious diseases. It was rst described in 1958 and named
“hand-foot-and-mouth disease” in 1960. HFMD mainly
occurs in children under 10years old in summer and autumn,
but it can also occur in adults. Coxsackievirus A16 and
Enterovirus 71 are the most common causes, but
Coxsackievirus A5, A6, A7, A9, A10, B1, B2, B3, B5, and
Echovirus and other enteroviruses can also cause the disease.
It is transmitted through fecal–oral route, respiratory droplets, saliva, or direct contact, and it is known that transmission can occur between children, from children to adults, and
recently, transmission between adults has been reported.
Clinically, after an incubation period of about 3–6 days,
symptoms such as low fever, discomfort, abdominal pain,
and upper respiratory symptoms appear, most of the painful
oral lesions appear on the tongue, buccal mucosa, hard palate, and oropharynx. The lesions change from a small pink
macules or papules to a 4–8mm vesicular lesions accompanied by erythema, soon becoming the erosions. Skin lesions
occur soon after the mouth lesions appear, mainly on the
palms, soles, and sides of the hands and feet, but can also
occasionally appear on the legs, buttocks, genitals, and face.
Vesicles develop from the red macules and appear as vesicles
surrounded by erythema, with improvement occurring after
7–10 days. The vesicles are 1–5 mm in size, slightly oval
Figs. 55.1 and 55.2 Hand, foot, and mouth disease blisters and rashes observed on an adult’s hands and feet
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
J. Y. Jeong, Dermatology Diaries, https://doi.org/10.1007/978-981-97-1578-7_55
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Figs. 55.3 and 55.4 Hand-foot-mouth disease in adults
55 Hand, Foot, andMouth Disease (HFMD)
Figs. 55.5–55.7 Hand-foot-mouth disease in children
55 Hand, Foot, andMouth Disease (HFMD)
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225
rather than round, supercial, thin, lled with clear uid, and
surrounded by a 1 mm wide erythema zone. Usually, the
vesicles are not painful or itchy. It usually has a benign
course and heals naturally, but in some cases, it can show a
widespread vesicular appearance similar to eczema herpeticum. In some cases, fever and rash may reappear 1–3days
after the symptoms disappear, so observation is necessary.
Also, rarely, complications such as aseptic meningitis,
encephalitis, encephalomyelitis, meningoencephalitis can
occur, and neurological complications with paralytic symptoms similar to those of polio, myocarditis, and pulmonary
edema can occur. Severe complications are mainly caused by
Enterovirus 71 rather than Coxsackievirus A16. Recently,
there have been many reports of onychomadesis occurring
after suffering from hand, foot, and mouth disease.
Onychomadesis is a disease in which the proximal nail plate
separates from the nail bed and nail matrix due to temporary
arrest in the activity of the nail matrix. Especially, onychomadesis, which occurs after the onset of hand, foot, and
mouth disease, has been known to occur in many countries,
including Korea, since it was rst reported in 2000. However,
the changes in the nails are temporary, and normal growth
spontaneously returns within 1–4 months without special
treatment.
Although it is easy to diagnose due to the distribution of
clinically characteristic lesions, the diagnosis can be conrmed by proving the causative virus in lesions near the skin
rash area. Atypical forms of hand–foot–mouth disease that do
not accompany oral lesions are rarely reported, and in such
cases, diagnosis can be made through virus culture or antibody tests in addition to clinical symptoms. It should be differentiated from aphthous stomatitis, herpangina, herpes
simplex, chickenpox, erythema multiforme, etc.
(Figs.55.5–55.7, 55.8–55.10, 55.11–55.14, 55.15 and 55.16).
The lesions of hand–foot–mouth disease heal naturally, so
symptomatic treatment is sufcient. Treatment for symptoms is necessary in cases where discomfort is caused by
oral lesions. The skin lesions disappear within a few days,
and there is no need to prescribe ointment. For prevention,
avoid contact with children who have hand, foot, and mouth
disease. During the epidemic season, avoid places with many
children and instruct to wash hands thoroughly and brush
teeth after going out. When neurological symptoms appear in
children with hand, foot, and mouth disease, the possibility
of infection by enterovirus 71 must be considered. Especially,
Figs. 55.8–55.10 Hand–foot–mouth disease in children
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55 Hand, Foot, andMouth Disease (HFMD)
Figs. 55.11–55.14 Hand–foot–mouth disease in adults
Fig. 55.15 Lesions on the thigh and buttocks
when hand, foot, and mouth disease is prevalent, careful
observation must be made to ensure that encephalitis, meningitis, and polyneuritis occur along with paralysis symptoms
among the clinical manifestations. It is necessary to reassure
parents that normal spontaneous growth of nails will return
Fig. 55.16 Onychomadesis of the nails after suffering from hand–
foot–mouth disease
within 1–4months without special treatment for onychomadesis that occurs after suffering from hand, foot, and mouth
disease. I told Ms. K that adults can also get hand–foot–
mouth disease, informed her of precautions, and prescribed
for simple symptoms.
Steroid-Induced Acne, Steroid Acne
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Suddenly, something like acne spread all over my chest
and back, is it because of the orthopedic medicine I’ve
been taking recently? (Fig.56.1).
A man in his 30s, Mr. M, recently took medication containing steroids for a few weeks due to an orthopedic disease
and suddenly developed acne-like rashes on his chest and
back. He came in for a consultation, saying, “I hardly ever
had acne even when I was in school, but I’m really worried
because these suddenly appeared on my body!” Upon closer
examination, there were hardly any comedones typically
seen in acne, but numerous small, red papules and pustules
of similar shape were primarily found (Fig.56.2).
There are quite a variety of drugs that can cause acneiform eruptions, but acneiform eruptions caused by steroids
are the most common, and this has been recognized as a distinct disease entity called steroid-induced acne or steroid
acne. Steroid acne is a type of folliculitis that occurs after
topical or systemic administration of steroids, and it shows
different clinical and histological ndings from acne vul-
garis. It can occur at any age, but it is common in adolescence and young and middle adulthood and rare in children
and the elderly. The time for acneiform eruptions to occur
after steroid administration is roughly within 2 weeks or
within 2–4 weeks. Lesions are primarily observed as erythematous papules and pustules of uniform shape, and comedones, nodules, and cysts are rare. Itching and
post-inammatory hyperpigmentation are common, but
scars are not common, which clearly distinguishes it from
true acne both clinically and histopathologically. The common sites are the chest, back, neck, shoulders, and upper
arms, and sometimes it appears on the face and scalp and
rarely on the arms and buttocks.
In a 1973 study testing the induction of acne by occlusive
topical steroid therapy in more than 350 adult male volunteers, red papules of the same shape appeared within
7–14 days, and comedones formed within a few weeks.
Factors that promote the occurrence of steroid acne after
topical steroid application include (1) high concentration, (2)
Fig. 56.1 Steroid acne observed on the body
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
J. Y. Jeong, Dermatology Diaries, https://doi.org/10.1007/978-981-97-1578-7_56
Fig. 56.2 Steroid acne on the back and shoulders
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Fig. 56.3 Steroid acne showing uniform erythematous papules and
pustules
56 Steroid-Induced Acne, Steroid Acne
persistent occlusion, (3) young age over 30, (4) whites more
than blacks, (5) history or signs of acne, and (6) application
to the face or upper body. Acneiform eruptions caused by
systemic administration of steroids appear suddenly. On the
body, shoulders, and upper arms rather than the face, erythematous 1–3 mm hemispherical papules and pustules
appear in one form and show symmetrical distribution.
Comedones do not appear initially but can appear later as
secondary lesions of the pustules. Lesions caused by topical
application are less inammatory than those caused by systemic administration.
Histologically, it is a local folliculitis with neutrophil
deposition in the follicles and surrounding area.
Hyperkeratosis is not a characteristic nding and differs
from typical acne lesions as a result of the destruction of follicular epithelium. These inammatory lesions are not
located deep and do not grow as large as nodules (Figs.56.3,
56.4, 56.5, 56.6, 56.7, 56.8 and 56.9).
Figs. 56.4 and 56.5 Steroid acne observed on the chest
Figs. 56.6 and 56.7 Steroid acne that occurred after systemic steroid administration
56 Steroid-Induced Acne, Steroid Acne
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Figs. 56.8 and 56.9 Steroid acne that occurred after applying steroid cream
229
For the treatment of steroid acne, the use of the causative
steroid must be stopped, and treatments similar to those for
acne vulgaris, such as topical or systemic retinoids, tetracycline antibiotics, etc., have been used. However, in cases
where the treatment results are not satisfactory, it has been
reported that antifungal treatments such as itraconazole are
effective in treating typical Malassezia folliculitis and acneiform eruptions induced by steroids, based on the fact that
steroids are one of the important triggers of Malassezia fol-
liculitis (Pityrosporum folliculitis), clinical similarities,
direct smear examination ndings, and treatment responses.
Mr. M said, “Fortunately, I don’t have to take orthopedic
medicine anymore, so I just need to get treatment, right?”
However, I explained in advance that even if the steroid is
stopped and treatment is started, the inammation in the follicle does not improve quickly and it takes some time to
disappear.
Cement Dermatitis
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While I was working, my pants got wet with cement and
came in contact with it for a while. It was burning and
very painful due to cement poisoning (Fig.57.1).
A 40-year-old man, K, came for treatment after his leg
had been in contact with cement for a while during cement
work, and countless small wounds were formed on his skin,
and he had severe itching, burning, and pain. “Is this the
cement poisoning? I didn’t know it would be this severe,” he
said (Fig.57.2).
Cement refers to an inorganic bonding hardener whose
main ingredient is lime, etc., which hardens when kneaded
with water or a solution and can act as a binder or adhesive.
Portland cement, which is most commonly used in construction and civil engineering sites, consists of calcium oxide,
silicon dioxide, aluminum oxide, iron oxide, magnesium
oxide, sulfur dioxide, hexavalent chromium, and other alkali
oxides. In the workplace, workers can easily be exposed to
cement, which can lead to various occupational skin diseases. These include irritant contact dermatitis and allergic
contact dermatitis, also called cement dermatitis, as well as
burns and skin ulcers.
When cement and water are mixed, the most abundant
calcium oxide turns into calcium hydroxide, which has a
strong alkalinity of pH12–13. This transformation is accompanied by an exothermic reaction, so contact with wet cement
can cause chemical burns and thermal damage, leading to
full-thickness burns, skin ulcers, and irritant contact dermatitis. If it comes into contact with the conjunctiva, it can
cause irritation, excessive tear secretion, ulcers, and even
perforation of the eyeball. It can also cause inammation,
ulcers, and perforation of the mucous membrane of the upper
respiratory tract, leaving serious sequelae if exposed in large
amounts occupationally. Chromium, although only about
0.002% of the cement’s composition, is a common cause of
allergic contact dermatitis, which can also be caused by
nickel or cobalt in some cases. Allergic contact dermatitis
caused by chromium has a very poor prognosis, and it often
does not improve even with a change of occupation, so it is
important to prevent initial exposure. Chromium is a silverwhite heavy metal that exists in various forms depending on
its valence, mainly in the stable forms of trivalent chrome
and hexavalent chrome. Trivalent chrome is generally found
Fig. 57.1 Cement dermatitis and burns observed on the leg
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
J. Y. Jeong, Dermatology Diaries, https://doi.org/10.1007/978-981-97-1578-7_57
Fig. 57.2 Cement dermatitis and burns that occur after contact with
cement
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57 Cement Dermatitis
in nature, while hexavalent chrome is mostly combined with
oxygen due to its insolubility and acts as a powerful oxidizing pigment, so it is widely used in industries such as plating,
corrosion inhibitors, pigment manufacturing, leather processing, cement, etc. (Figs.57.3 and 57.4).
Such chromium is highly corrosive and requires special
attention and appropriate protective equipment. If it comes
into direct contact with the skin, it can cause burns, ulcers,
and contact dermatitis. Also, if exposure to chromium continues for a long period, it can cause chrome ulcers on the
skin, allergic asthma in the respiratory system, perforation of
the nasal septum, and there are even reports that it can cause
cancer in the lungs, kidneys, and liver. Allergic contact dermatitis caused by chromium is more common in men and
usually occurs occupationally. Among many occupations,
cement workers are the most likely to have problems with
chromium. Like nickel, chromium contact dermatitis also
has a poor prognosis. Chromium dermatitis can persist long
after a worker changes jobs and is no longer exposed. Mr. K
was advised to avoid direct contact with cement in the future,
and he needs to receive burn dressings equivalent to burn
treatment along with drug treatment for 2weeks (Figs.57.5,
57.6, and 57.7–57.10).
Fig. 57.3 Irritant contact dermatitis, skin ulcers, and burns caused by
cement in a cement worker
Fig. 57.5 Cement dermatitis that occurred after working with cement
barefoot
Fig. 57.4 Irritant contact dermatitis, skin ulcers, and burns caused by
contact with cement
Fig. 57.6 Cement dermatitis and skin ulcers that occurred after contact
with cement
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