1._SKIN_DISEASES_IN_CHILDHOOD_template_2025_copy.pdf

Transcript

1. SKIN DISEASES IN CHILDHOOD Student: Veronika Vymlátilová Mentor: assist. prof. Mateja Starbek Zorko, MD, PhD
2. 1. TINEA CAPITIS 2. INFANTILE HEMANGIOMA 3. ATOPIC DERMATITIS
3. 1. TINEA CAPITIS ▪ETHIOLOGY ▪ Dermatophytes: ▪ in 90% Microsporium canis; ▪ Central and Southern Europe ▪ Cats, among siblings ▪ Seasonal: July-October ▪ Trichophyton tonsurans: ▪ North America ▪ Close contact with an infected person or subject. ▪ Trichophyton schoenleinii: ▪ - Poor hygienic conditions. ▪ - Tinea favosa. ▪ others: T. violaceum, T. schoenleinii, M. audouinii
4. PATHOGENESIS: 1. Fungal entry and colonization: dermatophytes from environment or fomites enter the scalp hair = Asymptomatic colonization 2. Enzyme production: keratinase → break down keratin = source of nutrients + weakening of the skin’s barrier → invade the stratum corneum of the epidermis 3. Hair follicles invasion (ectothrix or endothrix) and sebaceous gland ducts → after 3 weeks this leads to fragility, breakage and visible signs like patchy alopecia or grey-white scaling
5. TRANSMISSION o Person-to-person – most common o Animal-to-person – cats and dogs o Via fomites o Enviromental reservoairs (school furniture, floors, locker rooms) o Spores present on asymptomatic carriers, animals or inanimate objects.
6. Ectothrix: o Growth outside the hair shaft. o Zoophilic dermatophytes ( M. canis, Trichophyton verrucosum) Endothrix o Growth within the hair shaft. o Anthropophilic dermatophytes (Trichophyton spp) o Variants: a) Black dot (resembling seborrheic dermatitis) b) Kerion (with boggy inflammatory plaques) c) Favus (with arthroconidia and airspaces within hair shaft) CLASSIFICATION
7. EPIDEMIOLOGY ▪ In 85% of children up to 9 years (more common in boys) ▪ Densely populated areas, kindergartens, schools ▪ Immunocompromised ▪ Contact with animals (dogs, cats), close contact with peers, through objects (toothbrushes, combs, towels) ▪ Asymptomatic vectors (humans or animals) ▪ Geographical distribution of each fungus ▪ North and Central America: 90% T. tonsurans. Less common: M. canis. ▪ Europe: M. canis, T, violaceum, M. audouinii, ▪ Asia: T. violaceum, M. canis. ▪ Africa: T. violaceium, T. schonleinii, M. canis.
8. CLINICAL PICTURE CLINICAL PICTURE ▪ It depends on the causative agent and the inflammatory response of the host. ▪ Tinea capitis superficialis ▪ Tinea capitis profunda and Kerion celsi ▪ Tinea favosa / Favus
9. TINEA CAPTIS SUPERFICIALIS ▪ Mildest form ▪ One or more round foci with greyish scales. ▪ They may be without inflammatory signs or they may be mild (mild erythema). ▪ Uneven hair breakage → a few mm above the skin surface = “black dot” variant ▪ No pain or pus
10. TINEA CAPTIS PROFUNDA ▪ Broken hair, follicular pustules, pus leaking under pressure ▪ Reason: T. superficialis not treated for a longer time or treated incorrectly (f.e. with topical steroids) ▪ Severe (rare): Kerion Celsi ▪ Zoophilic dermatophytes (T. verrucosum, T. mentagrophytes vad. Mentagrophytes) ▪ Extensive, painful, inflamed area, carbuncle-like inflammation, pus leaking from follicular pustules, and sinuses may form at depth → characteristic regional lymphadenopathy, elevated temperature + often secondary bacterial infection ▪ Heals with SCARRING ALOPECIA
11. TINEA FAVOSA ▪ T. schoenleini ▪ Rare, poor hygiene. ▪ Chronic, usually from childhood onwards ▪ Early: Perifollicular erythema and matting of hair ▪ Later: Thick yellow adherent crusts (SCUTULA) composed of skin debris and hyphae that are pierced by remaining hair shafts Fetid odor. Unbroken hair grows without shine, below erosion ▪ Little tendency to clear spontaneously, often: SCARRING ALOPECIA
12. DIAGNOSIS o History and clinical picture o Dermatoscopy – comma hairs, corkscrew hairs, black dots o Microscopic examination of hair or scarification of the scalp (Hyphae and arthrospores) o Microbiological cultures of broken hair, skin scales (hyphae, macroconidia) o Growth in 10-14 days o Skin swab for pathogenic bacteria (usually S. aureus)
13. M. canis • Investigation with Wood's lamp: o M. canis: blue-green o T. schoenleinii: yellowish o T. tonsurans: without fluorescence
14. Seborrheic dermatitis DIFFERENTIAL DIAGNOSIS • Tinea capitis superficialis: seborrheic dermatitis, psoriasis, pityriasis sicca • Tinea capitis profunda: staphylococcal folliculitis or carbuncle, lichen planus, discoid lupus, other causes of alopecia • Favus: Impetigo, ecthyma and crusted scabies Lichen planus
15. Tinea capitis: favus COURSE • Good prognosis. • Without treatment, some of the forms can develop into a chronic form. • More severe/ chronic untreated forms (Kerion and favus) → SCARRING ALOPECIA. Scarring alopecia
16. TREATMENT • ALWAYS SYSTEMIC: o antifungals (itraconazole, fluconazole, griseofulvine, terbinafine) - terbinafine NOT a good option for T. capitis caused by M. canis -> other systemic antimycotic, f.e. itraconazole! • Additionally LOCAL antifungal cream: o terbinafine or azole antifungal • We recommend washing the scalp with an antifungal shampoo (ketoconazole, selenium sulfide) o Reducing the transfer of spores o Cover infected areas – NO transmission • Control mycological results 1x / 4-6 weeks: o 1. negative report → we cancel the SYSTEMIC TH o 2. negative report → cancel LOCAL TH • Systemic antibiotic (if associated bacterial infection)
17. 2. INFANTILE HEMANGIOMA ▪ Most frequent neonatal tumors - benign vascular tumors ▪ 2 types: CAPILLARY and CAVERNOUS ▪ Typical onset in first 4 weeks of life, rarely at birth – grow until 5 months of life, then shrink in size and disappear in next few years ▪ If at birth, mostly precursor lesions are seen ▪ 4-10 % prevalence ▪ More frequent in: white people, girls, prematurly born children (<1000g), older mothers, placenta previa and preeclampsia
18. CLINICAL PICTURE • PRECURSOR LESIONS: anemic patches with telangiectasias • Clinical appearance: red or redish-purple papules or plaques with a smooth surface, variable shapes and sizes, solitary, focal, superficial, on the head or neck • Typical 3 phase progression: 1. Proliferation phase: a few months 2. Involucion phase: shrinking, greyish and stripy patches 3. Regression phase: completly disapear or leave atrophic, binding/fatty tissue or telangiekctatic residual lesions.
19. COURSE  usualy asymptomatic  90% complete remission by 5 years  may ulcerate (mostly in proliferation phase)  possible local complications, depending on the site – more periocular, nasal, labial, on the chin, ear lobes, auditory canal, anogenital  in multiple and extensive segmented hemangiomas, consider systemic complications – may be linked with other syndromes, must involve other specialists ulcerated infantile hemangioma
20. DIAGNOSTICS, DIFFERENTIAL DIAGNOSIS AND TREATMENT • Dg: clinically (absent at birth, 3-phase progression) • If diagnosis is unclear: color ultrasound, MR, histology + immunohistochemistry. • Ddg: vascular malformations, other vascular tumors, tumors of different origin • Treatment: spontaneous remission • If not, in accordance with size, localisation, age, growth and acompanied complications – medications (systemic beta-blocker propranolole), surgical, laser
21. 3. ATOPIC DERMATITIS ▪ Also known as atopic eczema, is a long-term type of inflammation of the skin. ▪ The most common dermatitis of young age. ▪ It usually starts by the age of 3. ▪ The cause is unknown. ▪ Many people with atopic dermatitis develop hay fever or asthma.
22. ETIOPATOLOGY  GENETIC CAUSES  Mutation of filaggrin  ABNORMAL SKIN BARIER  Invasion of microorganisms  IMUNE RESPONSE:  Type 2 inflammation (Th2 and CD4+ helper cells)  SPECIFIC FACTORS  Food allergies - type 1 hypersensitivity reaction  S.aureus  PSYCHOSOMATIC RESPONSE Stress – worsens the symptoms
23. CLINICAL PICTURE Itchy, red, swollen and cracked skin. A) BABIES  Red skin (macules) and edema at the location of inflammation  Face, scalp, neck  Symmetric, raised lessions form in the bends of the arms or legs (vesicules, papules)  It speeds to the body and extremities  Not under the diaper  Due to itching and sleeplessness, the children loose appetite and weight
25. CLINICAL PICTURE B) AFTER 1 YEAR OF AGE  Disappears from the face  Distal parts of the extremities: wrists and ankles C) AFTER THE AGE OF 5 + ADOLTS  Neck, inner elbows and knees  Clear fluid may come from the affected areas D) OLDER CHILDREN + ADULTS, when chronic inflammation:  lichenified areas
26. DIAGNOSIS (HANIFIN & RAJKA) 4 main criteria:  Itch  Typical clinical picture according to age  Family history with atopy diseases  Chronicity Additional criteria  Dry skin  skin wrinkles on the neck  Dennie-Morgan infraorbital fold  Pale face  pityriasis alba  keratosis pilaris  Ichtyosis  Hyperlinearity of the palms  …
27. LAB TESTS  Allergic tests  skin prick test  Lab  Whole/specific IgE
28. TREATMENT  Basics  Parents awareness  Everyday skin care (emollients, synthetic soaps)  Avoiding the worsening causes/triggers  Inflammation  Antiseptic baths/soaps  Corticosteroids locally  Immunomodulators locally
29. TREATMENT  Itching  Systemic antihistaminics  Wet wraps  Moderate to severe/ generalised cases  Phototherapy (nbUVB)  Systemic immunomodulators and immunosuppressives (CyA, MTX – both off lable in childhood)  Newer: biological therapy (dupilumab – IL-4 and IL-13 inhibitor), JAK inhibitors (baricitinib, upadacitinib)  Hospitalization
30. DIFFERENTIAL DIAGNOSIS