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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5192_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Dedications
- •Contributors
- •Acknowledgments
- •Preface
- •1 Basic science
- •1.1 Structure and function of the skin
- •Epidermis
- •Cellular biology of the epidermis
- •Dermal cells of importance
- •Structural components and cell biology of the dermis
- •1.2 Embryology
- •1.3 Wound healing
- •Dermis
- •1.4 Genetics
- •Basic cell biology of genome
- •Inheritance patterns
- •1.5 Ultraviolet light
- •Ultraviolet light (Fig. 1.8)
- •Minimal erythema dose
- •1.6 Immunology
- •Innate immunity
- •Adaptive immunity
- •1.6.2 Immunologic mediators
- •Cytokines
- •Pattern recognition receptors
- •Antimicrobial proteins (AMPs)
- •The complement system
- •B cells
- •T cells (majority of lymphocytes)
- •Innate lymphoid cells
- •NK cells
- •Mononuclear phagocytes
- •Langerhans cells
- •Dendritic cells
- •Mast cells
- •Eosinophils
- •Neutrophils
- •1.6.4 Major histocompatibility complex
- •1.7 Laboratory techniques
- •1.7.1 Tissue acquisition and processing
- •Polymerase chain reaction (PCR)
- •Quantitative reverse transcriptase PCR (qRT-PCR)
- •16S ribosomal RNA (rRNA) sequencing
- •DNA sequencing
- •RNA sequencing
- •Fluorescence in situ hybridization (FISH)
- •Immunohistochemistry (IHC)
- •Enzyme-linked immunosorbent assay (ELISA)
- •1.7.3 Cellular engineering and gene therapy
- •2 Dermatopharmacology
- •2.1 ANTIHISTAMINES
- •Mechanism
- •Other antihistamines
- •Introduction
- •Mucocutaneous
- •Systemic
- •Teratogenicity
- •Contraindications
- •Interactions
- •2.3 CORTICOSTEROIDS
- •Hypothalamic-pituitary-adrenal (HPA) axis suppression (Box 2.1)
- •Psychiatric changes
- •Contraindications
- •Pregnancy
- •Clinical use
- •Intramuscular CS
- •Pulse IV CS
- •Adalimumab
- •Certolizumab pegol
- •Golimumab
- •Indications
- •Ustekinumab
- •IL-17 inhibitors
- •IL-23 inhibitors
- •Spesolimab
- •Rituximab
- •IL-1 inhibitors
- •Omalizumab
- •Dupilumab
- •Lebrikizumab and tralokinumab
- •Nemolizumab
- •Vismodegib and sonidegib
- •Intralesional CS
- •Monitoring
- •2.4 IMMUNOMODULATORY AGENTS
- •Apremilast and other PDE-4 inhibitors
- •Janus Kinase (JAK) and Tyro inhibitors
- •Agents used in dermatology
- •Laboratory monitoring
- •Azathioprine
- •Important monitoring points
- •Cyclosporine
- •Important pharmacology points
- •Indications
- •Important monitoring points
- •Methotrexate
- •Important pharmacology points
- •Indications and contraindications
- •Important monitoring points
- •Important pharmacology points
- •Indications
- •Monitoring guidelines
- •Cytotoxic agents
- •Hydroxyurea
- •Cyclophosphamide
- •Chlorambucil
- •Antimalarial agents
- •Important pharmacology points
- •Indications
- •Dapsone
- •Important pharmacology points
- •Indications
- •Important monitoring points
- •Etanercept
- •MEK inhibitors (trametinib, cobimetinib, binimetinib)
- •Ipilimumab
- •PD-1 inhibitors (pembrolizumab, nivolumab, cemiplimab) and PD-L1 inhibitors (avelumab, atezolizumab)
- •Imatinib mesylate
- •Ibrutinib
- •Talimogene
- •Mechlorethamine hydrochloride
- •Brentuximab vedotin
- •Mogamulizumab
- •Romidepsin and vorinostat
- •2.6 ANTIMICROBIAL AGENTS
- •Topical antibacterial agents
- •Bacitracin
- •Benzoyl peroxide
- •Metronidazole
- •Azelaic acid
- •Systemic antibacterial agents
- •Penicillins
- •Polymyxin B
- •Neomycin
- •Mupirocin
- •Retapamulin
- •Gentamicin
- •Iodoquinol
- •Cephalosporins
- •Vancomycin
- •Macrolides
- •Fluoroquinolones
- •Tetracyclines
- •Clindamycin
- •Carbapenems
- •Linezolid
- •Daptomycin
- •Others
- •Antiviral agents
- •Acyclovir
- •Valacyclovir
- •Famciclovir and penciclovir
- •Foscarnet
- •Bleomycin
- •Podophyllin resin and podophyllotoxin
- •Cantharidin
- •Sinecatechins
- •5-Fluorouracil and imiquimod (discussed in section 2.5)
- •I. Azoles
- •Itraconazole
- •Fluconazole
- •Ketoconazole
- •Voriconazole
- •Posaconazole
- •Miconazole, clotrimazole, and econazole
- •Efnaconazole
- •Luliconazole
- •II. Allylamines/benzylamines
- •Terbinafne
- •Butenafne
- •IV. Ciclopirox olamine
- •VI. Nystatin
- •VIII. Tavaborole
- •Antiparasitic agents (Tables 2.7 and 2.8)
- •2.7 PHOTOTHERAPY
- •UVA modalities
- •Psoralen plus UVA (PUVA)
- •UVA-1 (340–400 nm)
- •UVB modalities
- •Extracorporeal photochemotherapy
- •Photodynamic therapy (PDT)
- •2.8 MISCELLANEOUS AGENTS
- •Sunscreens
- •Topical cosmetic agents
- •Bimatoprost
- •Brimonidine and oxymetazoline
- •Hydroquinone
- •Psychiatric agents
- •Antiandrogens and androgen inhibitors
- •Spironolactone
- •Finasteride and dutasteride
- •Combination oral contraceptive pills
- •Clascoterone
- •Calcipotriene and calcitriol
- •Attenuated androgens
- •Danazol and stanozolol
- •Colchicine
- •Potassium iodide
- •Thalidomide
- •Topical calcineurin inhibitors
- •Pimecrolimus and tacrolimus
- •Intravenous immunoglobulin (IVIG)
- •Glycopyrrolate
- •Oxybutynin
- •Botulinum toxin
- •Aluminum chloride
- •2.9 DRUG INTERACTIONS AND THE CYTOCHROME P-450 SYSTEM
- •Key points
- •CYP1A2
- •CYP2C9
- •CYP2D6
- •CYP3A4 (most relevant to dermatologists)
- •Classic CYP mnemonics
- •2.10 DRUG REACTIONS
- •Urticaria, angioedema, and anaphylaxis
- •Fixed drug eruption/Stevens-Johnson syndrome/toxic epidermal necrolysis
- •Drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)
- •Acute generalized exanthematous pustulosis (AGEP)
- •Photosensitive drug reactions
- •Drug-induced pigmentary changes
- •Bullous drug reactions, lichenoid drug eruptions, drug-induced connective tissue disease
- •Other drug eruptions
- •3 General dermatology
- •3.1 Papulosquamous dermatoses
- •3.2 Eczematous dermatoses
- •3.3 Interface dermatitis
- •Vacuolar interface dermatitis
- •Autoimmune connective tissue disease (AICTD)
- •Erythema multiforme (EM)
- •Stevens-johnson syndrome (SJS), and toxic epidermal necrolysis (TEN, lyell’s syndrome)
- •Pityriasis lichenoides
- •Fixed drug eruption (FDE)
- •Graft- versus- host disease (GVHD)
- •Lichenoid interface dermatitis
- •Lichen planus (LP)
- •Keratosis lichenoides chronica (KLC)
- •Erythema dyschromicum perstans (ashy dermatosis)
- •Lichenoid keratosis (benign lichenoid keratosis [BLK], LP-like keratosis)
- •Lichen nitidus
- •3.4 Blistering diseases
- •Pemphigus disease family
- •Pemphigus vulgaris (PV)
- •Pemphigus foliaceus (PF)
- •Paraneoplastic pemphigus (PNP)/paraneoplastic autoimmune multiorgan syndrome (PAMS)
- •Autoimmune subepidermal blistering diseases
- •Bullous pemphigoid (BP; pemphigoid)
- •Mucous membrane pemphigoid (MMP; cicatricial pemphigoid)
- •Linear IgA bullous dermatosis/chronic bullous disease of childhood (LABD/CBDC)
- •Epidermolysis bullosa acquisita
- •Bullous systemic lupus erythematosus
- •Dermatitis herpetiformis (duhring disease)
- •Inherited blistering diseases
- •Epidermolysis bullosa (see chapter 4)
- •Darier disease (keratosis follicularis)
- •Other blistering diseases
- •Lupus band test (LBT)
- •Lupus erythematosus
- •Chronic cutaneous lupus erythematosus (CCLE)
- •Subacute cutaneous lupus erythematosus
- •Acute cutaneous lupus erythematosus (ACLE)
- •Other rare cutaneous lupus variants
- •Systemic lupus erythematosus (SLE)
- •Drug-induced SLE (DI-SLE)
- •Lupus-related diseases
- •Other autoimmune connective tissue diseases and sclerosing dermopathies
- •Dermatomyositis (DM)
- •Sjögren’s syndrome
- •Relapsing polychondritis
- •Mixed connective tissue disease (MCTD)
- •Rheumatoid arthritis
- •Systemic-onset juvenile idiopathic arthritis (still’s disease)
- •Morphea (localized scleroderma)
- •Eosinophilic fasciitis (shulman syndrome)
- •Abnormalities of connective tissue
- •3.6 Granulomatous/histiocytic disorders
- •Non-infectious granulomas
- •Granuloma annulare (GA)
- •Annular elastolytic giant cell granuloma (actinic granuloma of O’Brien
- •Interstitial granulomatous dermatitis and arthritis (IGDA) and palisaded neutrophilic granulomatous dermatitis (PNGD)
- •Interstitial granulomatous drug eruption
- •Necrobiosis lipoidica (necrobiosis lipoidica diabeticorum, NLD)
- •Necrobiotic xanthogranuloma (NXG)
- •Cutaneous crohn’s disease
- •Sarcoidosis
- •Histiocytoses
- •Langerhans cell histiocytosis (LCH)
- •Non-langerhans cell histiocytoses (discussed in Table 3.23)
- •Malignant histiocytic disorders
- •3.7 Monoclonal gammopathies of dermatologic interest
- •3.8 Xanthomas
- •3.9 Urticaria and angioedema
- •3.10 Neutrophilic dermatoses
- •Amicrobial pustulosis of the folds
- •3.11 Eosinophilic disorders
- •Granuloma faciale
- •Eosinophilic folliculitis
- •Papuloerythroderma of ofuji
- •Wells’ syndrome (eosinophilic cellulitis)
- •Hypereosinophilic syndrome (HES)
- •3.12 Figurate erythemas
- •3.13 Follicular and eccrine/apocrine disorders
- •Acne variants
- •Acne fulminans
- •Acne conglobata
- •Solid facial edema in acne
- •Acne mechanica
- •Neonatal acne (neonatal cephalic pustulosis)
- •Infantile acne
- •Transverse nasal crease
- •Acne in setting of endocrinologic abnormality
- •Acne cosmetica
- •Pomade acne
- •Chloracne
- •Radiation acne
- •Acneiform eruptions
- •Drug-induced acne
- •Acne-associated syndromes
- •SAPHO (chronic recurrent multifocal osteomyelitis)
- •PAPA
- •HAIR-AN
- •Apert syndrome (acrocephalosyndactyly)
- •Rosacea
- •Epidemiology
- •Rosacea subtypes
- •Erythematotelangiectatic (vascular)
- •Phymatous
- •Ocular
- •Rosacea variants
- •Solid facial edema in rosacea (morbihan disease and rosacea lymphedema)
- •Pyoderma faciale (rosacea fulminans)
- •Granulomatous rosacea
- •Lupus miliaris disseminatus faciei
- •Folliculitis
- •Gram-negative folliculitis
- •Hot tub folliculitis
- •Eosinophilic folliculitis
- •Disseminate and recurrent infundibulofolliculitis
- •Viral-associated trichodysplasia
- •Pseudofolliculitis barbae
- •Acne keloidalis nuchae
- •Follicular occlusion tetrad (acne conglobata, hidradenitis suppurativa, dissecting cellulitis of the scalp, and pilonidal cyst)
- •Hidradenitis suppurativa (acne inversa)
- •Pilonidal cyst
- •Dissecting cellulitis of the scalp and acne conglobata (discussed in alopecia and acne sections)
- •Other diseases of eccrine and apocrine sweat glands
- •Hyperhidrosis
- •Hypohidrosis and anhidrosis
- •Miliaria
- •Bromhidrosis
- •Chromhidrosis
- •Fox-fordyce disease (apocrine miliaria)
- •3.14 Drug reactions
- •3.15 Photodermatoses and other physical dermatoses
- •Temperature-related dermatoses
- •Thermal burns
- •Erythema ab igne
- •Cold injuries
- •Photoaging
- •Polymorphous light eruption
- •Hydroa vacciniforme (see Chapter 4)
- •Actinic folliculitis
- •Chronic actinic dermatitis
- •Actinic prurigo (see chapter 4)
- •Solar urticaria
- •Mechanical injuries
- •3.17 Neurodermatology and psychodermatology
- •Cutaneous manifestations of psychiatric illness or self-induction
- •Delusions of parasitosis
- •Excoriation disorder (neurotic excoriations)
- •Factitial dermatitis/dermatitis artefacta
- •Gardner-diamond syndrome
- •Body dysmorphic disorder
- •Cupping/coining
- •Other neurocutaneous dermatoses
- •Scalp dysesthesia/burning scalp syndrome
- •Burning mouth syndrome
- •Brachioradial pruritus
- •Notalgia paresthetica
- •Meralgia paresthetica
- •Trigeminal trophic syndrome
- •Familial dysautonomia/riley-day syndrome
- •Auriculotemporal nerve syndrome (frey syndrome)
- •3.18 Palmoplantar keratodermas
- •3.19 Nutritional disorders in dermatology
- •3.21 Ulcers (Table 3.33)
- •3.22 Vasculitides, vasculopathies, and other vascular disorders
- •Subtypes of cutaneous small vessel vasculitis
- •Henoch-schonlein purpura (HSP)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Key features of adult HSP
- •Key features of childhood HSP
- •Treatment
- •Laboratory testing: See CSVV section
- •Pathology
- •Acute hemorrhagic edema of infancy (Fig 3.86)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Treatment
- •Urticarial vasculitis
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory testing
- •Treatment (Table 3.41)
- •Erythema elevatum diutinum
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Treatment
- •Mixed cryoglobulinemia (see cryoglobulinemia section)
- •Small to medium vessel vasculitis
- •Granulomatosis with polyangiitis (wegener)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Treatment
- •Microscopic polyangiitis (MPA)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory testing: See CSVV, especially:
- •Treatment
- •Eosinophilic granulomatosis with polyangiitis (churg-strauss syndrome)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation: Three classic stages (Table 3.47)
- •Pathology
- •Laboratory testing
- •Treatment
- •Medium vessel vasculitis
- •Subtypes: PAN and kawasaki’s disease
- •Polyarteritis nodosa
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory testing: See CSVV
- •Treatment
- •Kawasaki disease (acute febrile mucocutaneous lymph node syndrome)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation (Fig. 3.90)
- •Laboratory testing
- •Treatment
- •Key testing facts
- •Large vessel vasculitis
- •Subtypes: Temporal arteritis and Takayasu’s arteritis
- •Temporal arteritis (giant cell arteritis)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory workup
- •Treatment
- •Takayasu’s arteritis
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory workup
- •Treatment
- •Summary of organ system involvement in various vasculitides (Table 3.49)
- •Cryoglobulinemias
- •Epidemiology
- •Thrombosis and thrombotic syndromes
- •Important subtypes
- •Calciphylaxis
- •Antiphospholipid syndrome
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Treatment
- •Pathogenesis
- •Clinical presentation
- •Pathology
- •Treatment
- •Other vasculopathies (Table 3.51)
- •Other vascular disorders
- •Venous lake
- •Telangiectasia
- •Erythromelalgia
- •Livedo reticularis (LR)
- •Angiospastic macules (bier spots)
- •3.23 Panniculitides and lipodystrophies
- •3.24 Dermatoses of pregnancy
- •3.25 Hair, nail, and mucosal disorders
- •Non-scarring alopecia
- •Androgenetic alopecia
- •Trichotillomania
- •Alopecia areata
- •Temporal triangular alopecia
- •Congenital atrichia with papules
- •Cicatricial (scarring) alopecia
- •Central centrifugal cicatricial alopecia
- •Lichen planopilaris
- •Acne keloidalis nuchae
- •Dissecting cellulitis of the scalp (perifolliculitis capitis abscedens et suffodiens)
- •Folliculitis decalvans
- •Traction alopecia
- •Hair shaft abnormalities
- •Hypertrichosis and hirsutism
- •Hypertrichosis
- •Nail disorders
- •Mucosal disorders
- •3.26 Pigmentary disorders
- •Disorders of hypopigmentation and depigmentation
- •Vitiligo
- •Halo nevus
- •Chemical and physical agent-induced hypopigmentation
- •Idiopathic guttate hypomelanosis
- •Progressive macular hypomelanosis
- •Nevus anemicus
- •Pigmentary mosaicism
- •Hypomelanosis of ito
- •Nevus depigmentosus
- •Disorders of hyperpigmentation
- •Melasma
- •Erythema dyschromicum perstans (ashy dermatosis) discussed in Section 3.3
- •Lichen planus pigmentosus
- •Linear and whorled nevoid hypermelanosis
- •Prurigo pigmentosa
- •Familial progressive hyperpigmentation
- •Endocrinopathies
- •Pigmentary demarcation lines (aka futcher’s lines, voight lines, ito’s lines)
- •4 Pediatric dermatology
- •4.1 Neonatal dermatology
- •4.2 Viral exanthems and select infectious disorders of childhood
- •4.3 Inherited pigmentary disorders
- •Hypo-/depigmentation
- •Pigmentary mosaicism
- •Oculocutaneous albinism (OCA)
- •Silvery hair syndromes
- •Griscelli syndrome
- •Hermansky-Pudlak syndrome
- •Piebaldism
- •Waardenburg syndrome
- •Hyperpigmentation
- •McCune-Albright syndrome
- •Lentiginoses syndromes
- •Hereditary dyschromatoses
- •Dyschromatosis symmetrica hereditaria (acropigmentation of Dohi)
- •Dyschromatosis universalis hereditaria
- •Naegeli-Franceschetti-Jadassohn syndrome (NFJS)/dermatopathia pigmentosa reticularis (DPR)
- •4.4 Epidermolysis bullosa
- •4.5 Tumor syndromes
- •4.6 Vascular tumors, malformations, and related vascular disorders
- •Vascular tumors
- •Phace syndrome
- •LUMBAR/SACRAL syndrome
- •Multiple hemangiomas
- •Kasabach-Merritt phenomenon
- •Vascular malformations
- •Capillary malformations (CM)
- •Sturge-Weber syndrome (encephalotrigeminal angiomatosis)
- •Phakomatosis pigmentovascularis
- •Phakomatosis pigmentokeratotica
- •PIK3CA-related overgrowth spectrum (PROS)
- •Klippel-trenaunay syndrome
- •Macrocephaly capillary malformation syndrome
- •Cloves syndrome
- •Proteus syndrome
- •Beckwith-wiedemann syndrome
- •Diffuse capillary malformation with overgrowth (DCMO)
- •Venous malformations
- •Maffucci syndrome (enchondromas with multiple angiomas)
- •Blue rubber bleb nevus syndrome
- •Glomulovenous malformations (GVMs; previously termed “glomangiomas”)
- •Lymphatic malformations
- •Macrocystic lymphatic malformations (cystic hygroma)
- •Gorham-stout (disappearing bone) disease
- •Congenital lymphedema (hereditary congenital lymphedema, Nonne-Milroy syndrome)
- •Arteriovenous malformations
- •AVMs
- •Parkes-weber syndrome
- •Cobb syndrome (cutaneomeningospinal angiomatosis)
- •Other vascular disorders
- •4.7 Disorders of hair and nails
- •Pachyonychia congenita
- •Ectodermal dysplasias
- •Hypohidrotic ectodermal dysplasia (Christ-Siemens-Touraine syndrome)
- •Hidrotic ectodermal dysplasia (Clouston syndrome)
- •Ectodermal dysplasias due to p63 mutation
- •Schöpf-Schulz-Passarge syndrome
- •Other disorders
- •Rubinstein-Taybi syndrome
- •Parakeratosis pustulosa
- •Congenital malalignment of the great toenails
- •4.8 Inherited metabolic and nutritional disorders
- •4.9 Inherited connective tissue disorders
- •4.10 Autoinflammatory disorders (periodic fever syndromes)
- •4.12 Premature aging syndromes and DNA repair disorders
- •4.13 Primary immunodeficiency disorders with cutaneous manifestations
- •4.14 Disorders of cornification
- •Actinic prurigo
- •Diaper dermatitis
- •Juvenile plantar dermatosis
- •Acropustulosis of infancy
- •Trichorhinophalangeal syndrome
- •Midas syndrome (also MLS or microphthalmia with linear skin defects)
- •H syndrome
- •Cutaneous mastocytosis
- •Neutrophilic eccrine hidradenitis of childhood
- •5 Infectious diseases
- •5.1 Viral diseases
- •Herpes simplex virus (HHV-1/HSV-1 and HHV-2/HSV-2)
- •Varicella zoster virus (VZV; HHV-3)
- •Epstein-Barr virus (HHV-4)
- •Cytomegalovirus (HHV-5)
- •HHV-6 (Roseola infantum, exanthem subitum, sixth disease)
- •HHV-7
- •HHV-8
- •Poxviruses
- •Zika virus
- •Dengue virus
- •Viral hepatitides (Table 5.2)
- •Viral-associated trichodysplasia of immunosuppression
- •COVID-19
- •5.2 HIV/AIDS dermatology
- •5.3 Bacterial infections
- •Staphylococcal skin infections
- •Corynebacterial skin infections
- •Clostridium skin infections
- •Filamentous bacteria
- •Other gram-positive infections
- •Pseudomonas
- •Bartonella
- •Rickettsia
- •Other gram-negative skin infections
- •Borrelia
- •Nonvenereal (endemic) treponematoses
- •Syphilis
- •Cutaneous tuberculosis
- •Leprosy (hansen’s disease)
- •Atypical mycobacteria
- •Tinea versicolor (pityriasis versicolor)
- •Piedra
- •Tinea nigra
- •Sporotrichosis
- •Lobomycosis
- •Mycetoma (madura foot)
- •Chromoblastomycosis
- •Histoplasmosis
- •Blastomycosis (“north American blastomycosis”)
- •Coccidioidomycosis
- •Paracoccidioidomycosis (“South American blastomycosis”)
- •Candidiasis
- •Cryptococcosis
- •Aspergillosis
- •Fusarium
- •Penicilliosis
- •Zygomycosis (mucormycosis)
- •Phaeohyphomycosis
- •Protothecosis
- •Rhinosporidiosis
- •5.5 Parasites and other creatures
- •Parasitic infestations
- •Scabies
- •Lice
- •Tungiasis
- •Myiasis
- •Protozoa
- •Leishmaniasis
- •Toxoplasmosis
- •Helminths
- •Cutaneous larva migrans
- •Larva currens
- •Onchocerciasis (“river blindness”)
- •Loiasis
- •Filariasis
- •Swimmer’s itch and seabather’s eruption
- •Trichinosis
- •Dracunculiasis (guinea worm)
- •Gnathosomiasis
- •Cysticercosis
- •Cutaneous amebiasis
- •Free-living amoeba
- •Gi-associated amoeba
- •Bites and stings
- •Biting and stinging insects
- •Arachnids (ticks, mites, spiders, and scorpions)
- •Millipedes and centipedes
- •Snake bites
- •6 Neoplastic dermatology
- •Neoplastic dermatology
- •6.1 Keratinocytic neoplasms
- •Premalignant/malignant
- •Actinic keratosis (AK)
- •Bowen’s disease (squamous cell carcinoma in situ)
- •Invasive cutaneous squamous cell carcinoma (cSCC, “SCC”)
- •Verrucous carcinoma
- •Keratoacanthoma
- •Basal cell carcinoma
- •6.2 Cysts
- •6.3 Melanocytic neoplasms
- •6.4 Adnexal neoplasms and hamartomas
- •Comparative dermatopathologic features of sweat gland neoplasms for board exam purposes
- •Poroma (classic juxtaepidermal type)
- •Hidroacanthoma simplex
- •Dermal duct tumor
- •Hidradenoma
- •Spiradenoma
- •Cylindroma
- •Syringoma
- •Mixed tumor (MT; “chondroid syringoma”)
- •Hidradenoma papilliferum (HPAP)
- •Syringocystadenoma papilliferum (SPAP, SCAP)
- •Papillary eccrine adenoma (PEA)
- •Tubular apocrine adenoma (TAA)
- •Porokeratotic eccrine ostial and dermal duct nevus
- •Microcystic adnexal carcinoma (MAC)
- •Aggressive digital papillary adenocarcinoma (ADPA)
- •Adenoid cystic carcinoma (ACC)
- •6.5 Hair follicle neoplasms/hamartomas
- •Folliculo-sebaceous-apocrine hamartomas
- •Trichofolliculoma
- •Fibrofolliculoma
- •Nevus sebaceus
- •Neoplasms with follicular germinative differentiation
- •Trichoepithelioma
- •Neoplasms with follicular matrix differentiation
- •Pilomatricoma (calcifying epithelioma of malherbe)
- •Neoplasms with follicular sheath (trichilemmal) differentiation
- •Trichilemmoma
- •Desmoplastic trichilemmoma (DTL)
- •Tumor of the follicular infundibulum (TFI)
- •Trichoadenoma (TA; of Nikolowski)
- •Proliferating pilar (trichilemmal) tumor
- •6.6 Sebaceous proliferations
- •6.7 Neural neoplasms
- •6.8 Smooth muscle neoplasms
- •6.9 Hematolymphoid neoplasms
- •6.10 Fibrohistiocytic neoplasms
- •Multinucleate cell angiohistiocytoma
- •Nodular fasciitis
- •Fibrous hamartoma of infancy
- •Giant cell tumor of tendon sheath (tenosynovial giant cell tumor)
- •Connective tissue nevus (collagenoma and elastoma)
- •6.11 Vascular proliferations
- •Benign vascular lesions
- •Vascular malformation (includes “port wine stain,” “cavernous hemangioma” old terminology)
- •Intravascular papillary endothelial hyperplasia (masson tumor, pseudoangiosarcoma)
- •Angiokeratoma
- •Infantile hemangioma
- •Pyogenic granuloma (lobular capillary hemangioma)
- •Epithelioid hemangioma (angiolymphoid hyperplasia with eosinophils, ALHE)
- •Targetoid hemosiderotic lymphatic malformation (hobnail hemangioma, targetoid hemosiderotic hemangioma)
- •Tufted angioma
- •Glomeruloid hemangioma
- •Glomus tumor/glomangioma
- •Borderline vascular neoplasms
- •Kaposiform hemangioendothelioma
- •Kaposi sarcoma (KS)
- •Other borderline vascular neoplasms (rare; not commonly tested)
- •High-grade malignant vascular neoplasms
- •Angiosarcoma
- •Vascular neoplasm associations
- •6.12 Neoplasms of adipocytic lineage
- •6.13 Dermoscopy
- •Seborrheic keratosis
- •Actinic keratosis
- •Basal cell carcinoma
- •Squamous cell carcinoma in situ
- •Squamous cell carcinoma
- •Ink spot lentigo
- •Vascular lesions (e.g., cherry angiomas)
- •Hemorrhage
- •Porokeratosis
- •Sebaceous hyperplasia
- •Dermoscopic patterns of melanocytic lesions
- •7 Dermatopathology
- •7.1 Essential concepts in dermatopathology
- •7.2 High-yield dermatopathology diagnoses at a glance
- •7.3 High-yield dermatopathology differential diagnoses
- •8 Dermatologic surgery
- •8.1 Surgical anatomy
- •8.2 Local anesthetics and perioperative pain control
- •8.3 Surgical instruments and needles
- •8.4 Suture techniques
- •8.5 Wound closure materials
- •8.7 Electrosurgery
- •8.8 Cryosurgery
- •8.9 Excisions
- •8.10 Mohs surgery
- •8.11 Flaps
- •8.12 Grafts
- •8.13 Surgical complications and measures to avoid them
- •8.14 Scar improvement
- •8.15 Nail surgery
- •8.16 Wound dressings
- •9 Cosmetic dermatology
- •9.1 Lasers

8.13 Surgical Complications and Measures to Avoid Them
Dermatologic Surgery
Procedure
High risk of
No Prophylaxis
No
surgical site
infection
High risk for prosthetic
joint infectionb or
infective endocarditisc?
No
Consider
prophylaxis
Lesions below the knee (including groin)
Cephalexin 2g PO
If PCN allergic,
Bactrim DS 1 tablet PO or
Levofloxacin 500 mg PO
Skin graft (any site)
Wedge excision (ear, lip)
Flap surgery on the nose and ear
Cephalexin 2g PO
If PCN allergic,
Clindamycin 600 mg PO or
Azithromycin 500 mg PO or
Clarithromycin 500 mg PO
Fig. 8.22 Updated prophylaxis algorithm for dermatologic surgery. (From Bae-Harboe YS, Liang CA. Perioperative antibiotic use of dermatologic surgeons in 2012.
Dermatol Surg. 2013;39[11]:1592–1601.)
Breach of oral mucosa?
No
a
?
Yes
Yes
Prophylaxis
recommended
Yes
High risk for
prosthetic joint
infectionb?
No
High risk for
infective
endocarditisc?
No
No prophylaxis
Yes
Yes
Consider
prophylaxis
Prophylaxis
Amoxicillin 2 g PO
If PCN allergic,
Clindamycin 600 mg PO
or
Azithromycin 500 mg PO
or
Clarithromycin 500 mg
PO
recommended
First 2 years following joint placement
Previous prosthetic joint infections
Immunocompromised/immunosuppressed patients
Diabetes (Type 1 and 2)
Autoimmune disease
Post organ transplants
Receiving Chemotherapy
Bone marrow transplant recipients
Chronic steroid users
Obesity
Tobacco exposure
Alcohol use
History of radiation therapy
Eiderly
HIV infection
Malignancy (including leukemia)
Malnourishment
Hemophilia
C) High risk of infective endocarditis
Prosthetic cardiac valve
Previous infective endocarditis
Unrepaired cyanotic congenital heart disease including palliative shunts and
conduits
Completely repaired congenital heart defects with prosthetic material or device < 6
months after procedure
Repaired congenital heart disease with residual defects at or adjacent to site of
prosthetic patch or device
Cardiac transplantation recipients who develop cardiac valvulopathy
Venous congestion: cyanotic-purple skin color,
↑ dark purple bleeding following pinprick test; aps
undergo rapid necrosis (,3–4 hours)
■
Risk factors:
Hematoma, infection, ↑ wound tension, tight
sutures (“edge necrosis”), extensive supercial
undermining (→ damage subdermal plexus),
insufcient or excessive electrocoagulation, poor
ap planning (narrow pedicle), smoking/nicotine
■
Prevention: appropriate intraoperative hemostasis,
minimize wound closure tension
■
Treatment: suture replacement (↓ tension), elevation
(↓ edema), heat application (↑ circulation), and
hyperbaric oxygen (↑ oxygenation)
Do NOT debride necrotic tissue (unless shows signs
of infection) since it serves as a biologic dressing
• Dehiscence
■
Separation of wound edges as a result of excessive
tension, hematoma, infection, or necrosis
■
Highest risk 5 time of suture removal (1–2 weeks)
Consider removing sutures in stages if prolonged
support is needed
■
Treatment:
Classic teaching: re-suture if within 24 hours; if
$ 24 hours → let it granulate on its own
Recent literature supports re-suturing if no infection,
hematoma, necrosis, or after underlying
complication has been treated
• Abnormal healing
■
Chondritis: painful (test by “icking” ear); may occur
after any ear procedure involving cartilage; may be a/w
Pseudomonas infection; treat w/ NSAIDs 1 quinolones
(if infected)
■
Contour irregularities: treated w/ dermabrasion/
dermasanding (6 weeks postoperatively), ablative
laser, or excision
■
Ectropion:
Cause: downward tension on lower lid
Risk factors: poor recoil on “snap test”
Prevention: tacking sutures to periosteum and Frost
suspension sutures
■
Eyebrow elevation: avoid closures that elevate brow
. 3 mm (classic teaching)
Recent studies have actually shown that any brow
asymmetry from horizontal forehead closures selfresolves over time
■
Free margin distortion: avoided w/ proper surgical design
■
Keloids: often patient- and site-specic (anterior neck,
chest, shoulders, and scars crossing jawline); treat w/
intralesional corticosteroids
475

CHAPTER 8 • Dermatologic Surgery
■
Pincushioning/trapdoor deformity:
Risk factors: frequently due to concentric
contractile forces → aps w/ curved incision lines
have highest risk (e.g., bilobed aps, nasolabial
transposition/interpolation aps)
Prevention: wide undermining, appropriate sizing
of ap, remove excess SQ fat on ap, ensure ap
adherence to wound base
Treatment: intralesional corticosteroids (into SQ)
1/– scar revision
■
Spitting sutures: ↑ risk w/ Vicryl, larger caliber sutures,
or sutures placed supercially in dermis; occurs
1 to 3 months postop; remove if possible (use
Jeweler’s forceps if suture not visible on surface)
■
Suture granuloma: ↑ risk w/ Vicryl, occurs 1 to 3
months postop; self-resolves without sequelae, but may
treat w/ intralesional steroids
■
on nose and central cheeks; treated w/ pulsed dye laser
■
Thickened scars: treated w/ massage or intralesional
corticosteroids
■
“Track marks”: do not tie sutures too tightly or leave in
place for too long; consider running subcuticular
epidermal closure
More common on trunk/extremity closures since
sutures typically left in longer and under greater
tension compared to face
■
Webbed or contracted scars: consider Z-plasty revision
• Motor nerve damage
■
Most severe if nerve transected at its proximal portion
→ frequently permanent
■
Avoided by staying above SMAS
• Sensory nerve damage
■
Generally improves with time
■
Minimize by avoiding transection of multiple sensory
nerve branches (e.g., orienting linear repairs on
forehead vertically rather than horizontally)
8.14 SCAR IMPROVEMENT
Overview
• Scars mature over at least 2 years, but if not exhibiting
favorable characteristics, may consider intervention after
60 to 90 days
• Manage expectations
■
Goal is to improve, not erase
• Result depends on
■
Size
■
Location
■
Patient’s predisposition for appropriate wound healing
• Favorable scars
■
Positioned along aesthetic subunit borders
■
Parallel with RSTLs
Nonsurgical modalities
• Watchful waiting
• Massage
■
Efcacy greatest in postsurgical scars
■
Often best for subtle imperfections
Mild webbing, scar depression, or pincushioning
• Pressure therapy
■
Efcacy greatest during scar maturation (rst year) and
limited thereafter
■
Mechanism of action
Pressure → ↓ blood ow and oxygen → ↑ collagen
breakdown
• Topical scar therapies
■
Silicone sheeting and gel
Mechanism unclear
Side effects: skin maceration and rash
■
Vitamin E
Efcacy not proven in clinical trials
Noted to cause allergic contact dermatitis
■
Steroids
Mechanism of action
♦ Binding of nuclear steroid receptor
♦ Decrease activity of broblasts and decreases
collagen production
Clinical activity
♦ Softens scars, ↓ hypertrophy, ↓ pincushioning
Group I steroids most efcacious, but ↑ risk of side
effects
■
Imiquimod
Mechanism of action
♦ Stimulates IFN-a → ↑ collagen breakdown,
↓ TGF-b (note: ↑ TGF-b levels are a/w keloid
formation)
Clinical activity
♦ Prevention of keloid recurrence after excision
♦ Results of studies have been mixed
Cream is applied nightly for 8 weeks
• Intralesional therapies
■
Steroids
Primarily used for hypertrophic and keloidal scars
Mechanism of action and clinical activity: same as
for topical steroids
Consider intraoperative injection if patient has a
history of keloids
■
5-FU
Primarily used for hypertrophic and keloidal
scars
Can be used in combination w/ steroids
Mechanism of action
♦ Blocks TGF-b2 gene in broblasts → ↓ collagen
production → softens scars and ↓ hypertrophy
• Lasers
■
Pulsed dye laser (585–595 nm)
Laser of choice for red, hyperemic, pigmented, or
hypertrophic scars and keloids
Patient phototype important as melanin competes
for laser absorption. Must use lower energy densities
in darker skin tones
Mechanism of action
♦ Keloids: nonspecic heating of dermal collagen
promotes scar remodeling
♦ Redness: destruction of dermal vessels
■
Nd:YAG (1064 nm)
Noted to improve pigmentation, vascularity, pliability
and height of keloids and hypertrophic scars
476

■
Resurfacing lasers
Mechanism of action
♦ Dermal heating leads to scar remodeling
Types
♦ Ablative (CO
Destroys stratum corneum (→ recontouring
10,600 nm; Erb:YAG 2940 nm)
2
surface irregularities) and deeper structures
(dermal heating → scar remodeling)
Uses: recontouring atrophic scars → reported
equivalent cosmesis to dermabrasion w/ faster
clinical recovery
♦ Nonablative
Preserves stratum corneum with destruction of
deeper structures
• Radiotherapy
■
Reserved for scars that are unresponsive to other
treatments
■
Not adequate as monotherapy for keloids
■
Frequently combined with surgical resection
■
Mechanism of action
↓ Collagen synthesis due to ↓ broblast
proliferation and ↑ apoptosis
■
Best results reported w/ 15 to 20 Gy over 5 to 6
sessions in early postoperative period; typically started
24 to 48 hours after surgery
Surgical modalities
• Dermabrasion/electrobrasion
■
Dermabrasion
Mechanism of action: epidermis and papillary
dermis are removed → allows wound to
reepithelialize from surrounding epithelium and
underlying adnexa
Best performed 6 to 8 weeks postoperatively
Re-wounding during brillogenesis → ↑ epidermal cell
migration into wound → improved appearance of scar
Variants:
♦ Wire brush
Creates microscopic lacerations
Less forgiving than diamond fraise
♦ Diamond fraise with hand engine
Should rotate in the direction of free
margin
Feathering used to avoid demarcation between
treated and untreated regions
♦ Dermasanding
Manually performed with medium-grade
drywall sanding screen, sandpaper, or surgical
scratch pad (presterilized, equivalent to 80
grit sandpaper)
No aerosolization of infectious particles or
blood splatter
Side effects
♦ Hyper/hypopigmentation
♦ Milia formation
♦ Persistent erythema
♦ Paradoxical worsening of scars
■
Electrobrasion
Mechanism of action: controlled skin ablation w/
hyfrecator (low power)
8.15 Nail Surgery
Similar results to dermabrasion
↓ Procedure and bleeding time (vs. dermabrasion)
• Subcision
■
Utilized on depressed facial scars
■
20-gauge tri-beveled hypodermic needle inserted in
the skin and sharp edges are maneuvered to release
brotic scar bands within dermis and subcutaneous
tissue
• Scar excision procedures
■
Linear excision of scar
■
W-plasty
Irregularization technique; typically followed by
dermabrasion
■
Geometric broken line
Irregularization technique; incise connected random
geometric gures (squares, rectangles, and triangles);
typically followed by dermabrasion
• Scar reorienting/lengthening techniques
■
V to Y
Can push (V–Y) or pull (Y–V) a free margin into
place
Less dramatic lengthening than Z-plasty
■
Z-plasty
Used to lengthen scar or release contractions
Angle of the lateral arms relative to the central limb
determines the amount of lengthening
Greater angles → more lengthening (though aps
become harder to transpose over one another)
♦ 30° lengthens by 25%
♦ 45° lengthens by 50%
♦ 60° lengthens by 75% (Fig. 8.23)
8.15 NAIL SURGERY
• Nail avulsion: typically undertaken for treatment of
onychomycosis, onychomadesis, nail biopsy, nail matrix
ablation, or nail unit excision
■
Distal nail avulsion (most commonly used technique):
entire nail is separated from distal nail bed to PNF
■
Proximal nail avulsion: less traumatic than distal nail
avulsion; undertaken when there is thick subungual
hyperkeratosis, prominent distal subungual damage or
no distal free edge
■
Partial nail avulsion: used for onychocryptosis or when
the exact location of the subungual lesion is already
known
• Nail biopsies (Fig. 8.24):
■
Nail bed:
Longitudinal excision; excision extends down to
periosteum; 1/– suturing of defect (not required if
defect width # 3 mm); minimal risk of nail
dystrophy
■
Nail matrix:
Horizontal excision; make diagonal 5 mm incision
from PNF (extending proximally on nger) to allow
visualization of matrix → biopsy carried down to
periosteum
Matrix biopsies have ↑ risk of nail dystrophy/
thinning; highest risk w/ proximal matrix biopsies
and if . 3 mm width
477

CHAPTER 8 • Dermatologic Surgery
B
b
B
60°
A
D
60°
C
c
A B C
Fig. 8.23 Single Z-plasty, 60 degrees. (A) Central scar is the common diagonal. (B) Two triangular aps are lifted and transposed. (C) Result is approximately 75%
increased tissue length. (From James WD, Elston DM, Treat JR, Rosenbach MA, Neuhaus IM. Dermatologic surgery. In: Andrews’ Diseases of the Skin. 13th ed.
Philadelphia: Elsevier; 2020:881–908.)
b
B
C
c
D
A
c
b
C
75% tissue gain
D
Nail biopsies
6 mm
2
1
1
3–4mm
3
Fig. 8.24 Nail biopsies. Nail bed biopsy (1), lateral longitudinal biopsy (2), and fusiform matrix biopsy (3). (From Haneke E. Nail surgery. In: Robinson JK, Hanke CW,
Siegel DM, Fratila A, eds. Surgery of the Skin . 3rd ed. Philadelphia, Elsevier, 2015:755–780.)
478

8.16 Wound Dressings
Most nail melanomas arise from matrix → matrix
biopsy required → ↑ risk of nail dystrophy
■
Lateral longitudinal nail biopsy:
Longitudinal excision of entire length of lateral nail
unit (nail matrix, folds, bed, plate and
hyponychium)
Useful for lateral nail pathology or inammatory
conditions in which nail matrix, folds, bed, and
plate are concurrently involved
Main risks 5 spicule or cyst formation
• Nail unit excision:
■
En bloc excision is typically used for removal of
malignancy such as subungual melanoma; aggressive
procedure that may result in permanent stiffness of
joint, but may be preferable to amputation
■
Excision must be taken back to DIP tendon insertion to
remove entire matrix
• Matricectomy
■
Removes nail matrix → inability to form new nail
■
Indications: ingrown nail/onychocryptosis (#1) and
intractable onychogryphosis
■
Typically only the part of the matrix causing problems
needs to be removed
Table 8.23 Types and Characteristics of Occlusive/Moisture-Retentive Wound Dressings
Type Advantages Disadvantages Indications Examples
Foams Absorbent, conform to body
Films Transparent, create bacterial barrier,
Hydrocolloids
Hydrogels Semitransparent, soothing, do not
Alginates Highly absorbent, hemostatic,
From Levin Y, Brown KL, Phillips TJ. Wound healing and its impact on dressings and postoperative care. In: Robinson JK, Hanke CW, Siegel DM, Fratila A, eds.
Surgery of the Skin. 3rd ed. Philadelphia: Elsevier; 2015:114–133.
contours
adhesive without secondary
dressing
(1) Autolytic debridement,
enhance angiogenesis, absorbent,
create bacterial and physical
barrier
adhere to wounds, hydrating
do not adhere to wounds, fewer
dressing changes
Opaque, require
secondary dressing
May adhere to wounds,
can cause fluid
collection
Opaque, gel has
unpleasant smell,
expensive
Require secondary
dressing, frequent
dressing changes
Require secondary
dressing, gel has
unpleasant smell
■
Phenol matricectomy
After avulsion, phenol (88%) applied to matrix w/
cotton tipped applicator (2–3 passes) for 3 minutes
total
♦ Attention to lateral matrix horns to avoid spicule
formation
Nail folds and nail bed should be protected from
phenol (w/ petrolatum) and phenol is neutralized
after nal pass w/ isopropyl alcohol
ECG monitoring is not necessary
■
Excision and electrodesiccation of the nail matrix have
been advocated by some authors as alternatives to
phenol; limited data exist on its benets and harms
relative to other forms of nail matricectomy
■
Subungual hematoma:
Trephination indicated if hematoma . 50% of nail
May occur in combination w/ fractured distal
phalanx → X-rays recommended
8.16 WOUND DRESSINGS
• See Table 8.23
Partial-thickness wounds, moderately to
heavily exudative wounds, pressure relief
Donor sites, superficial burns and ulcers,
partial-thickness wounds with minimal
exudates
Partial- or full-thickness wounds, mildly to
moderately exudative wounds, pressure
ulcers, venous ulcers, donor sites, acute
surgical wounds
Painful wounds, partial-thickness wounds,
wounds after laser, dermabrasion or
chemical peel, donor sites
Highly exudative wounds, partial- or full-
thickness wounds, after surgery
Allevyn
Flexzan
Hydrasorb
Lyofoam
Vigifoam
Tegaderm
Bioclusive
BlisterFilm
Omniderm
Transeal
Duoderm
Nu-Derm
Comfeel
Cutinova
Replicare
Vigilon
Tegagel
Curagel
ClearSite
Cural
Elasto-Gel
SoloSite wound gel
2nd Skin
AlgiDerm
AlgiSite
Algisorb
Kaltostat
Curasorb
Polymem
SeaSorb
Sorbsan
479

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9
Cosmetic Dermatology
Ronda S. Farah
CONTENTS LIST
9.1 LASERS
9.2 BOTULINUM TOXIN
9.3 DERMAL FILLERS
9.4 LIPOSUCTION AND FAT REDUCTION
9.5 SCLEROTHERAPY AND VEIN MANAGEMENT
9.6 COSMECEUTICALS, NUTRACEUTICALS, AND OTHER SUPPLEMENTS
9.7 HAIR TRANSPLANTATION
9.8 CHEMICAL PEELS
9.9 OTHER ESTHETIC PROCEDURES AND SCALES
Acknowledgments: With acknowledgments to Addison Demer MD,
Lori Fiessinger MD, Seaver Soon MD, Kaichu Lee MD, Neil Sadick
MD, and the original author, Raja K. Sivamani.
9.1 LASERS
• LASER 5 Light Amplication by Stimulated Emission of
Radiation (Table 9.1)
• Lasers are characterized by the “3 Cs”
■
Coherence: light waves travel together in-phase in time
and space
■
Collimation: light waves travel together in a parallel
fashion
■
(mono) Chromatic: light waves are all the same
wavelength
• Three different media exist (determine laser wavelength):
■
Gas: CO2, xenon chloride (excimer laser), krypton,
argon, copper vapor, helium-neon
■
Liquid: rhodamine dye (pulsed dye laser [PDL])
■
Solid: two classes exist
Crystal: alexandrite, Er-YAG, Nd-YAG, potassium
titanyl phosphate (KTP), and ruby
Semiconductor: diode
• Selective photothermolysis: using a laser to achieve
selective destruction of the target structure(s); depends on
three factors (Table 9.2):
■
Wavelength must target the desired chromophore and
reach an appropriate anatomic depth to destroy the
desired target tissue. Medium determines wavelength
of laser.
■
Pulse duration should be # thermal relaxation time
(TRT) → minimizes diffusion of heat and resultant
“collateral damage” to surrounding tissues
■
Fluence must be high enough to damage target tissue,
but not so high as to nonspecically damage bystander
tissue
• Four different types of laser wave forms:
■
Continuous: emit light continuously; low power (e.g.,
CO2 laser, and argon)
■
Pulsed: light is emitted periodically, with short pulse
durations (millisecond [ms] range), and high power
(e.g., PDL, ruby, alexandrite, diode, Erbium:glass, and
Erbium:YAG)
■
Quality switched (Q-switched [QS]): variant of pulsed
lasers with extremely short pulse durations
(nanosecond range); extremely high power (example:
all QS lasers)
For pigmented lesions, tattoos, and drug deposits
because target molecules are very small → very short
TRT (nanoseconds)
■
Quasicontinuous: emits multiple rapid bursts of lowenergy light → simulates continuous wave lasers (e.g.,
KTP and copper vapor)
• Treated skin will have at least one of the following four
interactions with emitted laser light particles:
■
Reection: 4%–7% of light is reected (“bounced
away”) by skin surface, as a result of the difference in
refractive index between air and stratum corneum; the
remaining 93%–96% of light enters skin and will
subsequently interact in one of three following ways:
Scattering: light bounces off bers within dermis/SQ
→ limits depth of penetration
↑ Spot size → ↓ scatter → ↑ depth of penetration
Transmission: light passes straight through the tissue
without interacting with anything → lack of any effect
Absorption (desired effect): light is absorbed by its
intended target → tissue effects
481

CHAPTER 9 • Cosmetic Dermatology
Table 9.1 Laser Terminology
Term Definition Unit Comments
Energy Fundamental unit of work Joules (J) —
Fluence Energy delivered per cm
Power Rate of energy delivery
Irradiance Power delivered per cm
Pulse width (pulse
duration)
Spot size Diameter of the laser beam hitting the
Wavelength Length of a specic laser’s light wave
Chromophore Absorptive target tissue of laser — Major chromophores in skin (boards favorite): melanin, hemoglo-
Thermal relaxation
time (TRT)
Photomechanical
effect
Duration of laser exposure (seconds) Seconds (or fractions
skin surface (mm)
Four categories:
UV (10–400 nm)
Visible (400–700 nm)
Infrared (700 nm–1 mm)
Radiofrequency/microwaves (.1 mm)
The time required for heated tissue to
dissipate 50% of its heat
Sudden heating produces thermal
expansion with acoustic and/or shock
waves → waves produce cavitation
(steam bubbles)
2
2
2
J/cm
Watts (W) 5 J/s
2
W/cm
of seconds)
mm
nm (most commonly) Longer wavelengths penetrate deeper (rule holds true until
Seconds (or fractions
of seconds);
proportional to the
diameter of target
squared
↑ fluence → ↑ energy of treatment per unit area
↑ Pulse duration 5 longer exposure to the laser → ↑ energy/heat
delivered to tissue
Ideally, pulse duration should be # TRT to prevent collateral dam-
age to bystander tissues
Larger spot size → ↓ scatter → ↑ depth of penetration
1300 nm, at which point penetration decreases as a result of
water absorption; Figure 9.1)
Most deeply penetrating wavelengths 5 650–1200 nm
Least penetrating wavelengths 5 far UV and far IR
bin (oxyhemoglobin and deoxyhemoglobin), and water
A laser/light source may target multiple chromophores to differing
degrees
TRT (seconds) is proportional to the square of the target’s
diameter (in mm)
Ideally, pulse duration should be # TRT
If pulse duration . TRT → ↑ undesired damage to surrounding tis-
sues (Table 9.2)
Cavitation is the primary mechanism of vessel rupture w/ PDL ,
and also is responsible for skin whitening during QS laser treatment
of tattoos
Table 9.2 Thermal Relaxation Times of Chromophore
Chromophore Diameter Thermal Relaxation Times Typical Pulse Duration
Tattoo ink particle 0.1 micrometer 10 nanoseconds a. 0.6–10 nanoseconds (if Q-switched lasers)
Melanosome 0.5 micrometers 250 nanoseconds 10–100 nanoseconds (requires Q-switched lasers)
PWS vessels 30–100 micrometers 1–10 milliseconds 0.4–20 milliseconds
Terminal hair follicle 300 micrometers 100 milliseconds 3–100 milliseconds
Leg vein 1 millimeter 1 second
Modied from Sakamoto FH, Avram MM, Anderson RR. Lasers and other energy-based technologies—principles and skin interactions. In: Bolognia JL,
Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier; 2018:2354–2363.
■
Epidermal damage is minimized via skin cooling (three
commonly used methods):
■
Precooling: most aggressive, most effective method
(e.g., cryogen [tetrauoroethane] spray)
Main side effect (SE) 5 hyper/hypo-pigmentation
■
Parallel cooling: only effective for pulses . 5 ms in
duration (e.g., solid cold sapphire window pressed
and reduction of periorbital rhytides; anti-aging/
photorejuventation applications exist (red light
633 nm and near-infrared light 800–830 nm)
• A variety of lasers exist, each with specic wavelengths, target
chromophores, and depths of penetration (Figs. 9.1 and 9.2)
• Non-laser light-based energy sources:
■
Intense pulsed light (IPL):
against skin)
■
Postcooling: used primarily to ↓ pain, erythema, and
edema (e.g., ice packs and cold air)
• Photobiomodulation (aka low level light therapy):
■
Mechanism unknown but chromophore thought to
be mitochondrial cytochrome c oxidase; sources of
light include lasers, light emitting diodes, broadband
light (within the visible and near infrared spectrum)
■
Used for androgenetic alopecia (typically 655–678 nm
and available as home or in-ofce devices), acne
vulgaris (blue light 415 nm and red light 633 nm)
0.1 seconds
Xenon ashlamp (light source) emits
noncollimated, noncoherent, and polychromatic
light (broad wavelength range: 500–1200 nm)
A variety of lters are utilized to narrow down the
range of wavelengths to target the same
chromophores that lasers do
Less selective and less powerful than lasers; can be
risky in patients with skin types IV–VI
Targets lentigines, vascular lesions such as
telangiectasias; caution when treating men on the
face as it also removes hair
482

DEPTH OF OPTICAL PENETRATION BY VARIOUS LASERS
483
Excimer
Stratum
corneum
Epidermis
1 mm
Superficial
dermal blood
vessels
2 mm
3 mm
4 mm
Fig. 9.1 Depth of optical penetration by various lasers. It should be noted that the treatment depth can greatly exceed the optical penetration depth for ablative lasers. On the face, fat can be
present at a depth of 2 to 3 mm. For example, the depth of optical penetration for CO2 lasers is only 20 microns, but fractional CO2 lasers can vaporize nearly full-thickness microchannels
through the dermis. KTP, Potassium titanyl phosphate; Nd, neodymium; PDL, pulsed dye laser; YAG, yttrium aluminum garnet. (From Sakamoto FH, Avram MM, Anderson RR. Lasers and other
energy-based technologies—principles and skin interactions. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier; 2018:2354–2363.)
Dermis
Deeper
dermal
blood vessels
Subcutaneous
308 nm
80 2 20
fat
Argon
488–514 nm
KTP
532 nm
PDL
585–600 nm
Ruby
694 nm
Alexandrite
755 nm
Diode
800 nm
Nd:YAG
1064 nm
Erbium: Glass
1540 nm
Thulium
1927 nm
Erbium:YAG
2940 nm
CO
2
10,600 nm
9.1 Lasers

CHAPTER 9 • Cosmetic Dermatology
100,000
)
-1
1000
Excimer
ABSORPTION SPECTRA
Ruby
Alexandrite
KTP, Nd:YAG
PDL
Diode
Nd:YAG
Er:Glass
Erbium
Thulium
YSGG
Er:YAG
Fig. 9.2 Absorption spectra. The heterogeneous absorption spectra of
chromophores allow selective photothermolysis to work. Er, Erbium;
KTP, potassium titanyl phosphate; Nd:YAG, neodymium-doped yttrium
aluminum garnet; PDL, pulsed dye laser; YSGG, yttrium scandium gallium
garnet. (From Sakamoto FH, Avram MM, Anderson RR. Lasers and other
energy-based technologies—principles and skin interactions. In: Bolognia
JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier;
2018:2354–2363.)
Laser safety
• Four main concerns: blindness, re hazards, cutaneous
burns, and inhalation of biohazardous plume
• Blindness
■
Up to 7% of emitted laser light is reected by the
stratum corneum → reected light can cause eye
damage/blindness (may occur if even 1% of the beam
is reected into eye!)
■
Blindness is rapid and painless
■
Any laser/light source in UV range (10–400nm) → lens
damage, cataracts
Example: excimer laser (308 nm)
■
Any laser/light source that targets melanin or
hemoglobin (visible light [400–700nm] and near-
infrared [700–1400nm] wavelengths) → retinal
damage (retina is highly pigmented); also damages
uvea and iris
Examples: KTP (532 nm), PDL (585–600 nm), ruby
(694 nm), IPL (various wavelengths), alexandrite
(755 nm), diode (800 nm), and Nd:YAG (532 and
1064 nm)
Highest risk 5 near-infrared and QS lasers
■
Any laser/light source that targets water (near-IR [upper
end], mid-IR, far-IR wavelengths) → corneal/scleral
damage
Examples: Nd:YAG (1320 nm), Erbium:glass (1550 nm),
Erbium:YAG (2940 nm), and CO2 (10,600 nm)
• Fire hazard
■
Greatest re risk with CO2 and Erbium:YAG ablative
and fractionated lasers
■
Risks: drapes, clothing, dry hair, and plastic tubes
(endotracheal tubes, especially if oxygen is being
administered)
■
Prevention: moisten hair near treatment eld, ensure
that any alcohol/acetone skin cleanser has fully dried
before using laser, and reduce intraoperative O
concentration , 40%
2
10
Absorption coefficient (cm
0.1
200 400 600 800 1000
Wavelength (nm)
Melanin
Oxyhemoglobin
Deoxyhemoglobin
Water
Fat
• Cutaneous burns: may occur with any laser or nonlaser
energy source (IPL and radiofrequency [RF]); as a result of
operator error or device malfunction (e.g., epidermal
cooling mechanism fails)
• Inhalation of biohazardous plume
■
HPV viral particles have been detected in carbon dioxide
laser plumes → cases of laser-surgeons developing HPV16–induced oral SCC related to inhalation
■
Hepatitis B and HIV also reported in plume
■
Prevention: smoke evacuator (rst line); also
recommend N95 mask
• Other safety facts:
■
QS lasers can eject tissue due to cavitation
■
Beware of diseases that koebnerize with lasers (e.g.,
psoriasis and lichen planus)
■
Lasers can damage tooth veneers/dentures
■
Optical density (O.D.): found on laser glasses; is a
logarithmic measure of the laser energy that will pass
through a lter; higher O.D. value = higher energy
attenuation → greater eye protection
Each unit represents a 10-fold reduction in transmitted
laser light (O.D. 1 5 10% energy transmittance; O.D.
2 5 1%; O.D. 3 = 0.1%, etc.) → there is a 10-fold increase
in eye protection for each additional O.D. unit
Additional general lasser points for
consideration
• There are increased risks of dyspigmentation with some
energy-based devices in darker skin types
• Strong sun protective counseling is key; avoid treating
tanned skin
• Decrease laser settings to avoid complications (consider
fewer passes, lower joules, decreased surface area treated,
and nonablative procedures)
• Isotretinoin and dermatologic procedures:
■
New data suggests insufcient evidence to delay
treatment with hair removal lasers, vascular lasers, and
5000
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