Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5192_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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

Body: middle portion; strongest part of needle →
always grasp here; various curvatures (3/8 circle
most common)
Tip: sharp tip that may be round (tapered) or
cutting; minimize grasping of tip → contact w/
other instruments quickly dulls the tip
■
Three types of needle tips:
Round (tapered): only tip pierces tissue (no sharp
edges along arc of needle); less likely than
cutting needles to tear tissues; used for deep
soft tissues (fat and muscle); difcult to pass
through skin
Cutting: triangular-shaped needle point; preferred for
skin because it easily passes through tissue; two types:
♦ Conventional cutting: cutting surface is on inner
portion of needle arc; ↑ risk of suture tearing/
cutting through wound edge (because cutting
edge of needle faces toward wound edge)
♦ Reverse cutting: cutting surface is on outer
portion of needle arc; ↓ risk of suture tearing/
cutting through wound edge
8.4 SUTURE TECHNIQUES
• Knots
■
Surgeon’s knot: most common; essentially a square
knot w/ rst knot double thrown to prevent slippage
■
Aberdeen hitch knot: used to tie the end of a running
subcuticular suture; more compact, more secure, and
uses less material than surgeon’s knot
• Epidermal (“cuticular”) suturing
■
Simple interrupted: used for wounds under moderate
to high tension; directing the needle away from the
wound results in ↑ eversion and ↓ risk of sunken scar
■
Simple running: used for wounds under minimal
tension; faster to place than interrupted sutures but
↑ risk of dehiscence
■
Running locked sutures: provides hemostasis but
↑ strangulation risk
■
Vertical mattress: strongly everts (Vertical 5 eVert)
wound edges; eliminates dead space, and decreases
wound edge tension
■
Horizontal mattress: provides Hemostasis (Horizontal 5
Hemostasis); eliminates dead space, and decreases wound
edge tension; signicant strangulation risk → do not use
in poorly vascularized areas
■
Pulley suture: modied vertical mattress suture; used
for wounds under high tension
■
Running horizontal mattress: same benets as simple
horizontal mattress, but is faster, provides ↑ eversion,
and ↓ strangulation risk; improved outcomes relative
to simple running sutures, but takes longer
■
Tip stitch: half-buried horizontal mattress used for
corners (aps and M-plasty tips)
■
High-low (step-off stitch): used to correct imprecise
dermal/subcuticular suturing, where one side of the
wound edge is higher than the other (“step-off deformity”)
• Dermal/subcutaneous (“subcuticular”) suturing
■
Simple buried suture: traditional deep suture; minimal
eversion; high rate of spitting sutures
8.5 Wound Closure Materials
■
Buried vertical mattress: better eversion; “heart shaped”
■
Set-back suture (“buried buttery”): suture entry and
exit points are both underneath the undermined
wound surface; maximal eversion; ↓ spitting sutures
and ↑ cosmetic outcomes (vs. buried vertical
mattress)
■
Running subcuticular: running sutures in supercial
dermis, instead of along epidermal surface; primary
advantage 5 lack of track marks; however, ↑ rate of
spitting sutures; typically used in combination w/
buried vertical mattress sutures
■
Purse-string: traditionally used to ↓ wound size and
↓ healing time, relative to second intention; a recent
RCT study did not demonstrate any difference in
cosmetic appearance or scar size, but there was a
trend toward faster healing time
■
Buried pulley suture: essentially just a series of two or
more buried sutures; primary advantage 5 permits
wound closure under high tension; disadvantage 5
tissue strangulation
■
Fascial plication suture: used to decrease tension on a
wound
■
“Figure of 8”: used to tie off bleeding vessels
• Suture removal recommendations (largely anecdotal):
head/neck # 7 days; trunk/extremities 5 10 to 14 days;
the longer sutures remain in place → ↓ likelihood of
dehiscence, but ↑ track-marks
• Suspension sutures: anchor the overlying tissue to
periosteum → removes tension from leading edge of ap
→ prevents distortion of a free margin (i.e., tacking
cheek rotation ap to lateral orbital rim periosteum to
remove tension from leading edge of ap covering lower
lid defect); also prevents ap “tenting” across concavity
(i.e., tacking underside of ap to nasal periosteum when
advancing cheek skin medially to cover a nasal sidewall
defect)
8.5 WOUND CLOSURE MATERIALS
• Suture types and properties (Tables 8.7–8.11)
• Suture coatings
■
Antifriction coatings present on some multilament
sutures → more easily pulls through tissue
■
Antibiotic (Triclosan most common) coating: shown
to ↓ surgery site infection relative to non-coated
• Barbed sutures
■
New, knotless suturing method; barbs hold tissue in
place; main benets 5 tension distributed evenly
along entire course of wound, faster to use than
traditional sutures; most common use 5 large wounds
under ↑ tension
• Tissue adhesives
■
Two categories:
Octyl: 2-octyl cyanoacrylate (Dermabond)
Butyl: n-butyl cyanoacrylate (Liquiband)
♦ GluSeal is a blend of n-butyl and 2-octyl
cyanoacrylate
Details:
♦ Butyl types dry faster than octyl type (30 vs. 150
seconds) but are more rigid
455

CHAPTER 8 • Dermatologic Surgery
Table 8.7 Suture Types
Term Definition Comments
Suture type (absorbable vs. nonabsorbable)
Absorbable sutures Lose most of their tensile strength within 60 days Most commonly used as “deep” sutures
Nonabsorbable sutures
Suture material (absorbable; natural vs. synthetic)
Natural Derived from natural proteins (gut, silk) Degraded by proteolysis
Synthetic Synthetic copolymers Degraded by hydrolysis
Conguration (monolament vs. multilament)
Monofilament Composed of a single filament
Multifilament (braided) Composed of multiple small filaments braided
COF, Coefcient of friction.
Maintains tensile strength for . 60 days
together
Tensile strength is lost long before suture is fully absorbed
↑ Absorption rate in moist areas, febrile or protein-decient patients
Most commonly used as epidermal sutures
↑ Inammatory reaction and rapidly degraded
↓ Inammatory reaction and slowly degraded
Advantages: slide easily through tissue (because of ↓ COF), harbors less bac-
teria than braided sutures (because of ↓ capillarity), and low-minimal inammatory reaction
Disadvantages: ↓ knot security (because of ↑ memory and ↓ COF); poor
“ease of handling” (because of ↓ pliability and ↑ memory)
Advantages: ↑ ease of handling (because of ↑ pliability and ↓ memory), ↑ ten-
sile strength, and ↑ knot security (because of ↑ COF and ↓ memory)
Disadvantages: ↑ bacterial infections (because of ↑ capillarity), and ↑ in-
ammatory reaction
Table 8.8 Specic Suture Properties
Term Definition Comments
Tensile strength Force needed to snap suture Synthetic sutures are generally stronger than natural materials
Size (USP size) Diameter of suture material necessary to
Coefficient of
friction (COF)
Knot security Strength of the knot Higher with multilament sutures
Ease of handling Ease with which suture is used
Pliability Ease with which suture can be bent into a
Memory Tendency of suture to retain its original
Plasticity Ability of suture to stretch while maintaining
Elasticity Ability of a suture to return to its original
Capillarity Ability of suture to absorb fluid
Tissue reactivity Amount of inflammation incited by suture Much higher with natural sutures (gut, silk) than synthetic
achieve a given tensile strength
Degree of friction encountered when
suture is pulled through tissue
knot; felt as “stiffness” of suture
shape; determined by elasticity,
plasticity, and suture diameter
its tensile strength
length after being stretched
A suture that has been knotted only has 1/3 of its original tensile strength
More zeroes 5 smaller suture diameter (6–0 suture is smaller than 5–0)
Inherent strength of the material also affects USP size (nylon is inherently stronger than
gut → 5–0 nylon is smaller in diameter than 5–0 gut)
↓ COF → ↓ knot stability (slippery)
Monolament sutures (particularly polypropylene) have ↓ COF → easily slides through tis-
sue but requires more throws to secure knot
Multilament sutures have ↑ COF → ↑ knot security
Directly proportional to COF
Inversely related to memory
Multilament sutures generally have ↑ ease of handling
Directly related to pliability
Inversely related to memory
Multilament sutures have ↑ pliability → easier to tie knots/↑ ease of handling
Pliability and memory are the two main determinants of “ease of handling”
↑ Memory → ↓ knot security and ↓ ease of handling
Memory is one of two main determinants of knot security (the other is COF)
Memory is one of two main determinants of “ease of handling” (the other is pliability)
Monolament sutures have ↑ memory relative to multilament sutures
↑ Plasticity allows suture to stretch to accommodate postoperative swelling without
cutting into tissue (polypropylene has ↑ plasticity than nylon)
↑ Elasticity is an ideal suture property: elasticity allows suture to stretch to accommo-
date swelling, and later, resume its original shape → keeps wound edges approximated
after edema has resolved
Polybutester and poliglecaprone-25 have ↑ elasticity → good for areas that are likely
to swell signicantly
↑ Capillarity → suture wicks more uid from wound surface into wound (conduit for
bacteria)
Multilament sutures have ↑ capillarity → ↑ infection
456

8.5 Wound Closure Materials
Table 8.9 Absorbable Sutures
Suture Configuration
Fast-absorbing
gut
Fast-absorbing
Polyglactin 910
(Vicryl Rapide™)
Plain gut Virtually
Poliglecaprone 25
(Monocryl™)
Chromic gut Virtually
Polyglycolic acid
(Dexon™)
Polyglactin 910
(Vicryl™ and
Coated Vicryl
Plus
Antibacterial™)
Polyglyconate,
a copolymer of
glycolic acid and
polytrimethylene
carbonate
(Maxon™)
Polydioxanone
(PDS II™)
Modied from Srivastava D, Taylor RS. Suturing technique and other closure materials. In: Robinson JK, Hanke, CW, Siegel DM, Fratila A, eds. Surgery of the
Skin. London: Elsevier, 2015:193–213.
Virtually
monofilament
Braided 5d 42d Good Good Low
monofilament
Monofilament 7–10d 90–120d Good Good Minimal
monofilament
Braided 14d 90d Good Excellent Low —
Braided 21d 56–70d Good Good Low
Monofilament 30–40d 180d Fair Good Low Nearly equivalent to PDS in terms of
Monofilament 30–50d 180–240d Poor Poor Low Longest lasting absorbable
Tensile
Strength (50%) Absorption
3–5d 21–42d Fair Poor Low Often used for skin grafts; pretreated
7d 70d Fair Poor Moderate-
10–14d 90d Poor Poor Moderate (but
Ease of
Handling
Knot
Security
Tissue
Reactivity Comments
w/heat → ↑ rate of absorption
Ionized w/ gamma rays → faster
absorption
high
↑ Knot security and ease of handling
relative to other monofilaments;
least inflammatory; highest initial
tensile strength
less than
plain gut)
Pretreated w/ chromium salts →
collagen cross-linking → slower
degradation
↑ Rate of spitting sutures relative
to Monocry; coated vicryl plus
antibacterial→ ↓pain and ↓ S.aureus
(MRSA and MSSA) infections; active
ingredient 5 Triclosan
durability, but has ↑ knot security
and is easier to handle
suture → good for high-tension
closures
Table 8.10 Nonabsorbable Sutures
Suture Configuration Ease of Handling Knot Security Tissue Reactivity Comments
Silk Braided Gold standard Good High Used on mucosal surfaces
Nylon (Ethilon™,
Dermalon™)
Polypropylene
(Prolene™,
Surgilene™)
Polyester
(Ethibond™,
Dacron™)
Polybutester
(Novafil™)
Modied from Srivastava D, Taylor RS. Suturing technique and other closure materials. In: Robinson JK, Hanke, CW, Siegel DM, Fratila A, eds. Surgery of the
Skin. London: Elsevier, 2015:193–213.
Monofilament
(braided form
also available)
Monofilament Good to fair Poor Least Least inammatory nonabsorbable suture;
Braided Very good Good Minimal Highest tensile strength of any nonabsorb-
Monofilament Good to fair Poor Low Most useful for skin closure when significant
Good to fair Poor Very low Most common suture used for skin surface
Best handling of any suture
Second highest tissue reactivity (#1 is
plain gut)
closure
Clear nylon may be used as a permanent
deep suture for periosteal tacking or to prevent scar spread
has extremely low coefcient of friction →
ideal for running subcuticular suturing
High plasticity (stretches with swelling
rather than cutting into tissue = an ideal suture property), but low elasticity (remains
stretched when swelling resolves = not an
ideal suture property)
able suture (excluding stainless steel)
Used on mucosal surfaces
Similar to silk, but less inammatory
edema is expected (because of ↑ elasticity)
457

CHAPTER 8 • Dermatologic Surgery
Table 8.11 High-Yield Suture Comparisons
Property Absorbable (Most to Least) Nonabsorbable (Most to Least)
Tissue reactivity
Initial tensile strength
Time required to
decrease to 50% of
initial tensile strength
Absorption time (Longest time to shortest)
Surgical gut . polyglycolic acid 5 polyglactin 910 . polydioxanone .
polyglyconate 5 poliglecaprone 25
Poliglecaprone 25 . polyglyconate . polydioxanone . polyglactin 910 .
polyglycolic acid .. surgical gut
(Longest time to shortest)
Polydioxanone 5 polyglyconate . polyglactin 910 . polyglycolic acid . chromic
gut . poliglecaprone 25 . plain gut . Vicryl Rapide™ . fast-absorbing gut
Polydioxanone . polyglyconate . poliglecaprone 25 5 polyglycolic acid . polygla-
ctin 910 . Vicryl Rapide™ . fast-absorbing gut
Silk . nylon . polyester5 polybutester .
polypropylene (least)
Stainless steel (#1 overall) . polyester
(#1 nonmetal suture) . nylon 5
polybutester . polypropylene . silk
♦ All are typically used in combination w/
subcuticular sutures
♦ ↑ Dehiscence rate and ↓eversion (vs. sutures)
• Adhesive strips
■
Applied in combination w/ subcuticular sutures, often
w/ topical skin adhesive (Mastisol)
■
Studies demonstrate similar cosmetic outcomes for the
combination of subcuticular sutures 1 adhesive strips
(vs. standard bilayered suture closure)
• Staples
■
Traditional staples: typically used on scalp; advantages
5 quick, easy application, lower risk of strangulation
and ↓ infection rates compared w/ sutures;
disadvantages 5 possible ↑ pain after closure
■
Absorbable staples: recently introduced; staples are
buried; ↓ pain, ↑ cosmesis compared w/ traditional
transcutaneous staples
8.6 ANTISEPSIS AND STERILIZATION
• Hair removal
■
Do NOT shave! Old dogma states that shaving
introduces microscopic abrasions → theoretical increase
in bacterial access into wound and subsequent infections
Recent study by Shaffer (JAAD 2022) found very low
risk of infection with razor hair removal → old
dogma saying not to shave may be false!
■
DO use clippers and/or chemical depilatories
• Hand hygiene
■
Skin ora is divided into two groups:
Transient bacteria (bad): reside supercially; easy
to remove w/ hand washing; responsible for most
surgical site and nosocomial infections
Resident bacteria (ok): reside deeper; difcult to
remove; not commonly a/w surgical site infections;
for example, Staphylococcus epidermidis and
diphtheroids
■
Hand hygiene agents: alcohol or alcohol 1
chlorhexidine reduces bacterial counts most, followed
by: chlorhexidine only . iodophors . triclosan . soap
• Antiseptic skin preparations (Table 8.12)
■
Activity of these agents is the same as for the hand
hygiene products above
■
Important considerations:
Alcohol: ammable → may lead to res, especially
in hair-bearing areas
Chlorhexidine: should never be used around the eye
(→ severe corneal damage) or ears (ototoxic); Serratia
may colonize chlorhexidine bottles → infection
• Sterilization methods
■
Steam autoclave: most common in ofce; steam under
pressure; may dull instruments
■
Chemical autoclave: heated chemical vapor; lower
humidity →less dulling
■
Dry heat (oven): high temperature, longer time; no humidity
→ no dulling; cannot use for cloth, paper, plastic
■
Gas sterilization: good for large volumes (used
primarily in hospitals); expensive, prolonged times and
mutagenic gas; effective for heat- and moisture-sensitive
instruments
■
Cold sterilization (chemical immersion): not considered
adequate for surgical instrument sterilization
8.7 ELECTROSURGERY
Introduction
• Electrocautery and electrosurgery often incorrectly used
interchangeably (differences shown in Table 8.13)
■
Electrosurgery: high-frequency alternating current to
conduct energy via an unheated (cold-tipped) electrode
High resistance of human tissue (a poor conductor
of electricity) to the passage of current causes
conversion of electrical energy to thermal energy
→ specic surgical effect (cutting or coagulation)
High-frequency current prevents the depolarization
of muscles and nerves
Types: electrosection, electrocoagulation,
electrodesiccation, and electrofulguration
■
Electrocautery: direct current → hot metallic probe
No ow of current through patient (vs.
electrosurgery); hemostasis is achieved by the direct
application of heat
Monopolar versus bipolar
• Terms traditionally used to describe the number of tissue
contact tips at the end of an electrode (i.e., “bipolar”
forceps have two tips)
• Best to abandon these two terms because “…polar”
implies polarity (and unlike direct current, the alternating
458

8.7 Electrosurgery
Table 8.12 Antiseptics
Agent Mechanism Onset Advantages Disadvantages Residual Activity Comments
Alcohol (isopropyl
and ethanol)
Chlorhexidine
(2%–4%)
Iodine and
iodophors
Chloroxylenol
(parachlorometaxylenol)
Hexachlorophene Inactivates
Quaternary
ammonium
compounds
(Benzalkonium)
Triclosan Alters cytoplasmic
Soap and water Detergent; removes
G(1), Gram-positive; G(–), gram-negative; SSI, surgical site infection.
Denatures cell walls;
100% alcohol is
less effective than
70% (optimal
strength)
Disrupts cell
membranes
Oxidation →
disruption of
protein synthesis
and cell
membranes
Deactivates
enzymes and
alters cell walls
enzymes
Induces leaks
in cytoplasmic
membranes
membrane and
synthesis of RNA,
fatty acids, and
proteins
dirt and organic
substances
Very rapid
(fastest)
Rapid Broad spectrum:
Rapid Broad spectrum:
Slow Reasonably broad
Slow Effective against
Slow
Rapid G(+), mycobacteria,
Very rapid Highly effective
Broad spectrum:
G(1), G(–),
mycobacteria, and
many viruses
G(1), G(–),
viruses, fungi, and
mycobacteria;
not inactivated by
organics (blood and
sputum)
G(1), G(–),
bacterial spores,
mycobacteria,
viruses, and fungi
spectrum: G(1) .
G(–), mycobacteria,
and viruses
staph
G(1) and lipophilic
viruses
and candida; not
inactivated by
organics (blood and
sputum)
against Clostridium
difficile and
Norwalk virus
Inactive against spores,
protozoan oocysts, and
certain nonenveloped
viruses; not effective
for soiled hands
Inactive against spores;
ototoxicity, keratitis,
and conjunctivitis
Skin irritation and
discoloration (less w/
iodophors); inactivated
by blood and sputum
Not as broad spectrum,
fast-acting, or long-lasting
as chlorhexidine; ↓ efficacy
in presence of organics
Ineffective against G(–),
fungi, and mycobacteria;
neurotoxicity;
teratogenic
Ineffective against G(–),
mycobacteria and fungi;
inactivated by organic
materials and cotton
gauze
Ineffective against G(–)
and filamentous fungi
Inconvenient; skin irritation None Most appropriate for
None
#1 overall
(.6 hours;
remains bound
to stratum
corneum)
Minimal Must wait for it to dry
Good Ineffective against
Modest No longer used
Good Used in eyedrops
Good Not as effective as
Flammable → caution
w/ electrosurgery and
lasers
Longest acting
Often avoided around
eyes/ears
Chlorhexidine 1 alcohol
combo antiseptics are
most effective at
preventing SSI
to be effective
Higher risk of SSI
compared with
chlorhexidine
pseudomonas unless
combined w/ EDTA
Highly absorbed through
skin → infants bathed
w/ this agent developed neurotoxicity
chlorhexadine,
iodophors, or alcohol;
Binds enoylacyl carrier
protein reductase in
bacteria; primary agent
used in antibacterial
suture coating
soiled hands
Table 8.13 Summary of Methods of Electrical Hemostasis
Type Current Voltage Amperage Terminal Waveform Tissue Destruction
Electrocautery Direct — — N/A None
Electrodesiccation Alternating High Low Monoterminal Markedly damped
Electrofulguration Alternating High Low Monoterminal Markedly damped
Electrocoagulation Alternating Low High Biterminal Moderately damped
Electrosection Alternating Low High Biterminal Undamped Minimal
current used in electrosurgery does not have set positive
and negative poles)
■
Monoterminal circuits (electrodesiccation and
electrofulguration) employ an active electrode without
1111
111
11
1111
a grounding pad
Monoterminal and biterminal devices
• Monoterminal and biterminal: refers to the absence or
presence of a grounding electrode (Table 8.14)
Because there is no dispersive electrode to dissipate
the accumulated current, higher voltages are needed
to reach the desired level of effective tissue
destruction
459

CHAPTER 8 • Dermatologic Surgery
Table 8.14 Monoterminal Versus Biterminal
Term Definition
Monoterminal No grounding electrode; electrons from patient disperse
Biterminal Presence of a grounding electrode (either grounding pad
Only electrical difference between electrofulguration
and electrodesiccation is that the probe does not
directly contact the skin in electrofulguration
■
Biterminal circuits (electrocoagulation and
electrosection) always employ a dispersive electrode
to recycle current
Current travels from the active electrode to the
dispersive electrode; if grounding pad is used →
current travels through the body, whereas if
biterminal forceps are used → current travels
between tips of forceps; dispersive electrode
provides an outlet of return of current to
electrosurgical device, permitting increased
amperage and reduced voltage
Only electrical difference between electrocoagulation
to table, floor, walls, and air
or biterminal forceps)
Waveforms
• Waveforms are used to describe the characteristics of a
wave’s amplitude, frequency, and continuity (continuous
waveforms result in ↑ heating compared to discontinuous
waveforms)
• “Undamped” waveform (may be continuous or
discontinuous): amplitude remains unchanged
throughout sine wave → pure cutting, no hemostasis
■
Example: pure electrosection
• “Damped” waveform (may be continuous or
discontinuous): amplitude decreases with time and
eventually reaches zero; the more rapidly the wave’s
amplitude diminishes to zero, the more damped the
current; increased damping results in greater coagulation/
destruction and less cutting
■
Examples: electrodesiccation, electrofulguration, and
electrocoagulation
Electrocautery
• Direct current supplies energy to device tip → generates
heat → red-hot tip is applied directly to tissue
■
Mnemonic: “Cautery is Hotery”
■
Electrocautery is distinguished from electrosurgery by
its absence of alternating current
• Current does not pass through the patient; destruction
is achieved solely by heat conducted to the tissue → safe
in patients w/ implantable cardioverter debrillators
(ICDs) and pacemakers
• Additional advantages: portable and effective in a wet
eld
Electrodesiccation
• Monoterminal device
• Low amperage, high voltage, markedly damped
• Probe directly contacts tissue → slowly heats tissue →
water loss w/ supercial skin dehydration and
mummication, but no signicant protein loss
Electrofulguration
• Monoterminal device (e.g., hyfrecator)
• Low amperage, high voltage, markedly damped
• Probe held at a distance (1–2 mm from tissue)
→ ionized current between probe and tissue (“spark
gap”) → supercial tissue ablation, but underlying tissue
protected from heat spread by supercial carbonization
→ more limited, supercial tissue destruction
• Similar to electrodesiccation in most respects, with the
exception that the spark gap and resultant supercial
carbonization result in more limited, supercial tissue
destruction
Electrocoagulation
• Biterminal device
• High amperage, low voltage, moderately damped
• Probe directly contacts tissue → slow cellular heating
→ intracellular uid evaporation, coagulum formation,
and resultant protein denaturation
• ↑ Current (amperage) penetrates more deeply than in
electrodesiccation → ↑ deep tissue destruction and hemostasis
Electrosection
• Biterminal device
• High amperage, low voltage
• Undamped → pure cutting
• Vaporization of tissue without hemostasis; majority of
energy dissipates during vaporization → minimal
collateral tissue damage
• If used on a “blended mode” with electrocoagulation →
provides a mixture of hemostasis and cutting
Complications
• Thermoelectric burns at site of current exit may occur if
the patient is not properly grounded
• Unwanted current ow through patient
■
Minimize distance a current travels in a patient’s body
by applying grounding pad to a highly vascularized
surface in proximity to operative site
■
Avoid positioning any implantable monitoring devices
between the active and dispersive electrodes
• Corneal damage (↑ risk w/ metal eye shields) → be
careful around eyes
Fire hazards
• Bowel gas (methane) → exercise caution when using
electrosurgery in perianal area
460

8.9 Excisions
• Aluminum chloride (ammable) → must wash off
• Oxygen should be temporarily disabled if operative site
is in close proximity to the oxygen source
• Avoid alcohol preps; use chlorhexidine or povidone-
iodine instead
Implantable electronic devices
• Pacemakers and ICDs
■
Most modern (1980s and on) implantable devices have
shielding that guards from external electrical
interference, though caution still advised
■
ICDs are more sensitive than pacemakers to
electromagnetic interference (because of the presence
of sensing circuits)
■
Electrocautery has 0% risk of electromagnetic
interference but is less effective
■
Biterminal (often erroneously referred to as “bipolar”)
forceps are effective and very unlikely to cause interference
Most surgeons prefer this approach (vs.
electrocautery)
■
Magnet application can be used to:
Temporarily deactivate ICD
Switch pacemaker to a preset pacing rate that
ignores all electrical signals
■
In cases in which biterminal forceps cannot be used or
are unavailable, caution should be taken:
Direct the path of current away from implantable
devices
Do not position implantable devices between the
active and dispersive electrodes
Use short bursts of energy (,5 seconds and spaced
.5 seconds apart)
Use lowest effective power settings
Avoid electrosection (highest risk!)
Do not use within 5 cm of implantable device
Have a crash cart and ACLS-trained staff ready
■
In cases of uncertainty → cardiology consultation
• Noncardiac implanted electronic devices
■
Examples: deep brain stimulators, spinal cord
stimulators, vagal and phrenic nerve stimulators, gastric
stimulators, and cochlear implants
■
In contrast to ICDs, patients are usually equipped with
an external remote control to power these devices off
8.8 CRYOSURGERY
• Application of low temperature substances → cellular
injury → sloughing of damaged tissue
• Mechanism of action (in order):
■
Formation of ice crystals rst in the extracellular space
causing hyperosmotic gradient that pulls water out of
cell → intracellular dehydration → membrane damage
■
Further freezing → intracellular ice crystal formation
→ further membrane damage
■
Extracellular thawing reverses gradient and draws water
back into cell → cellular swelling and rupture
■
Vasoconstriction from freezing → further damage
through anoxia
■
Vasodilation after thawing → release of harmful free
radicals into affected tissue → further tissue damage
• Specic cryogens:
■
Liquid nitrogen (boiling point: –196°C) is preferred
cryogen due to low boiling point and ease
■
Solid carbon dioxide (boiling point: –79°C):
occasionally used for chemical peels
• Temperature required for cell death (Boards favorite!):
■
By cell type:
Melanocytes (most sensitive): –5°C
Keratinocytes: –20°C to –30°C
Fibroblasts (least sensitive): –35°C to –40°C
■
Benign versus malignant
Benign: –25°C
Malignant: –50°C
• Optimal freezing technique 5 rapid freezing 1 slow
thawing (favors intracellular ice formation)
■
Open technique: most common; liquid nitrogen is
released through tips, needles, cannulas, or cones
■
Chamber technique: modication of “open technique”;
typically used only for malignancies; cryogen is
released into a chamber → turbulence within the
chamber → lower temperatures achieved, and in
shorter amount of time than w/ open technique
■
Closed technique: cooled probe is attached to cryogen
line in closed system → direct application → tissue
destruction
■
Intralesional technique: cryogen injected directly into
tissue via cannula or needle
8.9 EXCISIONS
• Indications: biopsy, removal of benign and malignant
lesions, and scar revision
• Design: closure of a circle results in large standing cones
on each side of the closed wound → therefore, most
excisions are executed in a fusiform fashion
■
Apical angles: angles at either end of the excision;
ideally # 30 degrees in order to avoid formation of
standing cones
■
Length-to-width ratio should be $3:1
■
Generally, place excisions parallel to RSTLs
• Variations:
■
Crescent excision: when one side of excision is
designed longer than the other, a curved/crescent shape
will result; common uses: sites where RSTLs are
curvilinear (cheek and chin)
■
M-plasty (Fig. 8.11): used to shorten length of excision
such that the incision does not extend into an
undesired location; common uses: near free margins
(perioral and periocular regions)
■
S-plasty (“lazy S”): ↑ total length of scar, but the linear
distance between two apices remains same as linear
closure; redistributes tension along different vectors →
↓ tension in central portion of scar → ↓ risk of centrally
depressed scar, ↓ dehiscence, and ↓ contraction of scar;
common uses: convex surfaces (forearm and shin) and
excisions that cross over a joint (elbow and knee)
461

CHAPTER 8 • Dermatologic Surgery
30º
30º
Fig. 8.11 M-plasty. Instead of completing the ellipse, the dashed lines are incised
as shown, reducing the length of the scar. (From Cosulich M, Etzkorn J, Shin TM,
Miller CJ. Second intention healing and primary closure. In: Rohrer TE, Cook JL,
Kaufman AJ, eds. Flaps and Grafts in Dermatologic Surgery. 2nd ed. Philadelphia: Elsevier. 2018:34–49.)
■
Lip wedge excision: full-thickness excision of the lip
with layered repair; may be used to repair defects up to
one third of the length of lower lip; must mark
vermillion border before anesthetizing → ensures
precise realignment; close lip in layered fashion in the
following order (high yield!):
Mucosal layer: use silk or braided polyester
Orbicularis oris muscle: use polyglactin 910; reapproximation is critical to maintain competence of
oral sphincter
Dermis and subcutaneous tissue: start by reapproximating vermilion border
Epidermis: hyper-eversion to prevent depressed scar
• Standing cones (“dog ears”):
■
Causes: apical angles that are too wide (.30 degrees),
length-to-width ratio ,3:1, unequal lengths on each
side of wound, convex surfaces, and insufcient
undermining at wound apices
■
Repair options (“dog ear repairs”):
Extending incision: ↑ excision length allows for
redistribution of excess skin
M-plasty: removes standing cones
Rule of halves: standing cone is redistributed along
entire excision length by “halving” it throughout
Excision of a Burow’s triangle: a triangle of tissue
removed from the side of the wound with the
standing cone
• Closure types:
■
Simple closure: one layer of sutures (epidermal closure
only)
■
Layered closure: two or more layers (epidermal 1
dermal, SQ or fascia) of sutures → ↓ tension on wound
edges (improved cosmesis), ↓ dead space (results in
↓ hematoma and seroma risk)
• Undermining planes (Boards favorite!):
■
Trunk/extremities: mid-deep SQ (for small or
supercial defects), or just above deep fascia (larger
excisions and invasive melanomas)
■
Head/neck: varies by subunit, but generally supercial
SQ on face (supercial to SMAS); preserves motor
nerves, which are all deep to SMAS
Cheek: mid SQ plane → avoids transecting parotid
duct, buccal and zygomatic branches of CN7, and
vascular structures
Ear: given the near lack of adipose tissue, dissection
is always just above perichondrium
Eyebrow: subcutis, deep to hair bulbs → minimizes
eyebrow hair loss
Eyelid: immediately above orbicularis oculi muscle
(because there is minimal SQ tissue)
Forehead: deep SQ plane, just above frontalis
(small, supercial defects); occasionally undermine
in avascular subgaleal plane (large or deep
defects); if desired, supercial SQ undermining may
preserve sensory nerves
Lateral neck: supercial SQ plane, above spinal
accessory nerve → avoids Erb’s point
Lip: immediately above orbicularis oris muscle
→ avoids cutting into vascular orbicularis muscle
and branches of labial artery
Mandible: supercial SQ plane, above marginal
mandibular nerve
Nose: submuscular plane immediately above
periosteum/perichondrium (deep to SMAS/nasalis
muscle) → relatively avascular plane
Scalp: subgaleal → avascular plane
Temple: supercial SQ plane → avoids transection
of temporal branch of facial nerve and artery
• Wound healing (see Chapter 1, Basic Science)
• Wound strength following surgery never returns to
100%; dehiscence risk is highest at the time of suture
removal (1–2 weeks)
■
1 week 5 5%
■
2 weeks 5 ,10%
■
1 month 5 40%
■
1 year and beyond 5 80% (maximum strength)
• Surgical margins:
■
Melanoma:
Melanoma in situ → 0.5 to 1 cm (upper end of range
if broad or ill-dened such as lentigo maligna (LM);
recent studies by Zitelli et al. recommend 0.9 cm)
Breslow depth # 1 mm → 1 cm wide local excision
(WLE) to deep fat or fascia (variable)
Breslow depth 1.01 to 2 mm → 1 to 2 cm WLE to
fascia
Breslow depth . 2 mm → 2 cm WLE to fascia
■
Basal cell carcinoma (BCC): 4 mm margins for most
tumors; 0.6 to 1 cm margins or Mohs for high-risk
BCC (high-risk BCC described in Box 8.1)
■
Squamous cell carcinoma (SCC): 4 mm margins for
most low-risk SCC; $0.6 cm margins or Mohs for highrisk SCC (high-risk features described in Box 8.1)
■
Dermatobrosarcoma protuberans (DFSP): 2 to 3 cm
margins extending at least to fascia is recommended,
but is a/w ↑ recurrence compared to Mohs
462

8.11 Flaps
Box 8.1 Mohs Appropriate Use Criteria
BCC/SCC with following features generally considered appropriate
for Mohs
Tumors involving:
Area H (“H-zone” or “mask areas” of face, hands/feet, genitalia, nipple/
areola): especially if $ 0.6 cm
Area M (remaining face, neck, scalp, pretibial): especially if . 1 cm
Area L: only if . 2 cm or other high-risk features
Recurrent
Perineural/perivascular invasion
Aggressive histologic features:
BCC: morpheaform, inltrative, micronodular, or metatypical/basosquamous
SCC: poor differentiation; depth $ 2 mm or $ Clark IV; sclerosing, small cell,
spindle cell, inltrating, clear cell, lymphoepithelial, or sarcomatoid subtypes
At site of prior radiation/scar
Immunosuppressed status (CLL, organ transplant, HIV, hematologic malig-
nancy, or pharmacologic immunosuppression)
Genetic syndromes (Gorlin’s, XP, etc.)
Data from Ad Hoc Task Force, Connolly SM, Baker DR, et al. AAD/ACMS/ASDSA/ASMS 2012 appropriate use criteria for Mohs micrographic surgery: a report
of the American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery Association, and the American Society for Mohs Surgery. J Am Acad Dermatol. 2012;67(4):531–550.
8.10 MOHS SURGERY
• Mohs micrographic surgery (MMS): specialized method of
skin cancer removal that provides complete 3608
(circumferential) microscopic margin control; by
denition, both the surgery and microscopic evaluation
must be performed by same provider
• Advantages:
■
Allows for microscopic evaluation of 100% of the
excision margins (vs. ,1% with “breadloang”
technique used for standard elliptical excisions) →
↑ cure rates due to ↓ false-negative margins
■
Tissue sparing (smaller margins can be taken w/
condence that the tumor is clear)
■
Compares favorably in terms of cost effectiveness
relative to other treatments
• MMS offers superior cure rates for most skin cancers,
including rare forms:
■
BCC/SCC: 97%–99% for primary lesions (vs. 93% for
conventional excision) and 90%–95% for recurrent
lesions (vs. 80% for conventional excision)
■
DFSP (treatment of choice): .98%
■
MMIS, including lentigo maligna: .98%
■
AFX: .95%
■
Microcystic adnexal carcinoma: 90%–95%
■
EMPD: 85% (potentially higher if intraoperative CK7
immunostain is used)
■
Leiomyosarcoma (supercial): .90%
■
Sebaceous carcinoma: .90%
■
Erythroplasia of Queyrat: .90%
■
Others: verrucous carcinoma, various adnexal
carcinomas, Merkel cell carcinoma (not generally
recommended), and angiosarcoma (not generally
recommended)
• Tumor must have a contiguous growth pattern to be
amenable to Mohs
• Essential steps of Mohs technique:
■
Clinically apparent residual tumor/biopsy site is
debulked with curette or scalpel
Lentigo maligna/MMIS with following features generally considered
appropriate for Mohs
Area H or Area M
Recurrent
Other rare tumors generally considered appropriate for Mohs
Adenoid cystic carcinoma, adnexal carcinoma, apocrine/eccrine carcinoma,
AFX/PDS/UPS, DFSP, EMPD, LMS, MCC (not generally recommended),
MAC, mucinous carcinoma, sebaceous carcinoma
■
Beveled excision (scalpel held at 45° angle) of tumor
plus a small (1–2 mm) margin of normal-appearing
skin
■
Hash marks (“notches”) are placed on excision
specimen and surrounding nonexcised skin to assist w/
orientation
■
Excised specimen may be divided into two or more
pieces (optional)
Central relaxing incisions (or “Pac Man” incision
of undivided specimen), and/or dividing into two
or more pieces helps atten tissue to ensure
epidermis lies in same plane as deep tissue
■
Excised specimen is inked with two or more colors
■
Histotechnician attens tissue to ensure that the epidermis
lies in the same plane as the deep tissue → allows for
horizontal processing of slides (stain 5 H&E or Toluidine
blue) → enables simultaneous microscopic evaluation of
supercial and deep margins
■
Surgeon evaluates slides for residual tumor
■
If tumor is present, the site is marked on the Mohs
map, and steps two to seven are repeated until tumor
has been eradicated
■
Once tumor is cleared, surgeon discusses reconstructive
options w/ patient
• Mohs Appropriate Use Criteria (AUC): criteria established
in 2012; developed to guide decision-making, not to
establish the standard of care (see Box 8.1)
8.11 FLAPS
• Indications:
■
Defects that will heal poorly by secondary intention
■
When linear repair would compromise function, result
in excessive tension, or distort a free margin
■
To maintain three-dimensional contour when there is
signicant tissue loss
• Advantages:
■
Excellent color, texture, and thickness match, as the
skin is recruited from adjacent tissue reservoirs
463

CHAPTER 8 • Dermatologic Surgery
■
Ability to redirect tension vectors
■
Can be used to cover cartilage/bone because of reliable
blood supply
■
Rapid healing
■
Replaces volume when there is signicant tissue loss
• Disadvantages:
■
Geometric scar lines if not concealed in RSTLs
■
Poor design can lead to functional compromise, free
margin distortion, poor esthetics, or ap necrosis
• Denitions (Fig. 8.12):
■
Primary defect: defect following tumor extirpation that
requires repair
■
Secondary defect: defect created by ap elevation and
closure of primary defect
■
Body: tissue that is being shifted (“apped”) onto the
defect
■
Pedicle (ap base): vascular base of ap → provides
blood ow to ap
■
Flap tip: portion of ap furthest away from the blood
supply/pedicle → area at highest risk for necrosis
■
Primary lobe (for multi-lobed aps): portion of ap
intended to cover primary defect
■
Secondary lobe (for multi-lobed aps): portion of ap
intended to cover secondary defect
■
Primary ap movement: motion of ap movement
required to close primary defect
■
Secondary ap movement: motion of ap movement
required to close secondary defect
■
Primary tension vector: direction of force resisting the
movement of the ap body
■
Secondary tension vector: direction of force created by
closure of donor site defect
■
Pivot point: point on the base of the ap around which
the ap transposes/rotates → critical to undermine this
area to obtain optimal ap movement
■
Flap size (required measurement for billing purposes):
entire surface area of ap elevation 1 surface area of
primary defect
■
Key stitch: critical initial stitch required to move the
ap onto the primary defect
■
Axial pattern ap: aps based on a named vessel
→ most reliable; includes paramedian forehead ap
(supratrochlear artery), dorsal nasal rotation “Rieger”
ap (angular artery), and Abbe cross-lip ap (labial
artery)
■
Random pattern ap: aps with unnamed
musculocutaneous arteries within pedicle; elevated portion
of ap is perfused by anastomotic subdermal and dermal
vascular plexuses; includes all aps not listed above
• There are many ways to classify aps (primary motion,
blood supply, shape, and eponymous name); however,
they are best classied according to primary motion:
■
Sliding: ap slides into place with linear or curvilinear
motion; redundant tissue can be excised anywhere
along length of ap; main tension vector 5 opposite
direction of ap movement; key stitch closes primary
defect (approximates ap edge to opposite edge of
primary defect)
Advancement ap (Table 8.15):
♦ Mechanics: does not redirect primary tension vector
♦ Goal: redistribute Burow’s triangle to a more
functionally or cosmetically desirable location
(e.g., away from free margins [eyelid, ear, lip,
and alar rim])
Fig. 8.12 Anatomy of a ap. (From Brodland DG. Flaps. In: Bolognia
JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia:
Elsevier; 2018:2495–2516.)
Secondary
tension vector
Rotation point
ANATOMY OF A FLAP
Secondary
flap movement
Secondary defect
Primary
tension
vector
Base of flap
or pedicle
Pivot point
Secondary
tension vector
Primary flap
movement
Body
Primary defect
464
Соседние файлы в папке Библиотека им академика М.И. Перельмана
