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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

Table 8.15 Advancement Flaps
Flap Category
(Variants/Other Names) Design Common Uses Comments
Unilateral Burow’s
advancement (A → L, O → L)
Unilateral crescentic
advancement (perialar
crescentic)
Unilateral O →U advancement
Bilateral A → T advancement
(O → T)
Bilateral O → H advancement Essentially a double O → U flap, w/
V →Y advancement flap
(formerly island pedicle flap)
Mucosal advancement Essentially a linear flap of lip mucosa;
NLF, Nasolabial fold.
Displaces one of the Burow’s triangles
to a more cosmetically or functionally
desirable location (away from free
margins or hidden between cosmetic
subunits)
Variant of A → L where a crescentic
standing cone is removed within flap
body → eliminates need to remove one
of the two Burow’s triangles
Incisions and Burow’s triangles oriented
in same direction away from defect →
a square or rectangle-shaped flap is
advanced onto defect
Divides one of the two standing cones
into two smaller Burow’s triangles; two
opposing flaps are bilaterally advanced
onto defect
mirror-image flaps on either end of
primary defect
Unlike other advancement flaps, area
under flap body is not undermined
(serves as random-pattern pedicle);
periphery is undermined widely, then
V-shaped island w/ deep pedicle is
advanced onto defect; key stitch:
connects midpoint of leading edge of
flap to midpoint of defect’s wound edge
undermine deep to minor salivary
glands, but superficial to orbicularis
muscle; undermine to gingival sulcus;
flap is advanced onto vermilion defect
Suprabrow (displaces Burow’s lateral to
eyebrow)
Off-center nasal dorsum/tip (“East-to-
West” ap; maintains nasal symmetry)
Lateral upper cutaneous lip (displaces
Burow’s into NLF)
Suprabrow (hides incision above eyebrow
hairline)
Cheek-to-nose perialar crescentic
advancement: defects immediately su-
perior to alar crease (hides incision in alar
crease 1/– NLF)
Helical rim advancement (useful for deeper
defects that are not amenable to FTSG
or second intention healing)
Eyebrow (used to preserve continuity of
brow; hides incision lines above and
below browline)
Similar to A → L, but can cover larger
defects
Chin (hides ap incisions in mental crease)
Suprabrow (when unilateral is not enough)
Eyebrow, forehead Disadvantages: multiple incision
Small defects on nasal tip or immediately
above alar crease
Small, deep alar defects (includes “shark
IPF”, which can re-create alar crease)
Medium to large defects on lateral
upper cutaneous lip (particularly those
involving the nose-lip-cheek junction)
Eyebrow defects
Repair of ectropion
Vermilion lip Disadvantages: lip numbness
Does not provide much added
laxity relative to linear closure
Cheek-to-nose flap may require
suspension/tacking suture from
body of flap to nasal periosteum
to recreate the nasofacial sulcus
and prevent “tenting”
Hyper-evert helical rim flaps →
prevents notching
Smaller pedicle → more prone to
ischemia
lines, forehead numbness (as a
result of long horizontal incisions)
In reality, a portion of pedicle must
be undermined to allow for
movement, but must ensure
that $ 40% of pedicle
remains intact
Tissue-efcient ap (no tissue
discarded)
Disadvantages: triangular-shaped
scar (often prominent); trap-
door effect
(improves over time); thinning
of lip
8.11 Flaps
♦ Disadvantages: limited by degree of elasticity of
surrounding tissue → suboptimal for large defects
that lack abundant adjacent tissue reservoir/laxity
Rotation ap (Table 8.16):
♦ Mechanics: redirects primary tension vector
along an arc adjacent to primary surgical defect
while simultaneously creating a secondary defect
along the ap arc
♦ Goal: take advantage of tissue reservoir/laxity at a
distance from primary defect
♦ Disadvantages: there is a functional loss of ap
length and height when ap is rotated onto
defect → length of ap arc must be much
longer than width of primary defect and height
of ap must be taller than height of primary
defect; is a heavy ap and prone to causing
unwanted secondary tension vectors → may
result in distortion of free margins (ectropion) if
not carefully executed → may require tacking
sutures to periosteum to minimize risk
♦ Main uses: large defects on medial cheek; large
defects on inelastic skin (scalp); areas w/ curved
RSTLs (chin and along mental crease);
redistribute tension away from free margins
(lower eyelid, nasal tip, and upper lip)
■
Lifting: ap is lifted and transposed (“leapfrogged”)
over normal intervening skin; has both pivotal and
rotational movements; redirects primary tension
vector to donor site; goal is to use nearby, but
“nonadjacent,” tissue reservoir (“nonadjacent”:
intervening normal skin is present between ap donor
site and primary defect) in order to close primary
defects at sites that have minimal inherent laxity
(nose, medial canthus, and ear); key stitch varies
depending on specic ap
Transposition (single-stage) aps (Table 8.17)
♦ Mechanics: redirects primary tension vector onto
donor site → results in loose ap of skin that can
be “plopped onto” primary defect → primary
defect closed under minimal to no tension
465

CHAPTER 8 • Dermatologic Surgery
Table 8.16 Rotation Flaps
Flap Category (Variants/Other
Names) Design Common Uses Comments
Unilateral rotation Curvilinear incision w/ arc length
Unilateral rotation, Rieger variant
(dorsal nasal rotation, Hatchet flap,
and glabellar turn-down)
Unilateral rotation, Mustarde/Tenzel
variant
Bilateral rotation (O → Z)
. defect width, and arc height
. defect height to compensate for
loss of length as flap rotates; area
of pivotal restraint must be
undermined extensively to allow
movement; back-cuts ↑ mobility,
but ↓ blood flow
Axial flap (angular artery) w/
back-cut in glabella; undermine
just above perichondrium; maximal
points of pivotal restraint 5
medial canthal tendon and
nasofacial sulcus
Laterally based rotation flap of
cheek/temple; Mustarde flaps
utilize entire cheek/temple
reservoir; Tenzel flaps are smaller
(partial-cheek)
Double rotation flap with yin-yang
shape
Upper cutaneous lip (hides incision
in melolabial fold)
Chin (hides incision in mental
crease)
Medium to large (up to 2.5 cm)
midline defects on lower 2/3 of
nose (tip/supratip)
Mustarde: larger lower lid defects
($50%)
Tenzel: smaller defects of mid to
lateral lower lid (,50% of lid)
Large defects involving inelastic skin
(mainly used for scalp)
On face, flap pedicle should be
inferior-lateral to ↑ lymphatic
drainage → ↓ flap lymphedema
Disadvantages: transposition of thick
glabellar skin onto medial canthus,
long incision lines, potential “pig-nose”
deformity (as a result of inadequate
undermining and unwanted secondary
tension vectors)
Tacking sutures to lateral orbital rim
periosteum → ↓ ectropion risk
Disadvantages: long, prominent incision
lines (minimize w/ good galeal suturing,
eversion)
Table 8.17 Transposition Flaps
Flap Category (Variants/Other
Names) Design Common Uses Comments
Rhombic flap Classic design (Limberg flap):
parallelogram-shaped flap w/ two
60-degree angles and two 120-degree
angles; flap takes off from defect at
90-degree angle; Burow’s triangle removed
at pivot point; secondary defect is
closed first (key stitch)
Bilobed flap (Zitelli modification) Multilobed transposition flap that
redistributes tension to areas of
greater tissue laxity (i.e., nasal dorsum/
sidewall); tension is shared between all
lobes; 1° lobe diameter 5 primary
defect diameter; 2° lobe diameter 5
1° lobe diameter (or slightly smaller); flap
takeoff point 5 midpoint of defect at a
45-degree angle; angle between 1° and 2°
lobe also 5 45 degrees → flap has overall
angle of 90 degrees; remove standing
cone at pivot point; undermine flap
in submuscular plane to nasofacial
sulcus to achieve adequate movement;
order of closure 5 tertiary defect (2°
lobe donor site; key stitch) → secondary
defect (1° lobe donor site) → primary
defect closed last
Banner transposition flap Long, narrow transposition flap w/ high
length:width ratio (3:1 to 5:1); flap is
raised along RSTLs and transposed onto
primary defect
Medial canthus
Cheek
Temple
Upper lateral 1/3 of nose
Distal 1/3 of nose May use as many lobes as necessary
Upper helical rim
Medial canthus and nasal
bridge (donor site: glabella)
Lateral lower lid (donor:
upper lid)
Medial lower lid (donor: naso-
facial sulcus)
Final suture line looks like a question
mark
Eight rhombic aps possible for any
rhombic-shaped defect
Dufourmental and Webster modica-
tions: ↓ angle of ap tip → shorter
arc of rotation → easier to close sec-
ondary defect, ↑ tension sharing be-
tween 1° and 2° defect, ↓ reorientation
of tension vectors, and ↑ risk of ischemia (as a result of a narrower pedicle)
(trilobe, tetralobe) to reach a tissue
reservoir where tension will not cause
distortion
Risk of pincushioning (trapdoor)
→ may be due to oversizing ap, insufcient undermining, ↑ bulkiness on
underside of ap, ap lymphedema
(self-resolves), peripheral contraction
(↑ risk w/ rounded aps), or insufcient
tacking of ap to wound base
Original bilobed ap design was inferior
to Zitelli’s: used 180-degree overall angle (vs. 90 degrees) and did not remove standing cone at pivot point →
↑ pincushioning of 1° lobe, ↑ standing
cone at pivot point
Narrow pedicle → must ensure ap has
robust blood supply to prevent necrosis
Prone to pincushioning (trapdoor)
effect → must undermine recipient
site widely, undersize ap or deepen
recipient bed, and use tacking sutures
to ↓ dead space between ap and recipient site
466

Table 8.17 Transposition Flaps—cont'd
Flap Category (Variants/Other
Names) Design Common Uses Comments
Nasolabial/melolabial
transposition flap
Z-plasty Transposition flap primarily used for
RSTLs, Relaxed skin tension lines.
Variant of banner flap w/ 60° angle of
transposition; tack pivot point to pyriform
aperture (near junction of lateral ala/
isthmus of upper lip); must thin distal
portion of flap extensively
lengthening a contracted scar and
redirecting tension; may use various
angles: ↑ angle size → ↑ length gain
and ↑ reorientation of tension
Medium-sized, deep defects
of nasal ala
Disadvantages: blunting of alar crease
(almost all cases), pincushioning
→ minimized w/ tacking sutures, ap
thinning, and wide undermining of recipient site
Many cases require revision
Spear ap (variant): used for full-thick-
ness alar defects; same general design, but ap is folded on itself to provide internal nasal lining 1 external
coverage
30° angle → 25% ↑ length and 40° ten-
sion reorientation
45° angle → 50% ↑ length and 65° ten-
sion reorientation
60° angle → 75% ↑ length and 90°
tension reorientation
8.11 Flaps
♦ Goal: utilize nearby tissue reservoirs in order to close
defects at sites that have minimal inherent laxity
♦ Disadvantages: prone to
pincushioning/“trapdooring” (→ must widely
undermine to prevent); technically challenging
Staged interpolation aps (Table 8.18)
♦ Mechanics: similar to single-stage transposition aps
but base of ap (pedicle) is not adjacent to defect
and must be divided in a second stage; thick
vascular pedicle (either random pattern or axial)
provides ↑ blood ow → allows for ↑↑↑ ap
length-to-width ratio (.4:1 maximum ratio seen w/
most other aps), and coverage of very large defects;
pedicle typically divided and inset at 3 weeks
♦ Goal: utilize nearby tissue reservoirs in order to
close defects at sites that have minimal inherent
laxity or limited blood supply
♦ Main uses: large defects on nose, large helical rim
• Sliding aps (noteworthy key stitches marked with
star)
■
Unilateral advancement ap (“O to U” or “U-plasty”)
(Fig. 8.13)
■
Bilateral advancement ap (“H-plasty”) (Fig. 8.14)
■
Bilateral advancement ap (“A-to-T” or “O-to-T”)
(Fig. 8.15)
■
Burow’s advancement ap, crescentic advancement ap
(Fig. 8.16)
■
V-to-Y advancement ap (formerly, “island pedicle
ap”): vascular supply derived from non-undermined
subcutaneous pedicle (Fig. 8.17)
■
Rotation ap (Mustarde type) (Fig. 8.18)
• Lifting aps
■
Rhombic ap (and variants) (Fig. 8.19)
■
Bilobed transposition ap (Fig. 8.20)
■
Single-stage nasolabial/melolabial transposition
(modied banner) ap (Fig. 8.21)
defects, and large lip defects
Table 8.18 Staged Interpolation Flaps
Flap Category (Variants/Other
Names) Design Common Uses Comments
Paramedian forehead flap (PMFF) Axial flap based on supratrochlear artery;
maximum length of flap 5 distance between
orbital rim to frontal hairline (if longer, will
transplant hair onto nose); pedicle arises at medial
brow contralateral to the predominant side of
nasal defect (minimize twisting); pedicle oriented
in vertical fashion; ideal pedicle width 5 1.0–
1.5 cm; flap body elevated from cephalad to
caudad in plane just above periosteum; flap tip
must be extensively thinned before suturing to nasal
tip; pedicle is divided and inset at 3 weeks
Abbe lip switch Axial flap based on labial artery; transfers both
skin, mucosa and orbicularis oris muscle to
recipient site; pedicle divided and inset at
3 weeks
Large nasal defects
Large (.1/3 of lip), full-
thickness defects of
upper or lower lip
Pedicle too narrow → fails to incorporate
artery → ischemia
Pedicle too wide → kinking of artery
→ ischemia and ↓ rotational ability
Most commonly used for upper lip
defects, because defects involving up
to 1/3 of lower lip can be repaired via
lip wedge
Risk of microstomia and oral
incompetence
Continued
467

CHAPTER 8 • Dermatologic Surgery
Table 8.18 Staged Interpolation Flaps—cont'd
Flap Category (Variants/Other
Names) Design Common Uses Comments
Nasolabial/melolabial interpolation
flap
Retroauricular (“book”) flap Random pattern flap; a rectangular-shaped
Random pattern flap perfused by small
perforators of angular artery; similar in design
to single-stage nasolabial transposition flap,
but retains a thick vascular pedicle; extensively
debulk flap tip before suturing onto primary
defect; pedicle divided and inset at 3 weeks
flap is raised in subcutaneous plane from
retroauricular sulcus to the hairline; flap tip is
thinned and sutured onto helix; pedicle divided
at 3 weeks
Nasal ala (primary use)
Large defects of upper
cutaneous lip
Large defects of
helical rim 1/– loss of
cartilage
Advantage: does not blunt alar crease
(unlike single-stage transposition)
Disadvantage: vascularity less reliable
than PMFF
Donor site often left to heal by second
intention
Fig. 8.13 Unilateral advancement ap. Key stitch indicated by yellow star. (Modied from Cook JL, Goldman GD, Holmes TE. Random pattern cutaneous aps. In:
Robinson JK, Hanke CW, Siegel DM, Fratila A, eds. Surgery of the Skin. 3rd ed. Philadelphia: Elsevier; 2015:252–285.)
Fig. 8.14 Bilateral advancement ap. Key stitch indicated by yellow star. (Modied from Cook JL, Goldman GD, Holmes TE. Random pattern cutaneous aps. In:
Robinson JK, Hanke CW, Siegel DM, Fratila A, eds. Surgery of the Skin. 3rd ed. Philadelphia: Elsevier; 2015:252–285.)
468

8.11 Flaps
Fig. 8.15 Bilateral advancement ap (“A-to-T”). Key stitch indicated by yellow star. (Modied from Cook JL, Goldman GD, Holmes TE. Random pattern cutaneous
aps. In: Robinson JK, Hanke CW, Siegel DM, Fratila A, eds. Surgery of the Skin. 3rd ed. Philadelphia: Elsevier; 2015:252–285.)
A B
C D
Fig. 8.16 Burow’s advancement ap (A and B); crescentic advancement ap (C and D). Key stitches indicated by yellow star.
469

CHAPTER 8 • Dermatologic Surgery
A B
Fig. 8.17 (A) and (B) V-to-Y advancement ap (formerly, “island pedicle ap”). Key stitch indicated by yellow star.
A
Fig. 8.18 (A) and (B) Rotation ap. Key stitch indicated by yellow star. (Modied from Chen TM, Wanitphakdeedecha R, Nguyen TH. Flaps. In: Vidimos AT, Ammirati
CT, Poblete-Lopez C, eds. Requisites in Dermatology: Dermatologic Surgery. Philadelphia: Elsevier; 2009:163–180.)
F4
F3
Defect
B
F1
X
F2
A
Fig. 8.19 (A) to (D) Rhombic transposition ap. Key stitch indicated by yellow star. (Modied from Kang AS, Kang KS. Rhomboid ap: indications, applications, techniques and results. A comprehensive view. Ann Med Surg. 2021;68:102544.)
F1
X
B
470

C D
Fig. 8.19, cont’d
8.11 Flaps
b
a
b
a
Fig. 8.20 Bilobed transposition ap using Zitelli’s modication. Key stitch indicated by yellow star. (Modied from Bhatia AC, Overman J, Rohrer TE. Transpositions
aps. In: Rohrer TE, Cook JL, Kaufman AJ, eds. Flaps and Grafts in Dermatologic Surgery. 2nd ed. Philadelphia: Elsevier. 2018:99–115.)
Fig. 8.21 Single-stage nasolabial/melolabial transposition (modied banner) ap. Key stitch indicated by yellow star. (From Cook JL, Goldman GD. Random pattern
cutaneous aps. In: Robinson JK, Hanke CW, Siegel DM, Fratila A, eds. Surgery of the Skin. 2nd ed. Philadelphia: Elsevier; 2010:251–287.)
471

CHAPTER 8 • Dermatologic Surgery
Table 8.19 Comparison of Graft Types Used in Soft Tissue Reconstruction
Graft Type
FTSG Good to
STSG Poor to fair Low Low Low High Fair to good Fair Poor
Composite Good Very high Very high Moderate Low Fair Fair Good
Free cartilage N/A Moderate High Moderate Migration or
FTSG, Full-thickness skin graft; STSG, split-thickness skin graft.
From Ratner D, Nayyar PM. Grafts. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier; 2018:2517–2530.
Tissue
Match
excellent
Nutritional
Requirements
High High Low Low Good to
8.12 GRAFTS
• Skin grafts often utilized when defect is not amenable to
primary or ap closure
• Four main categories of skin grafts are commonly used,
each w/ their own pros and cons (Table 8.19)
• Physiology
■
Imbibition (24–48 hours): rst stage, ischemic period
Fibrin attaches graft to bed
Graft is sustained by passive diffusion of nutrients
from plasma exudate of wound bed
Graft becomes edematous
■
Inosculation (48–72 hours, lasts 7–10 days): second
stage
Revascularization resulting in linkage of dermal
vessels between graft and recipient wound bed
■
Neovascularization (day 7): last stage critical to graft
survival, occurs in conjunction w/ inosculation
Capillary and lymphatic ingrowth from recipient to
graft → revascularization complete by day 7
Edema begins to resolve
■
Reinnervation/Maturation (starts within 2 months):
slow process that is not completed for many months
to years
• Types of grafts
■
Full-thickness skin graft (FTSG):
Composed of epidermis and full-thickness dermis
Primary goal: match donor skin w/ recipient site
based on skin color, texture, thickness, degree of
photo damage, and presence/absence of hair
(Table 8.20)
Advantages: better overall appearance than splitthickness skin graft (STSG), retains adnexal
structures (and function), better contour and
texture match; greater thickness → ↓ wound
contracture
Disadvantages: ↑ metabolic demand → ↑ rate of
graft failure
Oversize graft by 10%–20% to account for graft
shrinkage after harvesting
Defatting (classic teaching): leaving fat on
underside of graft has long been thought to reduce
survival → most books recommend complete
removal of adipose tissue on graft
Requirement for
Recipient Bed
Vascularity
Infection
Risk
Graft
Contraction Risk Durability Sensation
excellent
deformation
possible, with
subsequent
resorption
Table 8.20 Donor Sites for Full-Thickness Skin Grafts
Defect Sites Donor Sites
Nasal tip, ala Preauricular, postauricular neck, nasolabial fold,
Nasal dorsum, sidewalls Preauricular, postauricular neck/lateral neck,
Lower eyelid, medial
canthus
Ear Preauricular, postauricular sulcus, postauricular
Face, scalp Burow’s graft (usually saved during partial
Dorsal hand and fingers Ulnar wrist (smaller grafts), ventral forearm,
♦ However, recent studies suggest defatting is not
Good N/A N/A
conchal bowl, Burow’s graft (particularly at
junction of nasal tip and dorsum)
supraclavicular region (if large)
Upper eyelid, postauricular sulcus (slightly
thicker than upper eyelid donor site)
neck/lateral neck
closure of defect with flap), lateral neck,
supraclavicular region, medial upper arm
medial upper arm (larger grafts)
Good Excellent
necessary and skin-fat composite grafts survive
extremely well, especially on nose
Bolster dressing
♦ Purpose: graft immobilization → ↑ graft
adherence to wound bed
♦ Technique: Xeroform™ gauze or equivalent bulky
nonadherent dressing secured w/ tie-over sutures
Delayed grafting
♦ Useful for:
Deep defects that cannot be adequately lled
by FTSG alone
Defects w/ signicant amount of exposed bone
or cartilage (.25% of periosteum or
perichondrium is lacking)
♦ Wound is allowed to granulate for 1 to 3 weeks
before delayed grafting is performed →
granulation tissue provides well-vascularized bed
to promote graft survival
Burow’s graft (commonly used type of FTSG)
♦ FTSG derived from skin adjacent to the defect
(donor skin 5 discarded Burow’s triangle skin
resulting from partial primary closure of defect) →
provides excellent tissue color and texture match
compared with grafts harvested from distant sites
♦ Most often utilized when primary repair does not
fully close the defect or if complete closure would
Adnexal
Functions
472

8.13 Surgical Complications and Measures to Avoid Them
result in distortion of free anatomic margin (e.g.,
alar rim, perioral, and periorbital area)
♦ Also useful for defects that span two cosmetic
units (nasal dorsum and tip) as it allows primary
closure of one unit and graft of the second unit
Renement of FTSG w/ dermabrasion or
dermasanding (4–6 weeks postop) may
↑ cosmesis
Graft necrosis: indicated by black color (do not
confuse w/ purple venous congestion phase, which
is normal) → do NOT remove, serves as biologic
dressing
■
Split-thickness skin graft (STSG):
Composed of full-thickness epidermis and variable
amount of dermis
Advantages: covers larger defects (.5 cm), ↑ graft
survival (as a result of ↓ demand for nutritional
support), and easier detection of tumor recurrence
Disadvantages: ↓ cosmesis, ↑ contraction (→ not
recommended near free margins), lacks adnexal
structures, ↓ anchoring to BMZ (→ bullae within
graft site), requires specialized instruments, and
painful donor site
Classied by overall thickness:
♦ Thin (0.005–0.012 in)
♦ Medium (0.012–0.018 in) → head and neck
♦ Thick (0.018–0.030 in) → trunk and extremities
Instruments
♦ Weck blade: specialized free-hand knife with
accompanying templates for various graft thicknesses
♦ Zimmer: electric dermatome used to harvest large
STSGs of various thickness and width
♦ Mesher: at bed with roller that compresses STSG
on plastic template with grid-like etched pattern
that puts ne fenestrations into the graft
Meshing enlarges size of STSGs by 25%–35%
and increases exibility
Allows serosanguineous drainage from
recipient bed, which may otherwise interfere
with graft adherence and survivability
Disadvantage: fenestrations often permanent
→ ↓ cosmesis
■
Free cartilage graft:
Composed of cartilage and overlying perichondrium
Used to restore structural integrity, especially of
nasal ala; often used in conjunction with wellvascularized ap
Common donor sites include antihelix (thinner,
atter) and conchal bowl (thicker, curved)
■
Composite grafts: modied FTSG that contains more
than one tissue component, most often cartilage or fat;
dependent on bridging phenomenon (rapid
revascularization) for survival
Skin 1 cartilage graft
♦ Cartilage is used to restore structural integrity,
especially of the nasal ala, to prevent anatomic
distortion and alar collapse during inspiration;
very high metabolic demand → very high risk of
necrosis
♦ Cartilage portion needs to be oversized (10%–
15%) to tuck into subdermal space (the
“pocket”) of recipient site
Skin 1 fat graft
♦ More tenuous survival than FTSGs because of
reduced access to vascular supply; graft size
should be 1 to 2 cm in maximal diameter to
minimize risk of necrosis; consider delayed graft
to increase likelihood of survival
♦ Caution in elderly patients, smokers, and those
with conditions of vascular compromise
(diabetes, vasoocclusive disease, and h/o ionizing
radiation at graft recipient site)
■
Xenografts:
Temporary grafts, usually harvested as STSG from
swine; function as biologic dressings and promote
granulation; remain in place for 7 to 14 days; most
commonly utilized in secondary intention healing
or delayed repairs
Advantages: ↓ wound care demands for patient;
protect/preserve bone, cartilage, tendons, and
nerves; ↓ postoperative pain at granulating site
Disadvantages: must be replaced for continued
benet after 2 weeks, contraindicated in patients with
pork allergy, and is malodorous after 10 to 14 days
8.13 SURGICAL COMPLICATIONS
AND MEASURES TO AVOID THEM
• Infection
■
Vast majority of wounds created during cutaneous
surgery are classied as “clean” → low infection rates
(1%–2%) (Table 8.21)
■
A recent study (Derm Surg. 2020) refuted the
commonly-held dogma that “second intention wounds
have a LOWER rate of infection than sutured wounds”;
in their study, second intention wounds after Mohs
surgery had .2x increased rate of infection compared
to sutured wounds (6.8% vs 3.2%)
■
Presents 4 to 8 days postoperatively
■
Symptoms: rubor (erythema, often extending
asymmetrically from suture line), dolor (pain), calor
(warmth), and tumor (swelling); may also have
Table 8.21 Wound Classication
Class
I. Clean—non-contaminated
skin, sterile technique
II. Clean contaminated—Minor
breaks in sterile technique,
or GI/GU/respiratory tracts
entered without gross
contamination
III. Contaminated—Major
breaks in sterile technique,
or gross contamination from
GI/GU/respiratory tracts
IV. Infected—wound with acute
bacterial infection 1/ pus;
devitalized tissue
From Mariwalla K. Antibiotics. In: Robinson JK, Hanke CW, Siegel DM, Fratila A, eds. Surgery of the Skin. 3rd ed. Philadelphia, Elsevier, 2015:85–94.
Infection
Rate (%)
20–30 Yes
30–40 Antibiotics therapeutic, not
Consider Antibiotic
Prophylaxis for
Dermatologic Surgery
5 No
10 Rarely; case-by-case basis
prophylactic
473

CHAPTER 8 • Dermatologic Surgery
purulent discharge, lymphangitic streaks, fevers, and
chills
■
Staphylococcus aureus = #1 culprit overall
Pseudomonas is common on ear
■
Always obtain wound culture!
■
Treatment:
Abscesses: traditional dogma is to incise, drain, and
pack the infected wound until it heals by second
intention; recent studies suggest that wound may be
sutured immediately following drainage
Surgical site infection without abscess: start antibiotics
(rst-generation cephalosporin or b-lactamase-resistant
penicillin); consider clindamycin, doxycycline or
TMP-SMX if high index of suspicion for MRSA;
uoroquinolone if Pseudomonas suspected
■
Differential diagnosis: normal inammation a/w
healing and tension (presents earlier); contact
dermatitis (pruritic); inammatory suture reaction
(epidermal sutures—erythema surrounding each
suture; dermal/SQ sutures—inammatory papule/
pustule, usually presents later)
■
Prevention:
Surgical site infections: use sterile technique,
minimize wound tension, and consider antibiotic
prophylaxis if operating on inamed skin or highrisk areas (lower legs and groin)
Perioperative antibiotic prophylaxis
recommendations for prevention of infective
endocarditis and prosthetic joint infections
(Table 8.22 and Fig. 8.22)
• Bleeding
■
Bleeding may lead to hematoma → ↑ risk of infection,
↑ wound tension, and dehiscence
■
Highest risk 5 rst 48 hours postoperatively (majority
within rst 24 hours, after epinephrine wears off)
■
Patient risk factors:
Aspirin: irreversibly affects platelet throughout its
lifespan of 6 to 10 days; aspirin should not be held
in patients taking for secondary prevention; if
taking aspirin for primary prevention, may consider
withholding for 10 days before and 5 to 7 days after
surgery (BUT only if it does not pose a risk for
cardiac or neurologic event!)
♦ Other NSAIDs such as ibuprofen and naproxen
also affect platelets, but not as severely/irreversibly
Table 8.22 Antibiotics for Prevention of Surgical Site Infections
Method of Administration Effect Based on Available Data
Topical antibiotics (postoperative) No difference compared with
Topical antibiotics (preoperative nasal
mupirocin for Staphylococcus carriers)
Topical chlorhexidine (preoperative)
Intralesional antibiotics (clindamycin
solution mixed into local anesthetic)
Postoperative systemic antibiotic
prophylaxis
Preoperative systemic antibiotic
prophylaxis (single dose)
white petrolatum
↓ Infection rate
↓ Infection rate
g
Infection rate
Cohort studies suggest a minor
benefit (best data is for grafts),
but no large RCTs
Effective; recommended for
patients at risk of infective
endocarditis or prosthetic joint
infection
Thienopyridine antiplatelet agents (e.g., clopidogrel
and ticlopidine): do NOT stop
Novel Oral Anti-Coagulants / Direct Oral AntiCoagulants (NOAC / DOAC): includes dabigatran
(Pradaxa), rivaroxaban (Xarelto), apixaban
(Eliquis), edoxaban (Savaysa), and betrixaban
(Bevyxxa); current AAD recommendations =
continue these agents perioperatively
♦ Recent study by Siscos et. al (JAAD 2021) found
that stopping DOAC/NOAC perioperatively is
NOT associated with an increased risk of
thrombotic complications or mortality; holding
NOAC/DOAC perioperatively for 24-48hrs may
↓hematoma risk
Warfarin: check INR to ensure it is not
supratherapeutic (generally prefer , 3.0) before
proceeding w/ surgery
Herbs and supplements that enhance
anticoagulation effects of warfarin and/or inhibit
platelet adhesion: feverfew, sh oil, garlic, ginger,
ginkgo, ginseng, bilberry, chondroitin, vitamin E,
licorice, devil’s claw, danshen, dong quai, alcohol
■
Prevention: consider minimizing undermining;
consider linear closure rather than ap; drain
placement; apply pressure dressing immediately after
procedure and leave on for $ 24 hours
• Hematoma
■
Gelatin-like clots formed by blood collecting in “dead
space” of wound; presents with pain, swelling, and
red-purple discoloration
■
Hematomas may lead to dehiscence, necrosis, and
infection
■
Small hematoma → pressure sensation
Small and stable hematomas resolve on their own;
no intervention needed but may use warm
compresses to hasten resolution
■
Large expanding hematoma → acute throbbing pain
Requires evacuation
Expanding hematomas in periorbital region
(→ blindness), and neck (→ airway compromise)
are considered medical emergencies
■
Hematomas evolve through four stages:
Early: rst 48 hours postop; uctuant; active
hemorrhage and blood accumulation → easy to
aspirate with a 16- or 18-gauge needle
Gelatinous: spongy w/ purplish hue
Organized: .1 week postop; thick, brous, and
adherent to surrounding tissue (evacuation
possible, but more difcult; cannot be aspirated
via needle)
Liquefaction: begins at 7 to 10 days after organization
phase (2 weeks postop); organized hematoma
becomes liqueed → can now be aspirated, or left
alone to self-resorb over many months
■
Bromelain: oral concentrate of proteolytic enzymes
derived from the pineapple plant → expedites
hematoma resolution
• Ischemia/necrosis
■
Earliest sign of ischemia is pallor
Arterial insufciency: ↓ skin temperature, lack of
bleeding following pinprick test; aps can remain
viable for up to 12 to 14 hours
474
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