Plastic Surgery: Facts

Plastic Surgery: Facts

by Christopher Stone, Stone

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Overview

Plastic Surgery: Facts by Christopher Stone, Stone

The FRCS(Plast) is the final examination taken by plastic surgery trainees towards the end of their training in the UK. This book has been written to address the needs of the candidate for this examination and non-UK equivalents. It provides comprehensive coverage of plastic surgery in a format that is easy for the trainee to assimilate rapidly and as such, will not only be indispensable as a revision guide but also as a valuable quick reference for the busy practising surgeon on the wards or in the consulting room. One key feature of the book which will enhance its use as a self-learning tool is that it contains many sample examination questions with suggested answers.

Product Details

ISBN-13: 9781841100647
Publisher: Greenwich Medical Media Limited
Publication date: 01/10/2000
Series: Greenwich Medical Media Series
Pages: 504
Product dimensions: 6.14(w) x 9.21(h) x 1.14(d)

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Plastic Surgery

Cambridge University Press
0521674492 - Plastic Surgery - Facts - by Christopher Stone
Excerpt


Cutaneous neoplasia and hamartomas (BCC, SCC, melanoma, vascular malformations, sarcomas)

Overview of aetiology of neoplasms

Benign epithelial tumours

Hair follicle tumours

Tumours of sebaceous glands

Sweat gland tumours

Basal cell carcinoma (basal cell epithelioma, rodent ulcer)

Premalignant conditions

Squamous cell carcinoma (squamous epithelioma)

Epidermal naevi

Vascular birthmarks

Vascular malformations

Melanocytic naevi

Dermal melanocytosis

Malignant melanoma

Axillary lymphadenectomy

Inguinal lymphadenectomy

Soft tissue sarcoma

Cutaneous metastatic malignant tumours

Miscellaneous conditions

Overview of aetiology of neoplasms

Clin Plastic Surg 1997; 24(4)

A neoplasm is an abnormal mass of tissue, the growth of which exceeds, and is uncoordinated with that of the normal tissues and which persists in the same excessive manner after cessation of the stimulus which evoked the change

A malignant neoplasm is one that invades surrounding tissues and has a propensity to metastasize

Initiation, promotion and progression lead to unrestrained growth and proliferation:

Initiation: a change in the genome of a cell

Promotion: the change made permanent by cellular division (initiators and promoters include UV and ionizing radiation, chemical carcinogens, viruses)

Progression: further cell division to form an invasive tumour

Inappropriate activation of normal cellular proto-oncogenes to become oncogenes - these proto-oncogenes encode growth factors, growth factor receptors or transcription factors

Inactivation of other cellular genes called tumour suppresser genes

p53 tumour suppresser gene is mutated in the majority of human cancers

UV radiation is the most important factor

First, mutations in cellular DNA and a failure of DNA repair

Second, production of immunosuppressive cytokines, depletion and alteration of antigen-presenting LCs and systemic induction of Ts-cells by altered LCs, inflammatory macrophages and cytokines

Sunburn, suntanning, local and systemic immunosuppression, photo-ageing, skin cancer and precancer are attributed to UVB radiation (290-320 nm)

UVA radiation (320-400 nm) generates oxygen-free radicals that damage cell membranes and nuclear DNA, contributing to erythema, photo-ageing and carcinogenesis

Interruption of intercellular and intracellular signalling cascades regulating transcription and function of viral oncoproteins in human keratinocytes

Interaction between a physical carcinogen (UV part of the sunlight) and a 'low risk' (non-mutagenic) papillomavirus infection

Benign epithelial tumours

Seborrhoeic keratosis (seborrheic wart, senile wart, basal cell papilloma)

Incidence

Males = females, fifth decade onwards

White races

Stucco keratosis - non-pigmented seborrhoeic keratosis on the limbs

Dermatosis papulosa nigra - multiple facial lesions, dark skinned races, early onset

Aetiology

Familial - autosomal dominant

Inflammatory dermatosis

Manifestation of visceral malignancy

Oestrogen administration

Pathology

Accumulation of immature keratinocytes between basal and keratinizing layers

Acanthosis - thickening of the epidermis

Elongation of dermal papillae

Malignant transformation reported but rare (squamous type)

Clinical

Verrucous plaque

Face, hands and upper trunk

May be heavily pigmented

Multiple lesions aligned in direction of skin folds

May bleed, become inflamed and itch

May shed but then reform

Treatment

Curettage or excision

Cryotherapy

Topical trichloroacetic acid

Digital fibrokeratoma

Papillary or keratotic outgrowth in the region of a finger joint

Adults, males > females

Follows trauma

Hyperkeratosis and acanthosis (thickening of the epidermis, specifically the stratum spinosum)

Distinguish from supernumerary digit

Treat by excision

Keratoacanthoma (Molluscum sebaceum)

Rapidly evolving tumour which resolves untreated

Keratinizing squamous cells originating in pilosebaceous follicles

Incidence

White races

Males > females (×3)

One-third frequency of SCC

Middle age onwards

Aetiology

Sun exposure

Coal, tar and carcinogenic hydrocarbons (multiple lesions)

Injury and infection including skin graft donor sites

Association with carcinoma of the larynx, internal malignancies and leukaemia

Association with deficient cell-mediated immunity (multiple lesions)

Pathology

Keratin-filled crypt

Rapidly dividing squamous cells deriving from skin appendages

Atypical mitoses and loss of polarity

Clinical

Globular tumour

Keratin plug or horn

Radial symmetry

Resolution begins after 6 weeks, takes 3 months

Face, dorsum of hand

Torre's syndrome: multiple internal malignancies, KAS and sebaceous adenomas

Distinguish from SCC

Treatment

Excise to provide good histological specimen

Spontaneous resolution leaves unsightly scar

5-FU and radiotherapy shorten time to resolution

Hair follicle tumours

Trichilemmal cyst

Sebaceous cyst of hairy skin

Wall resembles hair follicle

Situated on the scalp

Women > men

Middle age

Familial (AD)

Rupture causes cell proliferation and occasionally malignant change

Ruptured cell wall may fuse with surrounding skin (marsupialization)

Treat by excision

Trichofolliculoma

Multiple malformed hair roots arising from an enlarged follicle canal

Keratin-filled crater

Hairs may emerge from a central punctum

Mainly on the face

Tricholemmoma

Hair follicle tumour usually diagnosed clinically as BCC

Plaques of squamous cells containing glycogen

Occurs on the face

Middle-aged/elderly men

Tricho-epithelioma

Epithelial tumour differentiating towards hair follicle cells

Incidence

Rare, onset at puberty

Aetiology

Familial (AD)

Pathology

Resembles BCC

Rounded masses of fusiform cells

Lacunae filled with keratin

Tumour islands may connect with hair follicles

Malignant change (BCC)

Clinical

Pinkish nodules

Cheeks, eyelids and nasolabial folds

Often diagnosed as BCC, pigmented lesions mistaken for MM

Treatment

Excision

Pilomatrixoma (benign calcifying epithelioma of Malherbe)

Hamartoma composed of dead, calcified cells, which resemble those of hair matrix

Incidence

Uncommon

Mainly <20 years

Females > males

Association with myotonia atrophica

Pathology

Well-circumscribed dermal tumour

Cells mature from outer to inner layers

Similar to hair matrix cells maturing from cortex to root sheath

Central calcification and ghost cells, lacking basophilic granules

Clinical

Dermal/subcutaneous tumour

Head, neck, upper extremity

Stony hard consistency

Treatment

Excision

Tumours of sebaceous glands

Sebaceous adenoma

Benign tumour composed of incompletely differentiated sebaceous cells

Incidence

Rare tumour

Either sex

Mainly in the elderly

Pathology

Multilobular tumour of the upper dermis

Small basophilic sebaceous matrix cells

Larger cells containing fat globules

Clinical

Ulcers/plaques/sessile or pedunculated lesions

Yellowish hue

Face (including eyelid) or scalp

Sudden increase in growth rate

Treatment

Excision

Recur if incompletely excised

Radiosensitive

Sebaceous carcinoma

Malignant growth of cells differentiating towards sebaceous epithelium

Incidence and aetiology

Rare - 0.2% of skin cancers

May follow radiodermatitis

Pathology

Deeply set in dermis, epidermis usually uninvolved

Outer basophilic undifferentiated cells

Central differentiating cells with cytological atypia

Cytoplasmic vacuolation and fat droplets

Invasion

Clinical

Yellowish nodules on face and scalp

Slow or rapid growth

Metastasis uncommon

Treatment

Excision

Epidermoid cyst (sebaceous cyst)

Incidence and aetiology

Young and middle-aged adults

Inflammation and obstruction of a pilosebaceous follicle

Pathology

Epidermal lining

Birefringent keratin and breakdown products

Cholesterol clefts

Clinical

Spherical cyst in the dermis

Tethered to epidermis

Enlarge and suppurate through punctum

Treatment

Excision

Sweat gland tumours

Apocrine glands release lipid secretions in membrane-bound vesicles (e.g. breasts)

Eccrine glands release secretions by exostosis into ducts

Holocrine glands discharge whole cells which then disintegrate to release secretions

Sweat glands: mainly eccrine secretion, some apocrine

Sebaceous glands: holocrine secretion of sebum

Three benign eccrine sweat gland tumours: syringoma, acrospiroma, cylindroma

Syringoma (papillary eccrine adenoma)

Benign tumour of eccrine sweat gland origin

Incidence

Uncommon

Females > males

Onset during adolescence

Multiple tumours associated with Down's syndrome

Pathology

Collections of convoluted sweat ducts in the upper dermis

Tail-like projection of cells - characteristic tadpole appearance

Clinical

Small, yellowish dermal papules, usually <3 mm

May appear cystic - injury may cause release of a small amount of clear fluid

Chest, face, neck

May resemble tricho-epithelioma or xanthelasma

Treatment

Excision

Intralesional electrodesiccation

Laser

Eccrine acrospiroma

Tumour derived from eccrine sweat duct epithelium

Epidermal, juxta-epidermal or dermal

Eccrine poroma commonest subtype: juxta-epidermal

Incidence

Male = female

Middle age

Usually acral - palms and soles

Pathology

Sweat gland duct cell proliferation

Cells contain glycogen and glycolytic enzymes

Overlying hyperkeratosis

Malignant change (malignant eccrine poroma) reported

Clinical

Hyperkeratotic plaque on sole or palm

May ulcerate

Treatment

Excision

Dermal cylindroma (dermal eccrine cylindroma, turban tumour, Spiegler's tumour)

Derived from the coiled part of sweat glands (part secretory, part duct)

Incidence

Uncommon

Females > males (×2)

Often familial (AD)

Early adult life

Pathology

Columns of cells interspersed with hyaline material

Large and small (peripheral) cell types

Clinical

Scalp and adjacent skin

Pinkish fleshy tumours

Usually multiple and hairless

May be painful

Malignant change very rare

Distinguish from trichilemmal cyst

Treatment

Excision

Adenoid cystic carcinoma of the scalp

Malignant tumour of eccrine glands

Usually arises in salivary glands

Lacrimal glands and mucous glands of upper respiratory tract

Rarely arises primarily in the skin, mainly eccrine sweat glands of the scalp

Slow growing

Invades fascial planes, nerves and bone

Characteristic lattice-type appearance microscopically

Rarely completely excised

Not radiosensitive

Treat by excision with histological control of margins

Sweat gland carcinoma

Malignant epithelial tumour of the sweat glands

Incidence

Rare

Males = females

Middle age onwards

Pathology

Adenocarcinoma within the dermis

Eccrine or apocrine varieties

Eccrine commonest, frequently metastasizes

Clinical

Painful, reddish nodules within the dermis

Firm/hard

Irregular border

Occur anywhere, mainly scalp and face

Slow growth but may metastasize

Treatment

Wide excision

Monitor lymph nodes

Basal cell carcinoma (basal cell epithelioma, rodent ulcer)

Malignant tumour composed of cells derived from the basal layer of the skin

Incidence

Commonest malignant tumour of the skin in white races

Increased prevalence in locations of high sunlight exposure

Males > females except lower extremity lesions (female:male ratio = 3:1)

Uncommon in non-Caucasians

75% of patients > 40 years old

Aetiology

UV and ionizing irradiation

Burn and vaccination scars

Arsenicals

Immunosuppression

Occasionally has a familial inheritance

Malignant change in sebaceous naevi and other adnexal hamartomas

Face at much greater risk than other sun-exposed areas (may be related to density of pilosebaceous follicles)

Pathology

Tumour cells arranged in palisades

Cell-cell desmosomes preserved

Well-organized surrounding stroma

Varying degrees of atypia

Small buds of tumour off the main mass

Occasionally harbour a melanocytic proliferation

Mucin accumulation and central necrosis characteristic of cystic lesions

Clinical

Pinkish, pearly nodules

Telangiectasia

May be ulcerated, encrusted or pigmented

Nodular, ulcerated, superficial, sclerosing, cystic, morphoeic, desmoplastic

Usually slow growing

Very rarely metastasize via lymphatics

Long-standing tumours may invade deep into subcutaneous tissues

Distinguish from sebaceous hyperplasia

Gorlin's syndrome (basal cell naevus syndrome): AD inheritance, multiple BCCs, palmar pits, jaw cysts, sebaceous cysts, abnormalities of ribs and vertebrae, dural calcification

Bazek's syndrome: association of multiple BCCs with follicular atrophoderma

Treatment

Excisional biopsy: 2-5 mm margins, antibiotic cover if ulcerated

35% of incompletely excised tumours recur; re-excision of incompletely excised tumours shows residual tumour in only 30% of cases

5-FU or photodynamic therapy for superficial lesions

Radiotherapy

Guidelines for the management of basal cell carcinoma

Telfer. Br J Dermatol 1999

  • Review of surgical and non-surgical modalities used in the treatment of BCCs including

    • Mohs' micrographic surgery

    • Radiotherapy


© Cambridge University Press

Table of Contents

Introduction; Part I: 1. Cutaneous neoplasia and hematomas (BCC, SCC, melanoma, vascular malformations, sarcomas); 2. Principles of plastic surgery (local and free flaps, skin grafts, wound healing); 3. Hypospadias (embryology, anatomy and clinical management of hypospadias); 4. Cleft surgery (embryology, anatomy and management of cleft lip, palate, pharyngoplasty, alveolar bone grafting); 5. Hand surgery (trauma, degenerative and inflammatory disease, nerve compression, congenital abnormalities); Part II: 6. Burns (pathophysiology and acute and long-term management); 7. Breast surgery (cosmetic breast surgery, reconstruction, reconstruction of abdomen and perineum); 8. Head and neck oncology and reconstruction, facial reanimation, maxillofacial trauma, craniofacial surgery); 9. Cosmetic surgery (lasers, facelift, chemical peel, dermabrasion, liposuction, abdominoplasty, rhinoplasty); 10. Miscellaneous (lower limb trauma, pressure sores, lymphoedema, VAC therapy, tissue expansion).

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