(BQ) Part 1 book Hamilton baileys physical signs presentation of content: Historytaking and general examination, bones and fractures, joints and muscles, peripheral nerve injuries, the knee joint, the leg and ankle joint, distinctive clinical syndromes, the skin,... and other contents.
Hamilton Bailey’s Demonstrations of Physical Signs in Clinical Surgery K17518_Book.indb 21/11/15 12:19 am This page intentionally left blank Hamilton Bailey’s Demonstrations of Physical Signs in Clinical Surgery 19th Edition Edited by John S P Lumley, Emeritus Professor of Vascular Surgery, University of London; Past Council Member and Chairman of Primary Fellowship Examinations, Royal College of Surgeons of England, UK Anil K D’Cruz, Director, Tata Memorial Hospital, Professor & Surgeon, Department of Head & Neck Surgery, Mumbai, India Jamal J Hoballah, Professor & Chairman, Department of Surgery, American University of Beirut Medical Center, Lebanon; Emeritus Professor of Surgery, Vascular Surgery Division, University of Iowa Hospitals and Clinics, Iowa City, USA Carol E H Scott-Conner, Emeritus Professor, Division of Surgical Oncology and Endocrine Surgery, Department of Surgery, University of Iowa Carver College of Medicine, Iowa City, USA K17518_Book.indb 21/11/15 12:19 am CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2016 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S Government works Version Date: 20160107 International Standard Book Number-13: 978-1-4987-7484-0 (eBook - PDF) This book contains information obtained from authentic and highly regarded sources While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and not necessarily reflect the views/opinions of the publishers The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint Except as permitted under U.S Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400 CCC is a not-for-profit organization that provides licenses and registration for a variety of users For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com Contents Biography of Hamilton Bailey vii Part Three: Skin List of contributors ix Preface xi 18 The Skin Part One: Principles Part Four: Head and neck 289 291 317 History-taking and General Examination3 19 The Head 319 Distinctive Clinical Syndromes 20 The Face and Jaws 335 21 The Ear 343 22 The Orbit 351 23 The Mouth 365 24 Nose and Throat 379 25 Salivary Glands 391 26 The Neck 397 23 Lumps, Ulcers, Sinuses and Fistulas53 Inflammation71 HIV and AIDS Part Two: Trauma and (elective) orthopaedics 101 135 M anagement of the Multiply Injured Patient137 Part Five: Breast and endocrine 407 27 The Thyroid and Parathyroids 409 28 Breast and Axilla 417 Bones and Fractures 147 Joints and Muscles 167 Peripheral Nerve Injuries 177 10 The Spine 187 Part Six: Cardiothoracic431 11 The Shoulder Joint and Pectoral Girdle 207 29 The Thorax (Including the Oesophagus)433 12 The Arm 217 13 The Hand 229 14 The Pelvis, Hip Joint and Thigh 237 Part Seven: Vascular467 15 The Knee Joint 253 16 The Leg and Ankle Joint 269 31 Arterial Disorders 17 The Foot 277 K17518_Book.indb 30 Evaluation of the Cardiac Surgical Patient455 469 32 Venous and Lymphatic Disorders495 21/11/15 12:19 am vi CONTENTS Part Eight: Abdominal515 38 The Alimentary Tract and Abdomen in Children 33 The Abdominal Wall, Umbilicus and Groin 517 34 Abdominal Hernias 531 35 Non-acute Abdominal Conditions 547 36 The Acute Abdomen 629 Part Nine: Genitourinary637 577 39 The Genitourinary System and Genitalia639 37 Anorectal and Vaginal Examination615 Index665 K17518_Book.indb 21/11/15 12:19 am Hamilton Bailey 1894–1961 Born in Bishopstoke, Hampshire, where his father was a general practitioner, Henry Hamilton Bailey grew up in Southport, Eastbourne, and Brighton, England, where his father was successfully in practice His mother was a nurse, so not surprisingly he became a medical student at the London Hospital at the early age of sixteen years, after schooling at St Lawrence College, Ramsgate At the outbreak of the First World War he was a fourth-year medical student, and volunteered for the Red Cross, being dispatched with the British Expeditionary Force to Belgium Almost inevitably he was taken prisoner-of-war and set to work on the German railways A troop train was wrecked and Bailey, with two Frenchmen, was held on suspicion of sabotage One of the latter was actually executed but Bailey was reprieved (apparently by the good offices of the American Ambassador in Berlin) and repatriated via Denmark, where he continued his medical studies temporarily In 1916 he joined the Royal Navy as a Surgeon-Probationer, serving in HMS Iron Duke at the Battle of Jutland During the battle he helped with casualties in near darkness, the electricity supply being damaged for most of the action While in the Navy he qualified, and later returned to the London Hospital, where he gained the FRCS (Eng) in 1920 During his period as surgical registrar at the London Hospital he pricked his left index finger, and tendon-sheath infection, a common sequel in those days, ensued The end result was an amputation of the stiff finger, but he soon overcame the disability Appointments as Assistant Surgeon at Liverpool Royal Infirmary, Surgeon to Dudley Road Hospital, Birmingham (1925), and finally as Surgeon to the Royal Northern Hospital, London (1931) followed In a quarter of a century Bailey produced this work, his Emergency Surgery, and Short Practice of Surgery [jointly with R.J McNeill Love (1891–1974), contemporary as a surgical registrar at the London Hospital and as a Surgeon at the Royal Northern Hospital], edited Surgery of Modern Warfare during the Second World War, and revitalized Pye’s Surgical Handicraft These were his most successful works; all rapidly attained a wide circulation with many editions, and it has been said “ it will readily be conceded that the present excellence of illustrations in medical textbooks owes much to his inspiration and striving for perfection” In addition to these major contributions, he wrote over 130 original papers and nine other books All this, together with a busy practice, particularly in surgical emergencies, was too much, even for Hamilton Bailey’s massive frame, and in 1948 he suffered a breakdown in health, aggravated, no doubt, by the death of his only child, a son, in a railway accident in 1943 He retired to Deal, Kent, and later to Malaga, Spain, but continued his literary work He died of carcinoma of the colon, and is buried in the peaceful little English cemetery in Malaga His missionary zeal for teaching medical students has been perpetuated by the use of the royalties from his books to expand medical libraries in developing countries K17518_Book.indb 21/11/15 12:19 am This page intentionally left blank Contributors Dr Ghassan S Abu-Sittah mbchb frcs (plast), Assistant Professor of Surgery, Head of Division of Plastic & Reconstructive Surgery, American University of Beirut Medical Center, Beirut, Lebanon; Honorary Senior Clinical Lecturer, Queen Mary University of London, UK Badih Adada md frcs, Cleveland Clinic Florida, FL, USA Muhyeddine Al-Taki md facs, Assistant Professor of Clinical Surgery, American University of Beirut Medical Center, Beirut, Lebanon Parth Amin md, Clinical Assistant Professor, Western Michigan University School of Medicine, Kalamazoo, MI, USA Evgeny V Arshava md facs, Clinical Assistant Professor, Division Acute Care Surgery, Department of Surgery, University of Iowa Hospitals and Clinics, Iowa City, IA, USA Andrea Badillo md, Assistant Professor of Surgery, Attending Pediatric Surgeon, Children’s National Healthcare System, George Washington University, Washington DC, USA Jamil Borgi md, Cardiothoracic Surgery Senior Staff, Division of Cardiac Surgery, Henry Ford Hospital, Detroit, MI, USA John Byrn md, Department of Surgery, University of Michigan, Ann Arbor, MI, USA Devendra Chaukar ms (general surgery) dnb, Professor and Head, Division of Head and Neck, Tata Memorial Hospital, Mumbai, India William Cross bmed sci bm bs frcs (urol) phd, Consultant Urological Surgeon, St James’s University Hospital, Leeds, UK Anil K D’Cruz ms dnb frcs (hon), Director, Tata Memorial Hospital, Professor and Surgeon, Head and Neck Services, Tata Memorial Hospital, Mumbai, India Mitali Dandekar ms dnb, Clinical Fellow, Department of Head Neck Surgery, Tata Memorial Centre, Mumbai, India Anuja D Deshmukh ms (ent) dlo dorl, Associate Professor and Associate Surgeon, Department of Head and Neck Surgical Oncology, Tata Memorial Centre, Mumbai, India K17518_Book.indb Shraddha Deshmukh ms dnb, Assistant Professor, Department of Otorhinolaryngology, Government Medical College, Nagpur, India Mandar S Deshpande ms (general surgery) dnb, Consultant Head and Neck Surgeon, Kokilaben Dhirubhai Ambani Hospital, Mumbai, India Parul Deshpande ms (ophthalmology) dnb, Fellowship (Cornea and Anterior segment) Ophthalmologist and Cornea Specialist, Sarvodaya Eye Hospital, Mumbai, India Jesse Dirksen md, Surgical Director, Edith Sanford Breast Center, Sioux Falls, SD, USA Celia M Divino md facs, Department of Surgery, Mount Sinai School of Medicine, New York, NY, USA Abdel Kader El Tal md, Procedural Dermatology, Dermatology Associates Inc Perrysburg, OH, USA Rachid Haidar md facs, Head of Division of Orthopedic Surgery, Professor of Clinical Orthopaedic Surgery, Department of Surgery, American University of Beirut Medical Center, Beirut, Lebanon Ali Hallal md frcs (ed), Assistant Professor of Clinical Surgery, General and Upper Gastro-Intestinal Surgery, Trauma Surgery and Intensive Care, Program Director, Trauma and Surgical Critical Care Fellowship, Department of Surgery, American University of Beirut Medical Center, Beirut, Lebanon Natalie Anne Hirst bsc mbbs mrcs, Clinical Research Fellow, St James’s University Hospital, Leeds, UK Jamal J Hoballah Professor & Chairman, Department of Surgery, American University of Beirut Medical Center, Beirut, Lebanon; Emeritus Professor of Surgery, Vascular Surgery Division, University of Iowa Hospitals and Clinics, Iowa City, IA, USA Maen Aboul Hosn md febs, Division of Vascular Surgery, University of Iowa Hospitals and Clinics, Iowa City, IA, USA Hamed Janom md, Surgical Resident, PGY5, Division of Plastic and Reconstructive Surgery, American University of Beirut Medical Center, Beirut, Lebanon Subbiah Kannan ms (ent), Fellow (Head and Neck Oncosurgery), Consultant Head and Neck Onco-surgeon, Apollo Speciality Hospital, Chennai, India 23/11/15 11:05 am 302 THE SKIN Other Tumours of Skin Appendages These are rare They include steatocystomas (which are true sebaceous cysts containing oily material; Figure 18.29), leiomyomas from the smooth erector pili muscle of the hairs (Figure 18.30) (which are usually painful and contract upon being touched), hidradenomas (benign tumours of the eccrine glands that might simulate a pyogenic granuloma), sebaceous adenomas, cylindromas and trichoepitheliomas Cylindromas (Figure 18.31) are tumours of the sweat glands, frequently multiple and commonly found on the scalp They can range from a few millimeters to several centimetres across, the latter producing disfigurement They are soft, boggy swellings but not fluctuate or indent They are rarely malignant Cylindromas are one of the causes of turban tumours of the scalp, the deformity being better known for its title than for its incidence Trichoepitheliomas are benign growth of the hair follicle epithelium Clinically, they consist of skin-coloured papules that can be confused with a basal cell carcinoma (BCC) Figure 18.29 Multiple steatocystomas Premalignant and Malignant Lesions of the Skin Exposure to sunlight can produce a number of skin disorders and aggravate many existing conditions Scantily clad sun-worshippers are at risk; blonde and red-headed individuals are particularly susceptible There is a high incidence of skin disorders in Australia, South Africa and the southern states of the USA Also at risk are outdoor workers such as fishermen, farmers and labourers Sunburn can occur within an hour of exposure in sensitiveskinned individuals, producing erythema, blistering and later peeling Continued exposure may give rise to severe, permanent skin damage even at an early age, leading to premature skin ageing, although the changes are usually degenerative and age-related The signs of ageing are fragile skin with loss of elasticity, increased keratosis, vascular changes such as spider navi and angioma, telangiectases, venous lakes and pronounced sebaceous glands Of particular concern is the predisposition to premalignant and malignant skin lesions, including solar keratosis, Bowen’s disease, BCC, SCC and malignant melanoma The risk of developing malignant melanoma increases mostly with sunburn-related incidents before age 18, while the risk of developing basal and squamous cell carcinomas is related to chronic sun exposure that accumulates during a person’s lifetime Figure 18.30 Leiomyomas PART 3 | SKIN Actinic Keratosis (Solar Keratosis) Actinic keratoses (Figure 18.32) are painless, hyperkeratotic, skin-coloured to erythematous, ‘rough’, non-indurated macules, related to prolonged exposure to sunlight Because of their rough surface, these lesions are more commonly felt than seen The risk of these lesions undergoing malignant transformation is 1–5 per cent The lesions usually occur in elderly persons and outdoor workers, and are seen over the tops of the ears, on the face and on the backs of the hands and fingers The lesions are usually painless Actinic keratosis, SCC in situ and SCC fall within a spectrum of the disease Microscopically, actinic keratosis reveals a dysplasia at the lower level of the epidermis (the basal and spinous layer) Once full-thickness involvement of the epidermis has occurred, this becomes SCC in situ or Bowen’s disease Invasion of the dermis by such tumours denotes a SCC K17518_Book.indb 302 Figure 18.31 A cylindroma Bowen’s Disease and Erythroplasia of Queyrat The lesions of Bowen’s disease or SCC in situ (Figure 18.33) are irregularly shaped, well-defined plaques that may be mistaken for a patch of eczema or psoriasis They therefore present late and 21/11/15 12:27 am Cutaneous Lesions of Epithelial, Mesenchymal and Adnexal Origin 303 Figure 18.34 Squamous cell carcinoma behind the ear Figure 18.32 Multiple actinic keratoses Figure 18.33 Squamous cell carcinoma in situ any such lesion that does not respond to topical steroids should be biopsied The lesions vary in size from mm to a few centimetres in diameter They are beefy red, erythematous areas that are slightly raised and have a scaly crust on their surface The skin beneath the crust is moist and papilliform Malignant changes produce papules and nodules Erythroplasia of Queyrat (see p 651) has features identical to those of Bowen’s disease but is situated on the penis Leukoplakia Leukoplakia can occur along the margins of the lips (see p 17) and on the vulva, although it is most common in the oral cavity It is a white coating of the mucous membrane that does not rub off, unlike Candida and some other infections The lesions are the result of multiple traumas such as from sharp teeth and dentures, K17518_Book.indb 303 spicy foods, sepsis, syphilis, pipe smoking and betel nut (areca nut) chewing The majority of lesions are benign, but some may show dysplastic changes, and there is an incidence of 13 per cent change to SCC This incidence rises to two-thirds in the floor of the mouth, where all lesions must be biopsied and carefully monitored Erythroplakia is a pink to red discoloration underlying the white coating, the cellular abnormality in this instance showing in situ or invasive SCC in all cases Squamous Cell Carcinoma Cutaneous SCC (Figures 18.34 and 18.35) is the second most common skin malignancy following BCC The sun is considered to be the most important culprit in inducing these tumours, but there are a number of other predisposing factors including exposure to chemical hydrocarbons, tar and mineral oils There is a high incidence of cutaneous SCC in patients living in tropical countries due to the high ultraviolet index in these areas When seen in sun-exposed skin, SCCs are mostly due to sun damage, whereas on the genitalia they are mostly due to chronic PART 3 | SKIN Figure 18.35 A fungating squamous cell carcinoma 21/11/15 12:27 am 304 THE SKIN human papillomavirus infection, and in the oral cavity they are mostly due to chronic alcohol ingestion and cigarette smoking Cutaneous SCCs occasionally arises from areas of chronic radiation damage or a chronic ulcer or scar and are then referred to as Marjolin’s ulcers Chronic immunosuppression (e.g in organ transplantation) is associated with an increased risk of SCC If any nodularities or changes in the skin edges are seen in a chronic non-healing ulcer, they must be biopsied to rule out SCC The behaviour of SCCs of the genitalia and oral mucosa is more aggressive and the risk of metastasis is higher compared with SCCs arising in sun-exposed skin Clinically, SCCs can initially present as a firm, round erythematous nodule that progressively enlarges and ulcerates The enlargement usually takes place over a few months The ulcer has a crusty or horny covering but as it becomes deeper it penetrates the dermis, exposing underlying tissues such as tendons, bones, cartilage and joints; the base of the ulcer bleeds easily and is very necrotic The ulcer’s edge is everted and local invasion of the surrounding tissues produces induration that is visible beyond the ulcer margin The rate of onset, progressive deepening and increased eversion are typical of malignant change There may be associated thrombosis and the ulcer may penetrate the adjacent vessels, producing severe and possibly fatal haemorrhage Metastasis is usually via the lymphatics, and the local nodes are commonly involved However, one-third of these prove to be due to infection rather than secondary malignancy Metastases can occur via the bloodstream but this is uncommon Histologically, there is full-thickness atypia of the epidermal cells together with invasion into the dermis According to the degree of atypia and differentiation, SCCs are divided into well, moderately or poorly differentiated tumours The degree of differentiation carries a prognostic indicator for their behaviour With well-differentiated SCCs, keratin deposition, often arranged in onion-like, concentric layers termed keratin pearls, may be seen within the masses extending into the dermis and are not to be confused with the keratin pearls that can be seen within the epidermis in a seborrheic keratosis The differential diagnosis of SCC includes solar keratosis, pyogenic granuloma, seborrhoeic keratosis, BCC and malignant melanoma PART 3 | SKIN Keratoacanthoma Keratoacanthoma (Figure 18.36) is an overgrowth of an unknown aetiology It has a characteristic rapid development to its full size in 3–5 weeks, and spontaneous regression occurs in 2–12 months Besides these two hallmarks of keratoacanthoma, differentiation from well-differentiated SCCs is extremely difficult both clinically and histologically The lesions are usually single and can occur anywhere on the body, although particularly on exposed areas such as the arms and around the nose The lesion is a discrete, dome-shaped nodule 1–2 cm in diameter and 2–3 mm high The firm, smooth outer rim is skin coloured, but the central core is of hard, irregular, keratinized white or black material Multiple keratoacanthomas are also encountered with familial inheritance (Ferguson-Smith syndrome) or as part of other syndromes such as Muir–Torre syndrome, in which colonic polyps, sebaceous tumours and keratoacanthomas are seen The major problems with keratoacanthomas are the possible disfigurement and the difficulty of differentiating them from SCCs, both K17518_Book.indb 304 clinically and histologically For these reasons, keratoacanthomas are better excised in order not to miss an SCC counterpart Basal Cell Carcinoma Basal cell carcinomas (Figures 18.37 and 18.38) are the most common type of skin cancer The ratio of BCC to SCC is 2:1 but this is reversed in chronic immunosuppression BCC reflects a Figure 18.36 Keratoacanthoma Figure 18.37 Basal cell carcinoma Figure 18.38 Basal cell carcinoma 21/11/15 12:27 am Cutaneous Lesions of Melanocytic Origins Paget’s Disease Paget’s disease (see p 421) consists of eczema-like skin patches over the nipple area that arise secondary to intraductal carcinoma A similar eruption – extramammary Paget’s disease – may occur over the anogenital area secondary to an adenocarcinoma of the gastrointestinal or genitourinary system The lesions are red, weeping, crusty and scaly plaques involving the nipple and surrounding areola Because of its eczema-like appearance, the lesion may be disregarded by the patient until there is retraction, ulceration and destruction of the nipple or until an underlying mass or regional lymph node becomes palpable Figure 18.39 Plaque-stage cutaneous T-cell lymphoma nodules and tumours Involvement of the bone marrow produces Sézary syndrome, which consists of diffuse redness over the skin, otherwise known as erythroderma There may be up to 20 years of progression before tumour formation, lymphadenopathy and visceral involvement occurs CUTANEOUS LESIONS OF MELANOCYTIC ORIGINS The pigment melanin is produced by melanocytes These are derived from neural crest cells that migrate during development and are scattered throughout the basal layer of the skin epidermis Although the number of melanocytes is similar in all races, the amount of melanin produced varies between blackand white-skinned individuals, and also increases in response to ultraviolet light Benign overgrowths of melanocytes are termed moles or pigmented naevi Pigmented lesions may also be produced by an overproduction of melanin from a normal number and distribution of melanocytes – for example, a freckle – or by an increased number of melanocytes within the basal layer of epidermis, as seen in lentigo and the pigmentation of Peutz–Jeghers syndrome In order to diagnose and treat malignant melanoma as early as possible, it is important to recognize typical benign lesions and to examine all doubtful lesions histologically Cutaneous Lymphoma Benign Melanocytic Lesions Pigmented Naevi – Moles Lymphomas may affect any organ in the body but some forms predominantly affect the skin Unlike those in the body, cutaneous lymphomas are most commonly of the T-cell type and less commonly of the B-cell type The name ‘mycosis fungoides’, which used to be used to describe these cases, is a misnomer and has now been replaced by the name ‘cutaneous T-cell lymphoma’ (CTCL).The name ‘Sézary syndrome’ is still used to describe the leukaemic form of the disease CTCL is most commonly found in middle-aged men Early lesions begin as non-specific, asymptomatic, flat, red, scaly eruptions suggestive of chronic eczema or psoriasis However, they have a typical distribution, often over non-exposed areas Lesions progress to become plaques (Figure 18.39), Moles or naevi (Figures 18.40 and 18.41) are very common and most white individuals have at least one at birth, the number increasing throughout life Moles may regress or disappear during childhood; pigmentation may also increase but malignant change is very rare before puberty Moles are less obvious in blackskinned individuals but are seen on the palms and soles The lesions may occur anywhere on the body and are usually discrete and 2–4 mm in diameter The colour varies from very pale to black, as does the amount of hair in the mole The symptoms are usually cosmetic but rough and protruding lesions may catch on clothing Although pain can occur because of trauma to the lesion or due to the inflammation of sebaceous glands within it, this is an unusual symptom, as are bleeding and itching K17518_Book.indb 305 PART 3 | SKIN malignant change in the basal layer of the epidermis The lesions undergo slow, steady enlargement, invading the adjacent skin, and are very destructive if left untreated They metastasize in less than per cent of the cases, and metastases to the lymph nodes, lung and brain are most common Lesions are most common in the elderly, being twice as common in men than women There is also a high incidence in sun-worshippers Although the lesions are most commonly seen on s un-exposed areas, BCCs can occur over sun-spared areas such as the genitals and buttocks, reflecting that although the majority are secondary to sun-induced mutations, a few are due to genetic mutations Clinically, BCC starts as a nodule with a slightly transparent, superficial epidermal layer giving a cystic appearance Lesions are occasionally pigmented The next stage is central erosion with intermittent bleeding The edge is characteristic and diagnostic, being raised and rolled, with a pearly appearance It may also be slightly pinkish due to telangiectases running over the surface If the lesion is untreated, local invasion progresses into both the underlying tissues and the peripheral edges of the tumour, making them irregular The presence of ulceration and irregular borders gave rise to the original nomenclature of ‘rodent ulcer’ The lesions can be differentiated from SCCs by the pearly translucent papules and the rolled pearly border, which are not present in cutaneous SCCs Histologically, BCC starts as a nidus of basal cells extending into the dermis The nidus grows into larger masses consisting of basaloid cells that display little atypia with only few mitoses, form characteristic palisades at the periphery and surround themselves with a concentric thin stroma from which the tumour frequently detaches or clefts The differential diagnosis of BCC is similar to that mentioned above for cutaneous SCC 305 21/11/15 12:27 am 306 THE SKIN Figure 18.40 A junctional naevus Figure 18.42 Freckles potential They frequently arise with sun exposure and may disappear with disciplined protection against the sun Individuals with freckles are more likely to develop skin cancers at later stages in their lives Lentigo A Hutchinson’s lentigo or solar lentigo (Figure 18.43) results from an increased number of melanocytes within the basal layer of the epidermis It is usually found in elderly people (reflected in the name ‘senile lentigo’), grows slowly usually over sun-exposed areas (hence the alternative name ‘solar lentigo’) and is darkly pigmented The irregular area may be a number of centimetres in diameter and is usually flat, but it may be a slightly raised plaque or have flat nodules within it Lentigines are usually found on the neck and the back of the hand Figure 18.41 A compound naevus PART 3 | SKIN The clinician must always be on the lookout for any changes in a lesion suggesting malignant change The clinical signs of malignant transformation can be remembered using ABCDE: • A – Asymmetry (note whether one side is larger than the other) • B – Border (jagged borders are suggestive of transformation) • C – Colour (multiple colours within a naevus should raise suspicion) • D – Diameter (any naevus that has grown to more than the size of the pencil eraser or mm in diameter should be examined) • E – Evolution (a lesion that is changing with time should be checked) Another easy method is the ‘ugly duckling’ sign, where patients’ naevi are examined and moles that show changes that are not present in most others are considered for biopsy Freckles A freckle (Figure 18.42) is an overproduction of melanin from a normal population of melanocytes Freckles are common and occur particularly on exposed areas such as the face and the dorsum of the hands They are pale brown lesions, 2–4 mm in diameter, and are usually multiple They have no malignant K17518_Book.indb 306 Café-au-lait Spots These pale brown, flat, multiple patches (Figure 18.44) are usually a few millimeters in diameter but may be larger in size; they are present at birth The lesions can be associated with neurofibromatosis – particularly if there are more than five of them – and occasionally phaeochromocytomas Histologically, the lesions can be due to increased melanin production or sometimes an increased number of basal melanocytes However, they have no malignant potential Pigmented Lesions in Peutz–Jeghers Syndrome These lesions (Figure 35.53; p 571), associated with multiple intestinal polyposis, are usually found over the mucous membrane of the lips and circumoral area They are 1–2 mm in diameter and asymptomatic Although they are to the result of an increased number of basal melanocytes, they have no malignant potential Malignant Melanocytic Lesions: Malignant Melanoma Malignant melanomas are highly malignant tumours of melanocytic origin Approximately half develop in pre-existing benign naevi, while the rest occur spontaneously in previously normal skin Melanoma occurs most commonly in white individuals, particularly those exposed to the sunlight of subtropical zones 21/11/15 12:27 am Cutaneous Lesions of Melanocytic Origins 307 Figure 18.43 Solar lentigines Figure 18.45 A superficial spreading melanoma Figure 18.44 A café-au-lait spot K17518_Book.indb 307 Figure 18.46 Nodular melanoma (Courtesy of Dr Shukrallah Zaynoun.) The lesions of nodular melanoma are more invasive, produce early nodal involvement and have the worst prognosis The third type is lentigo maligna melanoma (Figure 18.47), a variant form that occurs in the elderly over the head and neck region Finally, acral lentiginous melanoma (Figure 18.48) is a rare form that occurs beneath a nail and is the form seen in Afro-Asian races, often on the palms and soles Pathologically speaking, the lesions are generally poorly differentiated with abundant mitotic figures and can increase rapidly in size over a few weeks They are highly malignant and usually relentlessly progressive, yet they can also be unpredictable: the spontaneous regression even of nodal metastases has been recorded Secondary spread may become evident after removal of the primary lesion A number of clinical features should alert the clinician to a suspicion of primary malignant melanoma or malignant change PART 3 | SKIN The highest incidence is seen in northern Australia but the incidence is increasing in northern Europe Melanomas are unusual in black-skinned individuals, although Africans are susceptible to malignant melanomas of the palms and soles Short, sharp, repeated exposures to ultraviolet light are more harmful than an accumulated effect This suggests a possible immunological carcinogenic response In keeping with this is the fact that the lesions can occur anywhere on the body They may occur at any age but are very rare before puberty and are unusual under 20 years of age; they are most common between 40 and 60 years old The lentiginous group occurs in elderly individuals There is often a family history of atypical or multiple pigmented naevi or malignant melanoma, and it is essential that individuals with this history avoid the sun or use appropriate screening agents Although the lesions can occur anywhere, they are common over the trunk in men and lower legs in women Be suspicious of pigmented lesions on the palms and soles and under the nails Choroidal melanoma occurs in the eye, and lesions may also be seen in the oral or anal mucosa Men have a slightly higher incidence than women, but women have a better prognosis Multiple lesions are rare Clinically, four main varieties of lesions occur The first is the superficial spreading melanoma (Figure 18.45), which is the least aggressive and the most common variant, while nodular melanoma (Figure 18.46) is the second most common 21/11/15 12:27 am 308 THE SKIN The American Joint Committee on Cancer staging for melanoma, with the year corresponding survival rates, is as follows: Figure 18.47 Lentigo maligna melanoma (Courtesy of Dr Shukrallah Zaynoun.) • Stage 0: Melanoma in situ (Clark Level I), 99.9 per cent survival; • Stage I/II: Invasive melanoma, 89–95 per cent survival; • T1a: Less than 1.0 mm primary tumour thickness, without ulceration, and with mitosis