An Atlas of Diagnosis and Management

GENERAL
DERMATOLOGY
John SC English, FRCP
Department of Dermatology
Queen's Medical Centre
Nottingham University Hospitals NHS Trust
Nottingham, UK

CLINICAL PUBLISHING
OXFORD
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Contents
Preface vii 4 Skin tumours 47
VISHAL MADAN AND JOHN T LEAR
Acknowledgements vii Introduction 47
Nonmelanoma skin cancers 47
Contributors viii Actinic (solar) keratosis 48
Intraepithelial carcinomas
Abbreviations ix (IEC, Bowen’s disease) 49
Cutaneous horn 50
1 Introduction to diagnosing dermatological Disseminated superficial actinic
conditions (basic principles) 1 porokeratosis 50
G WHITLOCK, JOHN SC ENGLISH, Erythroplasia of Queyrat 51
AND IAIN H LEACH Radiation-induced keratoses 51
Essentials of cutaneous anatomy and Arsenical keratoses 52
physiology 1 Basal cell carcinoma 52
History taking 4 Squamous cell carcinoma 54
Examination of the skin 5 Melanoma and melanoma
Investigations 10 precursors 56
Further reading 11 Melanoma precursors 56
Malignant melanoma 59
2 Paediatric dermatoses 13 References 63
JANE C RAVENSCROFT
Introduction 13 5 Hand and foot dermatoses 65
Skin lesions 14 JOHN SC ENGLISH
Birthmarks 14 Introduction 65
Other childhood lesions 20 Hand and foot dermatitis 65
Rashes 23 Psoriasis 71
Neonatal and infantile rashes 23 Fungus infection 72
Childhood rashes 28 Palmo-plantar pustulosis 74
Further reading 32 Miscellaneous conditions affecting the
hands and feet 75
3 Widespread rashes 33 Further reading 76
GEORGINA E ELSTON AND
GRAHAM A JOHNSTON 6 Facial rashes 77
Introduction 33 PAUL FARRANT AND RUSSELL EMERSON
Urticaria 33 Introduction 77
Erythroderma 35 History 77
Atopic eczema 36 Acne 79
Discoid eczema 38 Perioral dermatitis 80
Psoriasis vulgaris 39 Rosacea 80
Scabies 42 Atopic eczema 82
Erythema multiforme 44 Contact dermatitis 82
Further reading 46 Seborrhoeic dermatitis 84
Psoriasis 84
vi

Melasma 86 9 Skin infections and infestations 113

Lupus erythematosus 86 NEILL C HEPBURN
Dermatomyositis 89 Introduction 113
Tuberous sclerosis 89 Bacterial infections 113
Keratosis pilaris 90 Impetigo 113
Further reading 90 Cellulitis 114
Pitted keratolysis 115
7 Genital and oral problems 91 Erythrasma 116
SHEELAGH M LITTLEWOOD Atypical mycobacterium infection 116
Introduction 91 Anthrax 118
Lichen sclerosus 91 Gonococcal septicaemia 118
Lichen planus 93 Secondary syphilis 118
Zoon’s balanitis 94 Viral infections 120
Zoon’s vulvitis 95 Herpes simplex 120
Autoimmune bullous diseases 95 Herpes zoster 120
Malignant lesions 96 Molluscum contagiosum 120
Eczematous conditions 97 Viral warts 122
Vulval ulceration 98 Orf 122
Further reading 98 Fungal and yeast infections 123
Pityriasis versicolor 124
8 Scalp and nail disorders 99 Infestations 124
STUART N COHEN Cutaneous larva migrans 124
Introduction 99 Tungiasis 125
Disorders of the scalp and hair 99 Leishmaniasis 126
Alopecia areata 99 Cutaneous myiasis 127
Trichotillomania 100 Further reading 128
Tinea capitis 101
Folliculitis decalvans 102 10 Leg ulcers and wound healing 129
Dissecting cellulitis of the scalp 102 ANNA RICH AND JOHN SC ENGLISH
Acne keloidalis nuchae 103 Introduction 129
Lichen planopilaris 103 Clinical presentation 129
Discoid lupus erythematosus 104 Assessment and investigations 133
Pseudopelade of Brocque 104 Differential diagnosis 133
Naevus sebaceus 104 Management 138
Diffuse hair loss 105 References 139
Traction alopecia 105
Disorders of nails 106 Index 141
Onychomycosis 106
Psoriasis 107
Eczema 108
Lichen planus 109
Alopecia areata 110
Yellow nail syndrome 110
Onychogryphosis 110
Pincer nail 110
Median nail dystrophy 111
Tumours of the nail unit 111
Further reading 112
 vii

Preface

Dermatology is about diagnosis, as without the correct whether they be GPs, medical students, hospital doctors,
diagnosis the patient cannot be managed well. In medicine, specialist nurses or community pharmacists. Nevertheless,
treatments are often administered empirically, especially experienced practitioners will find much here to refresh their
where there is uncertainty over the diagnosis. If one knows memory; for all health professionals, we hope this book will
what the condition is then one can give the best treatment help them make the correct diagnosis and so be able to offer
and an accurate prognosis. In this book we have tried to the best possible course of management.
facilitate the process of making a diagnosis and formulating
a differential diagnosis in dermatology patients. It is aimed
primarily at dermatology naive practitioners and students, John SC English

Acknowledgements
I thank Drs Andrew Affleck, Ruth Murphy, Kate Dalziel,
and Roger Allen for providing illustrations where needed.
My thanks also to all the chapter authors for their individual
contributions.
viii

Contributors

Stuart N Cohen, BMedSci, MRCP Iain H Leach, MD, FRCPath

Department of Dermatology Department of Dermatology and Histopathology
Queen’s Medical Centre Queen’s Medical Centre
Nottingham University Hospitals NHS Trust Nottingham University Hospitals NHS Trust
Nottingham, UK Nottingham, UK

Georgina E Elston, MRCP John T Lear, MD, MRCP

Department of Dermatology Department of Dermatology
Leicester Royal Infirmary Manchester Royal Infirmary
University Hospitals of Leicester NHS Trust Manchester, UK
Leicester, UK
Sheelagh M Littlewood, MBChB, FRCP
Russell Emerson, MD, MRCP Department of Dermatology
Department of Dermatology Queen’s Medical Centre
Brighton General Hospital Nottingham University Hospitals NHS Trust
Brighton, UK Nottingham, UK

John SC English, FRCP Vishal Madan, MBBS, MD, MRCP

Department of Dermatology The Dermatology Centre
Queen’s Medical Centre Hope Hospital
Nottingham University Hospitals NHS Trust Manchester, UK
Nottingham, UK
Jane C Ravenscroft, MRCP, MRCGP
Paul Farrant, MRCP Department of Dermatology
Department of Dermatology Queen’s Medical Centre
Brighton General Hospital Nottingham University Hospitals NHS Trust
Brighton, UK Nottingham, UK

Neill C Hepburn, MD, FRCP Anna Rich, RN (Dip BSc Hons)

Dermatology Suite Department of Dermatology
Lincoln County Hospital Queen’s Medical Centre
Lincoln, UK Nottingham University Hospitals NHS Trust
Nottingham, UK
Graham A Johnston, FRCP
Department of Dermatology G Whitlock, PhD, MRCP
Leicester Royal Infirmary Department of Dermatology
University Hospitals of Leicester NHS Trust Queen’s Medical Centre
Leicester, UK Nottingham University Hospitals NHS Trust
Nottingham, UK
 ix

Abbreviations

ABPI ankle brachial pressure index ICD irritant contact dermatitis

ACD allergic contact dermatitis IEC intraepithelial carcinoma
ACE angiotensin-converting enzyme JPD Juvenile plantar dermatosis
ALA-based PDT 5-aminolaevulinic acid-based KID keratosis, ichthyosis, deafness
photodynamic therapy LE lupus erythematosus
BCC basal cell carcinoma LP lichen planus
CIN cervical intraepithelial neoplasia LS lichen sclerosis
CMN congenital melanocytic naevus MRI magnetic resonance imaging
CT computed tomography NMSC nonmelanoma skin cancers
CYP cytochrome P PCR polymerase chain reaction
DLE discoid lupus erythematosus PIN penile intraepithelial neoplasia
DLSO distal and lateral subungual onychomycosis PUVA ultraviolet A light with psoralen
DSAP disseminated superficial actinic porokeratosis PV pityriasis versicolor
DVT deep vein thrombosis SCC squamous cell carcinoma
EM erythema multiforme SCLE subacute cutaneous lupus erythematosus
GST glutathione S-transferase SLE systemic lupus erythematosus
HPV human papilloma virus SSSS staphylococcal scalded skin syndrome
HSP Henoch–Schönlein purpura UVB ultraviolet B
HSV herpes simplex virus VIN vulval intraepithelial neoplasia
 Chapter 1 1

Introduction to diagnosing
dermatological conditions
(basic principles)
G Whitlock PhD, MRCP, John SC English FRCP,
and Iain H Leach MD, FRCPath

Essentials of cutaneous anatomy

and physiology
1
The skin is a large and specialized organ, which covers the
entire external surface of the body. It plays an important role
in protecting the body against external traumas and
injurious agents such as infection, trauma, UV radiation,
and extremes of temperature as well as providing
waterproofing. Additional functions include detection of
sensory stimuli and thermoregulation. 2
The skin has two main layers, the superficial epidermis
and the dermis, which lies between the epidermis and
subcutaneous fat (1.1). The microanatomy of the skin is
essentially similar throughout, but there is considerable
regional variation. For example, the surface keratin layer is
much thicker on the palms and soles (1.2) than elsewhere,
whilst the dermis is much thicker on the back than on the
eyelids. There is also considerable regional variation in the
numbers and size of skin appendages such as hair follicles,
sebaceous glands, and sweat glands.
The epidermis is the surface layer of the skin and is a
keratinizing stratified squamous epithelium, the principle 3
cell type being the keratinocyte. The basal layer of the
epidermis contains small cuboidal cells that continually
divide to replenish the cells lost from the skin surface. The 1.1 Normal skin: epidermis (1), dermis (2). and subcutis
bulk of the epidermis is composed of the stratum spinosum (fat) (3) (H&E x4).
or ‘prickle cell’ layer, so called because the intercellular
connections or desmosomes are visible on histological
sections as prickles surrounding each cell. The cells in this become flatter and accumulate dark keratohyalin granules to
layer are large with abundant cytoplasm containing keratin form the granular layer. These cells then lose their nuclei
tonofilaments. With maturation towards the surface the cells and the keratohyalin granules, and keratin filaments
2 Introduction to diagnosing dermatological conditions (basic principles)

1.2 Acral skin (H&E x4). 1.3 Racially pigmented skin (H&E x20).

combine to form the surface keratin layer. Epidermal from prolonged contact of nickel-containing metals with the
turnover is continuous throughout life, with the turnover skin. Merkel cells are difficult to visualize in routine
time from basal cell to desquamation estimated at 30–50 histological sections but can be identified with special stains.
days depending on site. Their precise function is not clear but they are thought to
The epidermis also contains small numbers of play a role in touch sensation. They can give rise to Merkel
melanocytes, Langerhans cells, and Merkel cells. cell carcinoma, a rare aggressive malignant tumour most
Melanocytes are present scattered along the basal epidermis. often seen in the elderly.
They have long dendritic cytoplasmic processes, which The dermis lies beneath the epidermis and is essentially
ramify between basal keratinocytes. Melanocytes synthesize fibrous connective tissue. The papillary dermis is a thin
melanin pigment that is passed to basal keratinocytes via the superficial layer containing fine collagen and elastic fibres,
dendritic processes in the form of granules or melanosomes. capillaries, and anchoring fibrils which help attach the
Melanin pigment varies in colour from red/yellow to epidermis to the dermis. The bulk of the dermis is formed
brown/black. It is responsible for skin pigmentation and has by the reticular dermis which is mainly composed of thick
an important role in protecting the skin from the effects of collagen fibres and thinner elastic fibres. The collagen fibres
UV radiation. There is some regional variation in the provide much of the substance and tensile strength of the
number of melanocytes, with more being present on sun- dermis, whilst elastic fibres provide the skin with elasticity.
exposed sites though the number is fairly constant between Small numbers of lymphocytes, macrophages, mast cells,
individuals. Racial skin pigmentation is related to increased and fibroblasts are present in the dermis together with blood
activity and increased amounts of pigment rather than vessels, lymphatic vessels, nerves, pressure receptors, and
increased numbers of melanocytes (1.3). the skin appendages. The junction between the epidermis
Langerhans cells are also dendritic cells and are located in and dermis is not flat but has a complex three dimensional
the basal epidermis and stratum spinosum. They act as arrangement of downgrowths from the epidermis (rete
antigen presenting cells and are an important part of the ridges) and upgrowths from the papillary dermis (dermal
immune system. Small numbers are present in normal skin, papillae). This arrangement increases the surface area of the
but numbers are increased in some inflammatory skin dermo-epidermal junction and enhances adhesion between
diseases, such as contact dermatitis. There are two types of the two layers.
allergic reaction in the skin: immediate reactions causing The skin appendages comprise the hair follicles with their
contact urticaria (hay fever is an immediate allergic reaction attached sebaceous glands, the eccrine sweat glands and the
of the nasal mucosa), and delayed allergic reactions. This apocrine glands (1.4–1.7). Hair follicles are widely
manifests as allergic contact dermatitis such as reactions distributed but are not present on the palms and soles. They
 Introduction to diagnosing dermatological conditions (basic principles) 3

1.4 Pilo-sebaceous unit (H&E x4). 1.5 Hair bulb (H&E x4).

1.7 Apocrine glands (H&E x4).

1.6 Eccrine glands (H&E x4).

4 Introduction to diagnosing dermatological conditions (basic principles)

vary considerably in size from the large follicles of the scalp dermis (1.6). The gland is composed of a tubular coil of
and male beard area to the more widespread small vellus secretory epithelial cells with an outer layer of contractile
follicles, present on the female face for example. The hair myoepithelial cells. Sweat is transported via a duct, which
follicle is a tubular epithelial structure, which opens onto the spirals upwards through the dermis to open onto the skin
skin surface and is responsible for producing hairs. The surface. Glandular secretion and sweating are controlled by
deepest part of the follicle, the hair bulb, is situated in the the autonomic nervous system.
dermis or subcutaneous fat. The germinal matrix of the bulb Apocrine glands are histologically similar to eccrine sweat
consists of actively dividing cells that give rise to the hair glands but are slightly larger (1.7). They are much less
shaft and inner root sheath. Keratinization of the epithelial widespread and are principally located in the axillae and
cells occurs without keratohyalin and with no granular layer; ano-genital region. Their precise function in man is unclear,
this produces ‘hard’ keratin as opposed to the ‘soft’ keratin though in some other mammals they have an important role
of the epidermis, which is produced with keratohyalin. The in scent production.
outer root sheath of the follicle is derived from a
downgrowth of the epidermis. Melanocytes in the hair bulb
produce melanin pigment, which is incorporated into the History taking
hair shaft and is responsible for hair colouration.
Hair follicle growth is cyclical with an active growth phase History taking is the first part of a skin consultation. This is
(anagen phase), which is followed by an involutional phase no different to any other medical specialty: one seeks to
(catagen), and a resting phase (telogen) during which time know when the condition started, which part of the body is
hairs are shed. The anagen phase (during which time hairs affected, and how the condition has progressed since
are growing) lasts for at least 3 years, catagen lasts for presentation. Clues to the diagnosis may come from asking
approximately 3 weeks, and telogen 3 months. At any one the patient’s profession, if other family members or personal
time the majority of hair follicles (>80%) are in anagen contacts are affected, and whether there has been exposure
phase, 1–2% are in catagen, and the remainder are in to allergens or irritants. Particular attention should be
telogen phase. afforded to any treatments, both topical or systemic, that
Sebaceous glands are normally associated with and have been tried previously and if these have changed the
attached to a hair follicle (1.4). They are widespread but are character of the condition. In the past medical history, one
particularly large and numerous on the central face and are considers whether the skin condition is a dermatological
absent from the palms and soles. Sebaceous glands are manifestation of a systemic disease, if there is a history of
largely inactive before puberty but subsequently enlarge and atopy (asthma, eczema, or hayfever), and also if the patient
become secretory. The glands are composed of lobules of has suffered from previous skin complaints. Related to this,
epithelial cells, the majority of which contain abundant lipid it is important to ask about family history of skin disease.
within the cytoplasm and appear clear on histological Medications themselves can provoke skin eruptions and so a
sections. The lipid-rich secretion, sebum, is formed through thorough drug history will include current and recent
necrosis of the epithelial cells and is secreted into the upper medications as well as any over-the-counter medicines or
portion of the hair follicle. The function of sebum may supplements. Often overlooked is the psychological impact
include waterproofing and protection of the hair shaft and of the skin condition. Changes in the patient’s quality of life
epidermis as well as inhibition of infection. The other main may be a major factor in the patient consulting the physician
component of the hair follicle is the arrector pili muscle. in the first place. Through questioning a patient about how
This is a small bundle of smooth muscle situated in the the condition affects the patient’s life, the physician will be
dermis but attached to the follicle. Contraction of the able to assess what in particular is worrying the patient and
muscle makes the hair more perpendicular. explore the expectations for the consultation.
Eccrine sweat glands are responsible for the production of
sweat and play an important role in temperature control.
They are widely distributed and are particularly numerous
on the palms and soles, the axillae, and the forehead. The
secretory glandular component is situated in deep reticular
 Introduction to diagnosing dermatological conditions (basic principles) 5

1.8 Macules and

patches forming
an area of lichen
aureus on a
child’s leg. This
is a harmless
superficial
capillaritis of the
skin which leaks
red cells leaving
golden
haemosiderin
staining of the 1.9 Vesicular hand eczema of the palms in a patient
skin. allergic to Compositae plants (see Chapter 5).

Examination of the skin

Dermatology has its own vocabulary to describe skin lesions.

Some of these terms (for example, nodule and plaque) are
also used in nonmedical contexts, and special care must be
given to their particular meaning in dermatology.
Flat lesions are discolourations of the skin and no change
in texture is felt when passing a finger over the affected area.
If the diameter of a flat lesion is smaller than 1–2 cm then it 1.10 Vesicles and a bulla in a patient with bullous
is called a macule. A larger flat lesion is known as a patch pemphigoid.
(1.8).
If the lesion is raised above the skin it may be a blister, a
collection of free fluid beneath the skin. Again the terms
used to refer to blisters depend on their diameter. A small
blister is called a vesicle and large one, >0.5 cm in diameter,
is a bulla (1.9, 1.10). If a lesion is raised above the skin and
contains pus, then it is known as a pustule (1.11).
The description of a solid raised lesion, or what would
commonly be called a ‘lump’, also depends on its diameter.
A small lesion is referred to as a papule and a large lesion,
>0.5 cm in diameter, as a nodule (1.12–1.14). However,
some dermatologists distinguish between the two terms,
with a nodule meaning a lesion that has a firmer consistency
than a papule. Plaque is used for a raised lesion of large
diameter (>2–3 cm) that is characteristically flat topped and
often oval or disc shaped (1.15). 1.11 Pustular drug eruption.
6 Introduction to diagnosing dermatological conditions (basic principles)

1.12 Papular acne lesions with inflammation and

hyperpigmentation due to minocycline.

1.13 Nodular intradermal naevus on the

side of the nose.

1.14 Keloid nodule on the back.

1.15 Hyperkeratotic plaques of

psoriasis with obvious silvery scale.
 Introduction to diagnosing dermatological conditions (basic principles) 7

Colour is also an important feature of a skin lesion. An ecchymosis (plural: ecchymoses), which is known to most
area may be brown with pigment; it may be less pigmented people as a bruise (1.18). By contrast, erythema refers to
than the surrounding skin or hypopigmented (1.16). In fact, skin reddening that does blanch on pressure.
it may have any colour. The physician should note if the area There may be changes in the skin overlying the area of
is uniformly coloured or not. Where a lesion is red, it is interest. The area may be scratched or excoriated, and with
useful to compress the overlying skin to see if it blanches on this there may be fresh or dried blood (1.19).Crust is dried
pressure. Red macules that do not blanch on pressure are serum that is typically golden in colour that can overlie a
known as purpura (1.17). The redness is due to blood lying lesion; it suggests inflammation due to eczema or impetigo
outside the blood vessels, which cannot be pushed away (1.20, 1.21). This must be differentiated from scale, which
with compression. A small purpuric lesion is referred to as a is the detached keratin of the top layer of skin. Depending
petechia (plural: petechiae) and a large purpuric lesion as an on the skin condition, scale will be of differing adherence to

1.16 Hyper- and hypopigmentation in a small plaque of 1.17 Purpuric rash on the abdomen of a patient with
discoid lupus erythematosus on the forehead (see vasculitis. Not the Koebner phenomenon where she has
Chapter 6). scratched the skin and the yellow-brown pigmentation
where the lesions have faded.

1.18 Haematoma in the stratum corneum of the second 1.19 Excoriated lesions on the feet.
toe mimicking an acral lentiginous melanoma.
8 Introduction to diagnosing dermatological conditions (basic principles)

the lesion’s surface. Often it is useful to remove overlying describe dermatological conditions: Distribution, Con-
scale and crust in order to look at the underlying skin. figuration, and Morphology.
When examining in dermatology, good lighting must be • Distribution: which area or areas of the skin are affected;
used. The skin should be observed and then palpated. for instance does the rash tend to affect the flexor or
Rashes and isolated lesions should be approached in the extensor surfaces of the skin (1.22, 1.23)?
same logical manner. The mnemonic DCM can be used to

1.20 Impetiginized eczema of the lips and 1.21 Weeping allergic dermatitis due to contact with nickel
surrounding skin. in the belt buckle.

1.23 Dermatitis herpetiformis classically shows

herpetiform lesions (vesicles grouped together like a cold
sore) on elbows, knees, buttocks, and shoulders.

1.22 Plaques of psoriasis affecting the extensor surface of

the lower leg.
 Introduction to diagnosing dermatological conditions (basic principles) 9

• Configuration: first, does the condition affect the body For a lesion that is changing, use of the ABCDE criteria
symmetrically or not? Second, is there a pattern to the can be a useful tool for suspecting malignancy (1.26, 1.27).
condition, such as linear, where lesions are in a line or This rule has been validated in scientific studies in the
annular, where they form a ring; are the lesions in groups prediction of malignant melanoma. Although it has not been
or isolated (1.24, 1.25)? When describing an isolated validated for nonmelanoma skin lesions, it is a useful
lesion, the physician should check if there are approach to all skin lesions that are reported as changing.
surrounding lesions and if so, do they form a pattern.
• Morphology: the form of the rash or lesion should be
described, its size, colour, and any associated features. If
the rash has different forms within it, each form should be
described separately, using the terms described in the
previous section. A general physical examination of the
patient should not be overlooked, especially where the
skin condition is a manifestation of systemic disease.

1.24 Herpes simplex infection of the palm. 1.25 Lichen striatus.

1.26 A superficial malignant melanoma on a woman’s leg. 1.27 The husband of the patient in
It is Asymmetrical, the Border is irregular, there is Colour 1.26 regularly measured the lesion.
variation, its Diameter is •6 mm, and it is Enlarging (1.27).
10 Introduction to diagnosing dermatological conditions (basic principles)

Malignancy should be suspected if one or more of the measuring up to 6 mm in diameter is removed using a
following criteria are fulfilled: circular blade called a punch biopsy. Biopsies can be
• Asymmetry: is the lesion asymmetrical in shape? analysed in a number of ways including histology, culture,
• Border: does the lesion have an irregular border? and immunofluorescence, which is a useful tool when
• Colour: is the colour of the lesion irregular or changing? considering the aetiology of immuno-bullous skin disease.
• Diameter: is the diameter >6 mm? Patch testing is useful in suspected contact dermatitis
• Enlargement: is the lesion growing, either vertically or (Table 1.1). Skin, usually on a patient’s back, is exposed to
horizontally along the skin surface? different allergens; each is placed onto a separate disc and
held in contact with the patient’s skin using tape (1.29).
These so-called patches are left in place for 2 days and then
Investigations removed. The skin is inspected after a further 2 days for any
reactions (1.30). Skill is required to discern irritant from
The skin can be viewed using a dermatoscope, a handheld allergic reaction. Various contact dermatitis groups set the
device that magnifies the field of view ×10. This is especially number of standard chemicals used, although additional
useful when looking at pigmented lesions (see Chapter 4). chemicals may be ‘patched’ if the history is relevant.
Where a fungal infection is suspected, skin scrapings, Skin prick tests are used to examine for atopy, latex
collected using brisk strokes of a scalpel blade across the allergy, and food allergy. A drop of allergen in solution is
affected area, may be sent for analysis by microscopy and placed on the patient’s forearm. The skin is pricked with a
culture (1.28). Likewise, fluids within blisters or exuding lancet through the drop and excess solution is then
from a lesion may be collected using a swab or syringe and removed. Skin is inspected after 20 minutes (1.31). Skill is
analysed for the presence of bacteria or viruses. again required in interpretation of these tests. These tests
An invasive investigation of skin disease is the removal of are not commonly used because of the limited information
affected skin for analysis. Commonly, a core of skin afforded by them.

Table 1.1 Indications for patch testing

• Treatment-resistant eczema
• Chronic hand eczema
• Gravitational eczema
• Occupational contact dermatitis

1.28 Fungal spores and hyphae seen on microscopy.

 Introduction to diagnosing dermatological conditions (basic principles) 11

1.29 Patch tests in place. 1.30 Positive allergic reactions at day 4.

Further reading

Burns T, Breathnach S, Cox N, Griffiths C (2004). Rook’s

Textbook of Dermatology (7th edn). Blackwell Science,
Oxford.
McKee PH, Calonje E, Grauter SR (2005). Pathology of
the Skin (3rd edn). Elsevier Mosby, Philadelphia.

1.31 A positive prick test to natural rubber

latex allergy.
 Chapter 2 13

Paediatric dermatoses
Jane C Ravenscroft, MRCP, MRCGP

Introduction

Skin conditions are very common in children. Many are atopic eczema. This chapter will illustrate some of the many
transient and of little importance; however, some may have different skin lesions (Table 2.1) and rashes (Table 2.2) which
important implications. Atopic eczema is very common, and can affect children, and help in accurate diagnosis and
because of this, any rash in a child is often diagnosed as management.

Table 2.1 Lesions presenting in children <10 years, by colour, or presence of blisters

Red/pink/blue Pigmented
• Abscess/boil • Acquired benign naevus
• Infantile haemangioma • Café au lait macule
• Lymphangioma circumscriptum • Congenital melanocytic naevus
• Naevus flammeus • Dermatofibroma
• Pilomatricoma • Epidermal naevus
• Port wine stain • Mastocytoma
• Pyogenic granuloma • Mongolian blue spot
• Ringworm • Naevus spilus
• Spider naevus
• Spitz naevus Hypopigmented
• Vascular malformations • Naevus depigmentosus
• Postinflammatory hypopigmentation
Skin coloured/yellow/orange • Pityriasis alba
• Aplasia cutis • Vitiligo
• Dermoid cyst
• Epidermal cyst Blisters
• Granuloma annulare • Bullous impetigo
• Molluscum contagiosum • Chicken pox
• Neurofibroma • Chronic bullous disease of childhood
• Sebaceous naevus • Dermatitis herpetiformis
• Xanthogranuloma • Epidermolysis bullosa
• Herpes simplex
• Mastocytosis
• Miliaria
• Papular urticaria
14 Paediatric dermatoses

Table 2.2 Rashes in children <10 years SKIN LESIONS

Birthmarks
Neonatal and infantile rashes
• Atopic eczema
Infantile haemangioma (strawberry naevus)
• Epidermolysis bullosa
• Erythema toxicum neonatorum Clinical presentation
• Ichthyosis Infantile haemangiomas are benign vascular tumours which
• Infantile acne affect 1–2% of infants, most commonly on the head and
• Miliaria crystallina neck. They are not present, or just visible at birth, and grow
• Miliaria rubra rapidly in the first 6 months of life to become distinctive
• Psoriasis
bright red nodules, sometimes with a deeper component
• Seborrhoeic dermatitis
(2.1). At around 12 months of age, they start to undergo
Rashes affecting the nappy area spontaneous resolution (2.2). Fifty per cent of lesions will
• Atopic eczema disappear by 5 years of age and 90% by 9 years. There may
• Bullous impetigo be residual flaccid skin and telangiectasia. Complications of
• Candida infection ulceration (2.3), haemorrhage, and interference with
• Irritant nappy rash
function may occur during the phase of rapid proliferation.
• Langerhans cell histiocytosis
• Perianal streptococcal disease Rarely, multiple haemangiomas occur, which may be
• Psoriasis associated with internal haemangiomas. Very infrequently,
• Seborrhoeic dermatitis large haemangiomas may be associated with structural brain
and cardiac abnormalities, or consumptive coagulopathy.
Acute childhood rashes
• Folliculitis
Differential diagnosis
• Henoch–Schönlein purpura
• Infections: Differential diagnosis is from other vascular birthmarks.
– Chicken pox Vascular lesions which do not show characteristic
– Erythema infectiosum proliferation after birth are not infantile haemangiomas and
– Hand, foot, and mouth disease should be referred for accurate diagnosis.
– Herpes simplex
– Kawasaki disease
Management
– Measles
– Roseola Due to the self-limiting nature of infantile haemangiomas,
– Rubella treatment is not required unless complications occur.
– Scabies Ulcerated lesions can be treated with topical steroid and
– Scarlet fever antibiotics. Pulsed dye laser may be used for prolonged
– Staphylococcal scalded skin syndrome ulceration, and for residual telangiectasia after resolution.
• Pityriasis rosea
Interference with function may require intralesional or oral
• Toxic erythema
• Urticaria steroids.

Chronic childhood rashes

• Acne
• Atopic eczema
• Chronic bullous disease of childhood
• Dermatitis herpetiformis
• Ichthyosis
• Juvenile plantar dermatosis
• Keratosis pilaris
• Pityriasis versicolour
• Psoriasis
• Urticaria pigmentosum
 Paediatric dermatoses 15

Naevus flammeus (salmon patch)

Clinical presentation Management
This is a pale pink vascular patch, present at birth, which Those on the forehead and eyelid tend to disappear during
commonly occurs on the nape of the neck, forehead, or the first year of life, but those on the neck (stork marks) will
eyelid (2.4). persist. Treatment is not usually indicated, but they will
respond to pulsed dye laser.
Differential diagnosis
Naevus flammeus can be distinguished from port wine stain
by its paler colour and typical site.

2.1 Infantile
haemangioma
at 5 months
of age.

2.2 The same child as in 2.1 aged 3 years.

2.3 A proliferating infantile haemangioma, which is 2.4 A salmon patch in a neonate.

ulcerated.
16 Paediatric dermatoses

Port wine stain Congenital melanocytic naevus

Clinical presentation Clinical presentation
Port wine stain is a vascular malformation which presents as Congenital melanocytic naevi are palpable brown lesions
a deep red/purple vascular patch, present at birth, most with some variation in pigment within them, seen in 1–2%
often unilateral on the face; however, any site can be affected of infants at birth (2.7; see Chapter 4, 4.20–4.22). Most are
(2.5). small (<1.5 cm) or medium sized (1.5–20 cm); a few may
cover large areas of the body surface. They persist lifelong
Differential diagnosis and may become more raised and develop coarse hairs
Salmon patch is paler, and occurs on the nape of the neck, within them as the child gets older.
forehead, and eyelid. Infantile haemangiomas will grow
larger in the first 4 weeks of life. Other vascular and Differential diagnosis
lymphatic malformations are usually associated with soft Congenital melanocytic naevi are generally darker brown
tissue swelling. than other pigmented birthmarks.

Management Management
Port wine stains persist and darken throughout life, and Management of congenital melenocytic naevi must consider
cause considerable psychological morbidity. They may risk of malignancy and cosmetic appearance. Risk of
rarely be associated with other abnormalities, e.g. lesions malignancy with small- and medium-sized lesions is
affecting the trigeminal area may be associated with ocular considered to be <5%, so prophylactic excision is not
or intracranial involvement leading to glaucoma, epilepsy, routinely recommended. Excision may be considered for
and developmental delay (Sturge–Weber syndrome). cosmetic reasons. Change within a congenital naevus should
Referral should be made in the first few months of life for prompt referral for consideration of biopsy. Large congenital
assessment for associated conditions, and consideration for melanocytic naevi are extremely complex to manage and
treatment with pulsed dye laser, if available. require specialist assessment.

Lymphangioma circumscriptum Café au lait macule

Clinical presentation Clinical presentation
This uncommon lymphatic malformation presents at birth These are tan coloured, evenly pigmented nonpalpable
with a cluster of papules varying in colour from clear to lesions up to around 10 cm in size, presenting at birth or in
straw coloured to deep purple, which resemble frogspawn the first few years of life, most often on the trunk and limbs
(2.6). There may be associated soft tissue swelling. (2.8).

Differential diagnosis Differential diagnosis

Other vascular birthmarks should be distinguished by colour Congenital melanocytic naevi are generally darker in colour,
or early proliferation. and may be palpable.

Management Management
Lymphangioma persist and may enlarge throughout life. Lesions persist throughout life but are not usually a
Surgical removal is difficult because there is a deep cosmetic problem; therefore, treatment is not required. If >5
component. If weeping and crusting is a problem, CO2 or café au lait macules are present, there is a high chance (up to
Erb YAG laser may give symptomatic relief. 95%), that the patient has neurofibromatosis, so the patient
should be referred for further assessment.
 Paediatric dermatoses 17

2.5 A port
wine stain
affecting the
trigeminal
area.

2.6 Lymphangioma circumscriptum.

2.7 A large 2.8 Café au lait

and a small patches in a child
congenital with neuro-
melanocytic fibromatosis.
naevus.
18 Paediatric dermatoses

Mongolian blue spot Epidermal naevus

Clinical presentation Clinical presentation
This is a large blue patch on the lower back, commonly seen Children present with a linear brown or skin coloured warty
in oriental babies at birth (2.9). plaque, which may be present at birth or develop in the first
few years of life. They are of variable size, from 1–2 cm to
Differential diagnosis the length of a limb (2.11), and will often extend during
Bruising, which may be mistaken for child abuse. early childhood. Occasionally, epidermal naevi are multiple
and may be associated with other abnormalities.
Management
Lesions generally disappear in the first few years of life. No Differential diagnosis
treatment is necessary. Other birthmarks are distinguished by lack of linear pattern.
Lichen striatus is an inflammatory linear condition that
Sebaceous naevus appears in later childhood and resolves in months to years.
Clinical features
This is an uncommon yellowish papule or plaque, present at Management
birth, which often presents as a hairless area on the scalp Epidermal naevi persist for life. Treatment, if needed, is by
(2.10). surgical removal or laser, but scarring or recurrence may
occur.
Differential diagnosis
Trauma from forceps/ventouse delivery; aplasia cutis. Aplasia cutis
Clinical presentation
Management Aplasia cutis is a developmental abnormality with an area of
Surgical removal can be considered if they are a cosmetic absence of skin. It presents as an ulcerated red area present
problem. There is a small increased risk of basal cell on the scalp at birth, which heals with a scar, within which
carcinoma in adult life. the hair does not grow (2.12).

Differential diagnosis
Sebaceous naevus has a warty surface and the skin is intact;
trauma from forceps/ventouse during delivery.

Management
Surgical excision of the scar can be considered, if it is a
cosmetic problem.
 Paediatric dermatoses 19

2.9 Mongolian blue spot. 2.10 Sebaceous naevus.

2.12 Aplasia cutis results in a localized bald

patch on the scalp.

2.11 A linear epidermal warty epidermal

naevus.
20 Paediatric dermatoses

Other childhood lesions

Pilomatricoma Mastocytosis
Clinical presentation Clinical presentation
Pilomatricoma is a benign adnexal tumour which presents in Collections of mast cells may form a solitary lesion, called a
childhood as a firm, solitary 0.5–3 cm blue-red nodule most mastocytoma, or may develop throughout the skin as a rash
commonly on the face (2.13). It grows slowly over months called urticaria pigmentosum (2.15). Approximately 50% of
and may calcify. all cases of mastocytosis occur in children, generally before
2 years of age.
Differential diagnosis A mastocytoma presents as a red/brown nodule, which
Pilomatricomas can be mistaken for epidermal cysts or produces wealing if the lesion is rubbed (Darier’s sign).
dermoid cysts, but are distinguished by bluish colour and Urticaria pigmentosum presents as a rash composed of
firmer texture. hundreds of pale brown macules predominantly over the
trunk. Often, parents have noticed wealing after pressure or
Management a hot bath.
These lesions should be surgically excised.
Differential diagnosis
Pyogenic granuloma Solitary mastocytomas and urticaria pigmentosum can be
Clinical presentation distinguished from other lesions and rashes by their
Pyogenic granuloma is a benign vascular tumour which often distinctive pale brown colour and presence of wealing on
follows minor injury to the skin. It presents as a bright red, rubbing.
shiny ‘wet’ nodule, most commonly on the face or fingers,
which bleeds easily on minor trauma (see Chapter 4, 4.41). Management
Mastocytomas resolve spontaneously over 2–3 years. No
Differential diagnosis treatment is needed. Urticaria pigmentosum shows slower
Appearance is characteristic. resolution, with around 50% clear by adolescence.
Troublesome wealing can be treated with antihistamines.
Management Patients with urticaria pigmentosum should avoid drugs
Treatment is with currettage or electrodesication. which release histamine, e.g. aspirin, codeine, as they can
precipitate severe urticaria and systemic effects.
Xanthogranuloma
Clinical presentation
Xanthogranuloma is a rare benign tumour of histiocytes
which presents in early childhood as an orange/yellow
nodule (2.14). It resolves spontaneously in 1–5 years.
Occasionally, multiple lesions occur. There is a rare
association with neurofibromatosis and juvenile leukaemia.

Differential diagnosis
Xanthogranulomas may mimic mastocytomas, but are
distinguished by absence of wealing.

Management
Treatment is not required because xanthogranulomas
undergo spontaneous resolution.
 Paediatric dermatoses 21

2.13 Pilomatricoma. 2.14 Xanthomgranuloma.

2.15 Urticaria pigmentosum.

22 Paediatric dermatoses

Granuloma annulare
Clinical presentation
Granuloma annulare is an inflammatory disorder of the skin
which presents as an annular ring of smooth, skin-coloured
or pink coalescing papules with central clearing (2.16).
Lesions are often solitary, but may be multiple, and most
commonly affect the dorsum of the feet.

Differential diagnosis
Granuloma annulare is frequently misdiagnosed as
ringworm, but is easily distinguished by lack of scale.

Management 2.16 Granuloma annulare.

There is no effective treatment for granuloma annulare.
Spontaneous resolution generally occurs over months to
years.

Spider naevus
Clinical presentation
Pre-adolescent children present with a red papule on the
face, made up of a central arteriole with peripheral vessels
radiating from it (2.17). Pressure on the arteriole will cause
blanching. May be solitary, or two or three may be present.
In children, there is not usually an association with liver
disease.

Differential diagnosis
The appearance is characteristic.

Management
Spider naevi will tend to resolve by the teenage years, so
treatment is not generally necessary. Very large lesions can 2.17 Spider naevus.
be treated with cautery or pulsed dye laser, if available.
 Paediatric dermatoses 23

RASHES

Neonatal and infantile rashes

Miliaria
Clinical presentation
Miliaria rubra is an eruption of erythematous papules and
vesicles 1–4 mm in diameter, affecting the face, upper trunk,
and flexures. It is common in the neonatal period, and
lesions may occur in crops (2.18). Miliaria crystallina is
much less common, and comprises a widespread eruption of
thin walled 1–2 mm vesicles without erythema, occurring in
the first 2 weeks of life. In both conditions the infant is well.
2.18 Miliaria rubra.
Differential diagnosis
Erythema toxicum neonatorum is diffuse erythema with
occasional papules, seen in 50% of newborns in the first few
days of life. Herpes simplex and staphylococcal infections
cause pustular/vesicular rashes in an unwell child.

Management
These conditions are self-limiting over a few weeks.

Irritant nappy rash

Clinical presentation
This is a bright red, glazed, confluent erythema affecting the
convex surfaces of the nappy area which are in contact with
the urine and faeces. Erosions and ulcers can occur when
severe (2.19). Groin flexures are spared.

Differential diagnosis
Irritant nappy rash, which does not respond to simple
treatment, should be reassessed with consideration of rarer 2.19 Irritant nappy rash.
causes of rash in the nappy area (Table 2.2).

Management
Frequent changing of the nappy is advised, with application
of a barrier cream.
24 Paediatric dermatoses

Seborrhoeic dermatitis
Clinical presentation
A bright red, confluent, nonitchy eruption of the nappy area,
sometimes also involving the scalp, face, and trunk,
occurring in infants under 3 months (2.20).

Differential diagnosis
Psoriasis and seborrhoeic dermatitis can look very similar in
infancy. Atopic eczema is itchy, and associated with dry
skin. Irritant nappy rash is confined to the convex surfaces
and is painful. Candida infection has characteristic satellite
papules (2.21). Langerhans cell histiocytosis is a very rare,
more papular, brownish eruption of the groin and scalp,
which progresses over weeks to months (2.22, 2.23).

Management
This condition is self-limiting over weeks to months.
Combination therapy with a cream containing 1%
hydrocortisone and an antifungal can improve the
appearance.

Atopic eczema in infancy 2.20 Infantile seborrhoeic dermatitis.

Clinical presentation
Atopic eczema in infancy usually presents after 4 weeks of
age as a dry, scaly, erythematous rash affecting the face,
scalp, and sometimes the trunk and limbs (2.24, 2.25). The
rash is poorly demarcated, blending into normal skin. It is
itchy and causes distress to the child. There is usually a
family history of eczema, asthma, or hay fever.

Differential diagnosis
Seborrhoeic dermatitis is brighter red, affects the nappy area
and is nonitchy. Ichthyosis is present at, or soon after, birth
as a dry scaly skin, without a rash. Scabies is a generalized
papular rash, including palms, soles, and genitals, of sudden
onset, without associated dry skin.

Management
Emollients can be used to relieve dry skin. Mild topical
steroid can be applied to red areas in bursts of up to 7 days
when needed.

2.21 Candida infection of the nappy area.

 Paediatric dermatoses 25

2.23 Langerhans cell histiocytosis of the groin

resembling psoriasis.

2.22 Langerhans cell histiocytosis of the

scalp resembling seborrhoeic dermatitis.

2.25 Atopic eczema affecting the knee flexures.

2.24 Atopic eczema affecting the face.

26 Paediatric dermatoses

Psoriasis in infancy Epidermolysis bullosa

Clinical presentation Clinical presentation
Infants present with a salmon pink, well demarcated, scaly Abnormal blistering occurs due to skin fragility. The
erythema often affecting the nappy area (2.26, 2.27); the commonest type, epidermolysis bullosa simplex (autosomal
scalp, face, and trunk may also be involved (2.28). It is dominant), presents with blisters of the feet (2.30). It may
usually nonitchy and not too distressing for the child. There be mild with onset after the child starts to walk, and is often
may be a family history of psoriasis. exacerbated by heat. Other, more severe forms, present in
infancy with widespread blistering and scarring.
Differential diagnosis
Irritant nappy rash is localized to concave skin in contact Differential diagnosis
with urine and faeces. Seborrhoeic eczema is less well Epidermolysis bullosa simplex is distinguished from simple
demarcated, and responds more easily to treatment. friction blisters by extent and severity of blistering, and by
family history.
Management
Nappy psoriasis can be difficult to treat. It usually requires a Management
topical steroid of at least moderate strength. Patients with suspected epidermolysis bullosa should be
referred for accurate diagnosis. The charity DebRA
Ichthyosis (www.debra.org.uk) will provide education, nursing input,
Clinical presentation and genetic testing for patients with all forms of
Ichthyosis is a genetic condition in which the skin fails to epidermolysis bullosa.
shed normally, resulting in a build up of adherent scale. The
most common type, ichthyosis vulgaris (autosomal Infantile acne
dominant), causes fine white scaling which becomes Clinical presentation
apparent in the first year of life, and spares the flexures Infants present with papules, pustules, and comedones
(2.29). The rarer X-linked ichthyosis may affect all areas of (blackheads and whiteheads) on the central cheeks. It
the body with large, fish-like scales. Other, very rare usually occurs in boys aged 3–24 months (2.31).
subtypes may be associated with erythema and sparse hair.
Differential diagnosis
Differential diagnosis Eczema and impetigo can present with a red face, but
Atopic eczema causes erythema and characteristically comedones only occur in acne.
involves the flexures. However, atopic eczema coexists in
50% of patients with ichthyosis vulgaris, so distinction can Management
be difficult. Infantile acne tends to resolve by 5 years. Treatment may be
needed to prevent scarring. Topical benzoyl peroxide,
Management antibiotics, and retinoids can be used. Oral tetracyclines are
Simple emollients can be used to hydrate the skin. Referral contraindicated, but oral erythromycin may be helpful.
is recommended for genetic advice/testing in severe cases.
 Paediatric dermatoses 27

2.26 Nappy psoriasis.

2.27 Perianal psoriasis.

2.28 Facial psoriasis. 2.29 Ichthyosis vulgaris.

2.30 Epidermolysis bullosa simplex.

2.31 Infantile acne.

28 Paediatric dermatoses

Childhood rashes

Toxic erythema Henoch–Schönlein purpura (HSP)

Clinical presentation Clinical presentation
This is a term used to describe an acute, morbilliform, A purpuric rash develops predominantly over the lower
erythematous eruption due to drugs, virus, or bacteria limbs and buttocks, most commonly in children aged 4–7
(2.32). The child is often mildly unwell. Spontaneous years (2.34). This is an allergic vasculitis, and may be
resolution occurs over 1–2 weeks, followed by precipitated by an upper respiratory tract infection. There
desquamation. may be associated abdominal or renal involvement. Most
children have self-limiting disease over 4–6 weeks, but
Differential diagnosis relapses can occur.
Toxic erythema needs to be distinguished from specific
dermatological diseases and viral infections. Differential diagnosis
HSP must be distinguished from meningococcal
Management septicaemia
Simple emollients and antihistamines can give symptomatic
relief. Suspected drugs should be stopped. Management
Treatment consists of symptomatic relief and skin care.
Staphylococcal scalded skin syndrome (SSSS) Systemic steroids are given if there is significant abdominal
Clinical presentation or renal involvement, but benefit is uncertain.
SSSS is a serious but treatable, toxin mediated reaction to
staphylococcal infection. Infants and young children present Pityriasis rosea
with sudden onset of fever, skin tenderness, and erythema Clinical presentation
with denudation or blistering of skin, often accentuated in Pityriasis rosea consists of a rash of fine, scaly, pale pink
the flexures (2.33). plaques typically in a fir tree distribution over the trunk
(2.35). A history of a single, ‘herald’ patch 1–2 weeks earlier
Differential diagnosis can usually be obtained. Pityriasis rosea is probably due to
The main differential diagnosis is toxic epidermal necrosis an unidentified viral infection. It typically lasts 4–6 weeks
which is a type of severe drug eruption. before gradually resolving.

Management Differential diagnosis

Antistaphylococcal antibiotics, analgesia, and supportive Pityriasis rosea can mimic guttate psoriasis.
skin care should be given as a matter of urgency. Hospital
admission is required in all but the mildest cases. Management
No treatment is generally required.
 Paediatric dermatoses 29

2.33 Staphylococcal scalded skin syndrome.

2.32 Toxic erythema.

2.34 Henoch–Schönlein purpura.

2.35 Pityriasis rosea.

30 Paediatric dermatoses

Keratosis pilaris Pityriasis alba

Clinical presentation Clinical presentation
This condition presents with rough skin on the upper arms Multiple, poorly defined hypopigmented patches occur in
due to follicular plugs of keratin, sometimes with associated this condition on the cheeks in children, often appearing
erythema (2.36); it less frequently affects the cheeks and after a sunny holiday (2.38).
thighs. The condition is very common, often runs in
families, and is frequently not noticed by patients. Differential diagnosis
Pityriasis alba should be distinguished from vitiligo and
Differential diagnosis postinflammatory hypopigmentation.
Diagnosis is usually straightforward from the distribution
and follicular pattern. Management
Reassurance that the pigment will return to normal is
Management usually sufficient. Sun protection may prevent recurrence.
Frequently no treatment is required. The condition tends to
improve in the summer and as the patient gets older. Chronic bullous disease of childhood
Emollients may make the skin feel smoother. Clinical presentation
Children present with groups of blisters, often occurring in
Vitiligo rings on the face, trunk, and genitals, starting at age 3–5
Clinical presentation years. The blisters are nonitchy. This is a rare, autoimmune
Patients present with well-defined depigmented (white) condition.
nonscaly patches, often in a symmetrical pattern on the face,
trunk, or limbs (2.37). Differential diagnosis
Blisters may occur in several skin conditions (Table 2.1).
Differential diagnosis Diagnosis of chronic bullous disease of childhood can be
Pityriasis versicolour (trunk) and pityriasis alba (face) have confirmed by the appearance of a linear band of IgA on
a scaly surface, and are less pale and well-defined. In biopsy immunofluorescence. In the genetic group of
postinflammatory hypopigmentation, there is a clear history conditions epidermolysis bullosa, blistering occurs from
of preceding inflammation. Naevus depigmentosum is a infancy at sites of trauma. In papular urticaria, a cluster of
form of hypopigmented birthmark, which is stable bites and blisters occur, which quickly heal. In dermatitis
throughout life. herpetiformis, blisters are intensely itchy, and occur on the
extensor surfaces of limbs and buttocks, usually in older
Management children or adults (2.39).
Vitiligo may remain stable, partially resolve, or progress over
months to years. A trial of potent topical steroid is Management
worthwhile in the early stages. Light therapy can be helpful. Oral dapsone will usually control the blistering until it
Referral should be offered for cosmetic camouflage. resolves spontaneously over a few years.
 Paediatric dermatoses 31

2.36 Keratosis pilaris. 2.37 Localized vitiligo.

2.39 Dermatitis herpetiformis.

2.38 Pityriais alba.

32 Paediatric dermatoses

Juvenile plantar dermatosis (JPD)

Clinical presentation
This is a common condition affecting prepubertal children.
They complain of painful, itchy feet; examination shows
glazed erythema, hyperkeratosis, and fissuring affecting the
anterior third of the sole (2.40). The condition lasts months
to years with intermittent flares.

Differential diagnosis
JPD should be differentiated from pitted keratolysis, which
is a corynebacter infection causing maceration of the
forefoot; tinea pedis, which is concentrated in the toe webs;
and allergic contact dermatitis, which affects the whole sole.

Management
JPD is helped by reducing sweating with measures such as
avoiding occlusive footwear, and wearing cotton socks.
Emollients may give symptomatic relief.
2.40 Juvenile plantar dermatosis.
Striae
Clinical presentation
Adolescent children may develop linear, atrophic,
purple/red striae on the lower back or inner thighs due to
disruption of connective tissue during a period of rapid
growth (2.41).
Striae may also be due to excess topical steroid use, or,
very rarely, Cushing’s disease or genetic connective tissue
abnormalities.

Differential diagnosis
Appearance is characteristic.

Management
There is no effective treatment. Severe striae or atypical sites
should be referred for exclusion of underlying disease.

Further reading 2.41 Striae due to rapid growth in adolescence.

Harper J, Oranje A, Prose N (eds) (2005). Textbook of

Paediatric Dermatology (2nd edn). Blackwell Scientific,
Oxford.
Spitz JL (2005). Genodermatoses. A Clinical Guide to
Genetic Skin Disorders, 2nd edn. Lippincott Williams &
Wilkins, Philadelphia.
Verbov J (1988). Essential Paediatric Dermatology. Clinical
Press, Bristol.
 Chapter 3 33

Widespread rashes
Georgina E Elston, MRCP and
Graham A Johnston, FRCP

Introduction Clinical presentation

An urticarial rash consists of weals: pruritic, raised,
In order to diagnose a rash correctly, a history and oedematous papules and plaques, usually erythematous with
examination are necessary. An experienced dermatologist a pale centre. Scaling is always absent. An important clinical
may be able to take one look at a rash and come up with a clue is that individual lesions appear on any part of the skin
diagnosis but, for the less experienced, the history, within a few minutes and will have resolved within 24 hours,
distribution, configuration, and morphology of the rash will although new lesions may be appearing elsewhere on the
point to the correct diagnosis or differential. skin. Another clue to the diagnosis is if the patient is
dermographic (although not demonstrable in all cases)
(3.2). A firm, but gentle, scratch of the skin with an orange
Urticaria stick will produce a linear weal within 5–10 minutes. Rarely,
the condition is associated with angio-oedema where
Introduction there can be swelling of the lips, tongue, and around the
Urticaria is characterized by an acute eruption of recurring, eyes (3.3).
pruritic papules and plaques (3.1). It is often self-limiting,
but in many patients becomes chronic and relapsing where
it can greatly impair quality of life.

3.1 Chronic idiopathic urticaria on the back. 3.2 Dermographism.

34 Widespread rashes

3.3 Urticaria and angio-oedema of 3.4 Fixed drug eruption from

the face. temazepam.

Histopathology
A biopsy is not usually indicated for diagnostic purposes, as
the features are nonspecific, with oedema and a mixed
dermal inflammatory infiltrate. However, histology can
exclude the possibility of urticarial vasculitis.

Differential diagnosis
Drug reactions should be considered if there is a history of
new drugs preceding the rash (3.4). In urticarial vasculitis,
lesions persist for more than 24 hours and resolve with
bruising. Contact urticaria should be considered if local
applications of products preceded the rash (3.5). Papular
urticaria is possible if there is a history of contact with
mosquitoes, bed bugs, or fleas (are their pets scratching 3.5 Contact urticaria from perfume.
too?) (3.6, 3.7).

Management
Acute urticaria, normally triggered by drugs, food, or
infections has a good prognosis, resolving in less than
1 month. Treatment is symptomatic with high-dose
antihistamines. antihistamines and avoidance of associated triggers (which
Chronic urticaria lasts longer than 6 weeks and may may include pressure, sun exposure, and exercise, although
continue for many years in some cases. It is idiopathic in the there is usually no history of a trigger). Addition of H2
vast majority of cases and investigations are not indicated. blockers such as cimetidine as well as the tricyclic
Again treatment is with single or combination high-dose antidepressant doxepin can also be helpful.
 Widespread rashes 35

3.6 Papular urticaria on the arm. Note the close proximity

of the lesions ‘breakfast, lunch and tea’ for the flea!
3.7 Excoriated papular urticarial lesions on the ankle.

Erythroderma

Introduction Clinical presentation

Erythroderma is an acute and serious medical condition Erythroderma simply means red skin with involvement of
that can make patients feel shivery and unwell. Patients over 90% of the skin surface area. The skin is angry,
should be admitted to hospital for close monitoring and inflamed, and hot to touch. Usually there is a surface scale,
treatment. which may be fine or coarse (3.8–3.10). The skin is not
always itchy. Patients become acutely unwell with fever,

3.8 Erythrodermic cutaneous T-cell 3.9 Erythrodermic psoriasis. 3.10 Erythrodermic atopic eczema.
lymphoma (Sezary’s syndrome).
36 Widespread rashes

shivering, malaise, and lethargy due to the considerable loss Management

of heat, fluid, and protein from their inflamed skin. Palmo- Patients should be admitted to hospital. Liberal and
plantar involvement is common, with hyperkeratosis and frequent application of bland emollients should be applied
fissuring. Nails can exhibit onycholysis or may even shed. to the whole skin. Careful attention to fluid and electrolyte
Hair loss can occur with scalp involvement. Patients become balance is needed, and protein replacement with high
dehydrated and hypothermic as a result of insensible fluid calorie/protein supplements should be considered. This
loss from the skin. Peripheral oedema develops due to low condition can be life threatening, particularly in the elderly,
albumin and high output cardiac failure. Lymphadenopathy who may develop infections, hypothermia, and associated
may be found but should alert one to the possibility of high output cardiac failure.
cutaneous lymphoma.

Histopathology Atopic eczema

A biopsy may be nonspecific in the early stages but can help
differentiate psoriasis and eczema. The presence of Introduction
eosinophils would lead to a careful inquiry about drugs Atopic eczema usually presents in childhood and settles
including nonprescribed medication. spontaneously by the teenage years. In some patients atopic
eczema persists into adult life or can start for the first time in
Differential diagnosis adulthood. Asthma and hay fever are commonly associated
There are four main causes of erythroderma: with this condition or may be found in first-degree relatives.
• Psoriasis (3.9).
• Eczema (3.10). Clinical presentation
• Drug reaction (3.11). The clinical features include generalized xerosis (dry skin)
• Cutaneous lymphoma (mycosis fungoides) (3.8). and red, itchy, patches and plaques of dry, scaly skin with
overlying excoriations (3.10, 3.12). More chronic disease
Less common causes include pityriasis rubra pilaris and presents with thickening of the skin with accentuation of the
seborrhoeic dermatitis. Clues to the cause include a pre- surface markings (lichenification) (3.12). This is a
existing dermatosis or recent changes of medication. consequence of continual scratching. In patients with darker
Consider lymph node biopsy and CT/MRI imaging if skin there will also be hyperpigmentation at the site of the
lymphoma is suspected. eczema. The distribution usually includes the popliteal and
antecubital fossae but may involve any site (3.12–3.14).
White dermographism is a clue to the diagnosis, being a
white line produced after gentle scratching of the skin.
Palmo-plantar involvement often presents with erythema,
vesicles, scaling, and painful fissures.

Histopathology
Intercellular oedema (spongiosis) is the hallmark of eczema.
Intraepidermal vesicles associated with a lymphocytic
infiltrate are also seen. In more chronic disease, psoriasiform
hyperplasia occurs.

Differential diagnosis
Seborrhoeic and discoid dermatitis need to be considered.
Patch testing is helpful if the history is suggestive of allergic
contact dermatitis. In scabies, which is often complicated by
an infected eczema, look for the presence of burrows,
3.11 Erythrodermic drug reaction from prednisolone. particularly with genital involvement.
 Widespread rashes 37

Management
Emollients should be applied regularly to the dry skin and Coal tar is now less commonly used but remains useful as
used as soap substitutes. Topical steroids are the mainstay of it has anti-inflammatory properties and comes in the form of
treatment and the strength needed varies depending on the pastes, creams, bandages, shampoos, and bath additives.
site, severity, and chronicity of the eczema. Ointments are Bandaging is a useful way to intensify the effect of topical
preferable to creams in the majority of cases where the skin agents while preventing further damage by scratching.
is dry and scaly. Calcinuerin inhibitors are useful alternatives Sedative antihistamines can help patients to sleep at night but
to steroids for facial eczema. They should not be used if are best used intermittently. Cyclosporin is of proven use in
patients get recurrent herpes infections, and patients should severe chronic eczema but is only licensed for short-term use
avoid direct sunlight. Oral steroids are sometimes required in the UK. Phototherapy can benefit patients when used in
for severe flares of eczema and are preferred in short courses. addition to other therapy, but the total lifetime dose is limited.

3.12 Flexural eczema in the popliteal fossae.

3.14 Facial
atopic
eczema.

3.13 Flexural eczema in the cubital fossae.

38 Widespread rashes

Discoid eczema

Introduction Differential diagnosis

Discoid eczema is also known as nummular eczema, which In psoriasis, scale predominates and vesicles are absent; look
simply describes the coin shaped plaques. for clues at other sites such as nail changes or scalp
involvement. In tinea corporis lesions are flatter with a fine
Clinical presentation scale. A skin scraping is often useful (3.16). In primary
Intensely itchy, erythematous, dry, scaly, papules and vesicles impetigo lesions are flat, superficial, and painful rather than
coalesce into well-defined annular plaques, which can be itchy. A skin swab is helpful in guiding treatment (see
several centimetres in diameter. Golden crusting due to Chapter 9).
secondary infection with Staphylococcus aureus is common
(3.15). Lesions typically occur over the legs at first but may be Management
scattered over the trunk, arms, and hands. Excoriations and Discoid dermatitis is typically unresponsive to standard
lichenification may be evident. It is mainly seen in elderly topical corticosteroids. A combination of super-potent
males where it is not associated with atopy and IgE levels are steroid and antibiotic is often needed, and systemic steroids
usually normal. It is also seen in some young adults. are sometimes required in widespread cases. It can run a
chronic course.
Histopathology
The typical eczematous feature, spongiosis, is seen with
acanthosis of the epidermis.

3.15 Discoid eczema on

the arms.

3.16 Tinea corporis on the back.

 Widespread rashes 39

Psoriasis vulgaris

Introduction with a salmon-pink base and overlying silvery scale (3.17,

Psoriasis is a chronic inflammatory condition affecting 2% 3.18). The extensor aspects of the elbows and knees are
of the population. It can have widespread involvement of the frequently affected sites as well as the scalp and lower back
skin, nails, and joints and patients can feel very self- (3.19, 3.20). This common presentation is relatively easy to
conscious about their appearance and constant scaling. diagnose. However, psoriasis can affect other areas of the
skin including face, palms and soles, flexor areas, and nails,
Clinical presentation all showing very different clinical features and making the
Psoriasis occurs in many guises. Chronic plaque psoriasis correct diagnosis more challenging (3.21, 3.22). The clinical
typically produces well-demarcated papules and plaques features and possible differential diagnoses can be seen in

3.18 Widespread
chronic plaque
psoriasis on the
legs.

3.17 Chronic plaque psoriasis on the trunk.

3.19 Scalp psoriasis. 3.20 Perianal and natal cleft psoriasis.

40 Widespread rashes

3.21 Distal 3.22 Localized

interphalangeal pustular
psoriatic psoriasis of
arthritis. Notice the sole of
the psoriatic the foot.
nail changes.

Table 3.1. Clues to the diagnosis include a positive family psoriasis. They remain an important treatment in all types of
history of psoriasis, scalp involvement, and nail changes. psoriasis including erythroderma.
Triggers known to exacerbate psoriasis include trauma Vitamin D analogues are mainly used for chronic plaque
(Koebner’s phenomenon), streptococcal infections psoriasis. They can irritate the skin and should therefore not
(especially in guttate psoriasis), stress, and drugs such as be used in more inflammatory disease. The creams and
beta-blockers, lithium, antimalarials, nonsteroidal anti- ointments do not stain skin or clothes and do not smell,
inflammatory drugs, and ACE inhibitors. Roughly 5% of making this a more acceptable treatment to patients.
patients with psoriasis will develop an associated psoriatic Mild to moderate topical steroids can be used on flexural
arthropathy. There are five different types that may often and facial areas. Moderate to potent steroids can be used on
overlap (Table 3.2). affected areas of the trunk and limbs. Very potent steroids
should be limited to areas on the palms, soles, and scalp.
Histopathology Extensive use of very potent topical steroids may precipitate
In the epidermis, parakeratosis (nuclei retained in the acute generalized pustular psoriasis. Systemic steroids
stratum corneum) and acanthosis (thickening) are seen. should be avoided altogether as they may produce a
Dilated capillary loops are seen in the elongated dermal rebound phenomenon on reducing or stopping treatment.
papillae. A T-lymphocytic infiltrate in the upper dermis and Dithranol is an effective treatment but can stain skin and
epidermis forms microabscesses (of Munro) in the stratum clothing. Low concentrations of 0.1% are used initially as it
corneum. can be an irritant to the skin. Increasing concentrations are
used every few days as tolerated. A short-contact
Differential diagnosis preparation is available for patients to use at home.
Differential diagnoses are listed in Table 3.1. Coal tar preparations have anti-inflammatory properties
and also reduce the scale of psoriasis. Preparations can be
Management made in concentrations from 1–10%. The treatment is
Topical treatments messy and smelly and is generally applied under bandages
Emollients are safe and easy to use. They can sooth and although some ‘cleaner’ preparations are available which are
hydrate the skin and may have an antiproliferative effect in more practical for home use.
 Widespread rashes 41

Table 3.1 Clinical features and differential diagnoses of psoriasis

Clinical features Differential diagnosis

Plaque psoriasis Bilateral, relatively symmetrical involvement commonly Lichen simplex chronicus;
affecting the extensor aspects of elbows, knees, sacrum, tinea corporis; discoid eczema;
and umbilicus. Involvement on any other area may also occur mycosis fungoides

Guttate psoriasis Disseminated small round papules appear over the body, Pityriasis rosea;
often precipitated by a streptococcal tonsillitis secondary syphilis

Flexural psoriasis Red shiny, nonscaly well-defined plaques in the axillae, Candida; intertrigo;
groins, submammary, perineal, and natal cleft areas. tinea cruris; erythrasma
Fissures can be seen deep in the skin folds

Palmo-plantar Acral involvement can be very difficult to differentiate from Palmo-plantar dermatitis;
psoriasis eczema with scaling, erythema, and fissures. Vesicles are palmo-plantar keratoderma
absent in psoriasis

Scalp psoriasis There can be diffuse involvement of the scalp or discrete Seborrhoeic dermatitis;
red plaques with a thick adherent scale scalp eczema; lichen simplex
chronicus

Psoriatic nails Pitting, onycholysis (separation of the nail from the nail bed), Tinea unguium; yeast
hyperkeratosis, and oil spot (yellow-brown spot seen under infection of nail plate
the nail plate) may be seen

Pustular psoriasis This may be localized (e.g. to the palms and soles [3.22]) Pustular drug eruption;
or may be generalized – von Zumbusch. Multiple sterile folliculitis; bullous impetigo
pustules occur in waves. Patients are often very unwell with
a fever and are prone to dehydration, hypothermia, and
sepsis, which may prove fatal

Erythrodermic Erythematous skin involving the majority of the skin. Patients Causes of erythroderma
psoriasis can also be unwell with loss of heat, protein, and fluids from such as: eczema; drug
the inflamed skin reaction; cutaneous lymphoma

Keratolytics such as salicylic acid can be helpful, lamps are used to irradiate the skin several times a week and
particularly for thick scaly scalps, palms, or soles. produce a response that can often be prolonged. PUVA
Tazarotene is a topical retinoid. This can irritate the skin, (ultraviolet A light with oral psoralen) enhances the
especially the flexures, and should be avoided in pregnancy. therapeutic effect of the radiation. Due to the increased risks
of skin cancer, the total amount of phototherapy used in a
Systemic treatments patient’s lifetime is limited. Other side-effects include
Systemic treatments should be reserved for severe, resistant, burning, tanning, and ageing of the skin.
complicated, and unstable psoriasis. Phototherapy can be Methotrexate is an effective and relatively safe treatment.
useful for extensive disease including guttate psoriasis but Once established on treatment patients can continue for
does not help genital or scalp psoriasis. Ultraviolet B (UVB) many years. Side-effects include myelosuppression,
42 Widespread rashes

Table 3.2 Types of psoriatic arthritis

Type Clinical features

Distal interphalangeal joint involvement (3.21) Predominantly the distal interphalangeal joints are affected

Mono- or oligoarthropathy The commonest form associated with psoriasis – asymmetrical

Rheumatoid arthritis-like A symmetrical polyarthritis as seen in rheumatoid arthritis but

the patient is seronegative

Ankylosing spondylitis-like May involve spine and/or sacroiliac joints, with or without
peripheral arthropathy

Arthritis mutilans A rare and destructive arthritis with telescoping of the fingers
and toes due to gross osteolysis

hepatotoxicity, and teratogenicity. Both male and female Scabies

patients should use adequate contraception during, and for
6 months after treatment. Regular monitoring of full blood Introduction
count, liver function tests, and urea and electrolytes should Scabies is an intensely itchy dermatosis caused by the mite
take place throughout treatment. Liver biopsy should be Sarcoptes scabiei. The infestation occurs at all ages, but
considered after a total cumulative dose of 1.5 g has been particularly in children. Scabies is highly contagious and
taken, to rule out liver fibrosis. person-to-person spread occurs via direct contact with the
Cyclosporin is highly effective with a swift onset of action skin. Scabies is transmitted by close personal contact.
but long-term use is limited due to its nephrotoxicity. Infants and children are therefore particularly liable to
Regular monitoring of serum creatinine is required. Other infection. Outbreaks can occur among the elderly in nursing
side-effects include hypertension, which should be homes and can be transmitted to nursing staff. Transmission
monitored, and there is an increased risk of developing between adults is often by sexual contact.
lymphoma with prolonged treatment.
Acitretin is a systemic retinoid and must therefore not be Clinical presentation
used in pregnancy. Its teratogenic risk persists up to 2 years A history of itching in several members of the family over the
after stopping treatment and so is not the treatment of same period is almost pathognomonic. Pruritus is the
choice in women of childbearing age. It flattens down hallmark of scabies, regardless of age. In adults, scabies is
psoriatic plaques particularly when used in conjunction with characterized by intractable pruritus (worse at night) and with
PUVA. Common side-effects include dry lips and hair lesions in the web spaces, fingers, flexor surfaces of the wrists,
thinning. Less commonly, serum triglycerides may become and genital areas. The most common presenting lesions are
raised. These should be monitored along with renal and papules, vesicles, pustules, and nodules. The pathognomonic
liver function. sign is the burrow; a short, wavy, scaly, grey line on the skin
Fumaric acid esters are licensed for use outside the UK. surface. These burrows are most easily found on the hands
They are indicated in severe chronic stable plaque psoriasis. and feet, particularly in the finger web spaces, thenar and
Side-effects include abdominal cramps and diarrhoea along hypothenar eminences, and on the wrists (3.23–3.25). In
with flushing and headaches. These are dose-dependent. men, itchy papules on the scrotum and penis are
Lymphopenia is commonly seen and treatment should be pathognomonic. Definitive diagnosis relies on microscopic
reduced or withdrawn if levels are less than 0.5 × 109/l. identification of mites or eggs from skin scrapings of a burrow.
Hepatotoxicity and nephrotoxicity have been reported.
 Widespread rashes 43

Management
Permethrin 5% dermal cream is the treatment of choice for should not be used in children. Treatment of contacts
scabies in the UK, Australia, and the USA. It is the most should take place on the same days as treatment of the
effective topical agent, is well tolerated, and has low toxicity. patient to avoid reinfection.
Malathion should be used as second choice. Children After successful treatment to kill the scabies mite, itching
should be given aqueous preparations because alcoholic can persist for up to 6 weeks as the eczematous reaction
lotions sting and can cause wheeze. Lindane is less effective settles down. Patients can be treated as for regular eczema
than permethrin. It has been withdrawn in many countries with emollients and topical steroids with or without topical
because of reports of aplastic anaemia and concerns about antibiotics, depending on the clinical presence of secondary
potential neurotoxicity. Benzyl benzoate is irritant and infection with Staphylococcus aureus.

3.23 Scabies rash on the forearm.

3.24 Scabies rash on the back of the hand with

burrows visible in the finger webs.

3.25 Burrows on the palm of the hand.

44 Widespread rashes

Erythema multiforme

Introduction Histopathology
Erythema multiforme (EM) is an acute, self-limiting Typical histological changes include variable degrees of a
mucocutaneous disorder of variable severity and is perivascular lymphohistiocytic inflammatory infiltrate,
commonest in adolescents and young adults. It is usually dermal oedema, and basal cell vacuolation, which can be
divided into major and minor forms. Classically, all forms of very marked, together with keratinocyte necrosis.
EM are thought to represent different points in a spectrum
of disease severity and are simply divided into minor and Differential diagnosis
major depending on whether there is mucosal involvement, Target lesions are characteristic of EM. Among the
when the eponym Stevens–Johnson syndrome is used. differential diagnoses to be considered are: bullous impetigo
(see Chapter 9); primary herpes simplex infection (see
Clinical presentation Chapter 9); immuno-bullous disorders (3.28, 3.29); and
The minor form classically presents with indurated annular cutaneous lupus (see Chapter 6).
lesions with central clearing (target lesions) on the palms Bullous impetigo can be identified by a positive
and soles but these may occur at any site (3.26, 3.27). This microbacterial swab. Herpes simplex virus (HSV) per se or as
often develops following an infectious illness and presents an antecedent trigger for the development of EM is an
little diagnostic difficulty in adults. Lesions appear over important differential diagnosis. If mucosae are involved,
7–14 days and resolve spontaneously. The development of then immunobullous disorders such as pemphigus vulgaris
lesions at the site of prior trauma to the skin (the isomorphic or mucous membrane pemphigoid should be considered.
phenomenon) is well recognized. Immunobullous disorders can be excluded by histo-
The major form implies more extensive skin involvement pathological examination, plus direct immunofluorescence,
and lesions can coalesce with development of central and the presence of circulating anti-epidermal antibodies.
blisters. Mucosal involvement occurs and conjunctival Lupus is excluded not only histologically but, more
involvement may lead to keratitis and corneal ulceration. In importantly, by the absence of antinuclear antibodies and
EM major pulmonary symptoms, often with X-ray changes, antibodies to the extractable nuclear antigens.
are common. These may be attributed to an antecedent
upper respiratory tract infection, typically Mycoplasma Management
pneumoniae. EM is a self-limiting condition and simply needs treating
The two main causes are drugs (including symptomatically. Eye involvement should prompt a referral
sulphonamides, allopurinol, and phenytoin), and infection, to ophthalmology. If the condition becomes recurrent
particularly herpes simplex and mycoplasma. Frequently no secondary to recurrent HSV, then long-term prophylactic
cause is identified. Recurrent EM suggests recurrent aciclovir could be used.
infection with herpes simplex.
 Widespread rashes 45

3.26 Erythema multiforme on the foot.

3.27 Erythema multiforme on the hand.

3.29 Bullous
pemphigoid on
the thigh.

3.28 Widespread bullous pemphigoid on the trunk and

arms.
46 Widespread rashes

Further reading

Johnston GA (2004). Treatment of bullous impetigo and Sladden MJ, Johnston GA (2005). Current options for the
the staphylococcal scalded skin syndrome in infants. treatment of impetigo in children. Expert Opin
Expert Rev Anti Infect Ther 2:439–446. Pharmacother 6:2245–2256.
Johnston GA, Sladden MJ (2005). Scabies: diagnosis and Wakelin SH (2002). Handbook of Systemic Drug Treatment
treatment. BMJ 331:619–622. in Dermatology. Manson Publishing, London.
Lebwohl MG, Berth-Jones J, Coulson IM, Heymann W Walker GJA, Johnstone PW (2000). Interventions for
(eds) (2006). Treatment of Skin Disease: Therapeutic treating scabies. Cochrane Database of Systematic
Strategies for the Dermatologist. (2nd edn). Mosby, Reviews 3:CD000320.
London. DOI:10.1002/14651858.CD000320.
Sladden MJ, Johnston GA (2004). Common skin
infections in children. BMJ 329:95–99.
 Chapter 4 47

Skin tumours
Vishal Madan, MBBS, MD, MRCP and
John T Lear, MD, MRCP

Introduction NONMELANOMA SKIN CANCERS

Tumours in the skin can be conveniently divided into Nonmelanoma skin cancers (NMSC), which include basal
benign or malignant. Recognition of which group a (BCC) and squamous cell cancers (SCC), are the most
particular tumour falls into is paramount. Benign tumours common human cancers. Because of their relatively low
tend to be slow growing, symmetrical lesions (4.1) whereas metastatic rate and relatively slow growth, these are
malignant ones usually grow faster and keep growing and frequently underreported. The high prevalence and the
will expand in a haphazard manner, so will often be frequent occurrence of multiple primary tumours in affected
asymmetrical (4.2). The history and the ABCDE system individuals make NMSCs an important but underestimated
(Chapter 1) of examining tumours will help in making a public health problem.
diagnosis.

4.1 A benign pigmented dermatofibroma on the shin. 4.2 Nodular melanoma of the scalp. This was a rapidly
growing tumour that was asymmetrical and ulcerating and
had a very poor prognosis.
48 Skin tumours

The recognition of premalignant skin lesions and dry, rough, adherent yellow or brownish scaly surface (4.3,
conditions is important, as early treatment may allow 4.4) that are better recognized by palpation than by
prevention of the malignant process. It may also allow for inspection. Diagnosis is usually made clinically. The lesional
these lesions and conditions to be followed carefully and any size varies from 1 mm to over 2 cm and the usual sites of
malignancy that develops may be recognized and treated at involvement are the sun-exposed sites such as the face,
an early stage. This chapter deals with such premalignant scalp, and dorsa of hands of middle-aged or elderly patients.
skin lesions and conditions and the tumours that may Left untreated, these lesions often persist but regression may
develop if these are left undiagnosed or untreated. follow irritation of the individual lesion.

Differential diagnosis
Actinic (solar) keratosis Differentiation from early SCC may sometimes be difficult,
especially for smaller lesions. Other differentials include
Introduction viral warts, seborrhoeic keratoses, and discoid lupus
These are focal areas of abnormal proliferation and erythematosus.
differentiation occurring on chronically ultraviolet (UV)
irradiated skin, and appear as circumscribed, hyperkeratotic Management
lesions carrying a variable but low (0.025–16%) risk of Sun avoidance and sunscreen use should be advised. For
progression to invasive SCC1. Their presence is an limited numbers of superficial lesions, cryotherapy is the
important indicator of excessive UV exposure and increased treatment of choice and gives excellent cosmetic results. If
risk of NMSC. the clinical diagnosis is doubtful, larger lesions can be
Risk factors for the development of actinic keratoses curetted and the specimen can be assessed
include excessive (lifetime) exposure to UV or ionizing histopathologically. Excision is usually not required except
radiation, radiant heat or tanning beds in individuals with where diagnostic uncertainty exists.
fair skin, blond hair, and blue eyes, low latitude, working Topical treatments with 5-fluorouracil cream, diclofenac
outdoors, light skin, history of sunburn, immunosuppressive gel and imiquimod cream3 offer the benefit of treating early
therapy for cancers, inflammatory disorders, and organ lesions and those covering large areas, but with a varying
recipients2. degree of erythema and inflammation. Topical 6-
aminolevulinic acid-based photodynamic therapy, chemical
Clinical presentation peels, cryotherapy, and dermabrasion are other techniques
The lesions are asymptomatic papules or macules with a used in the treatment of actinic keratoses.

4.3 Multiple keratotic lesions on the back of the hands and 4.4 Multiple actinic keratoses on the scalp.
forearms. Most were actinic keratoses and the larger
lesions were intraepithelial carcinomas.
 Skin tumours 49

Intraepithelial carcinomas
(IEC, Bowen’s disease)

Introduction Differential diagnosis

Also known as squamous cell carcinoma in situ, these are Conditions from which Bowen’s disease must be
usually solitary, slowly enlarging erythematous lesions on differentiated include lichen simplex, psoriasis, and actinic
sun-exposed and nonexposed sites, with a small potential for keratoses.
invasive malignancy. UV irradiation is an important cause,
especially in white populations. Arsenic exposure (ingestion Management
of trivalent inorganic arsenic) seems important in the As with actinic keratoses, the treatment options include
development of lesions in populations consuming destructive measures like curettage and cautery, cryotherapy
contaminated water4. Radiation and viral agents have also and surgical excision for larger lesions; delayed wound
been implicated, although a combination of these factors healing following destructive treatments may be an issue.
may be involved in some patients. Topical treatments include 5-fluorouracil and imiquimod.
Topical 5-aminolaevulinic acid-based photodynamic
Clinical presentation therapy (ALA-based PDT) is also an established treatment
Lower legs of elderly women are most frequently involved. for Bowen’s disease.
Individual lesions are asymptomatic, discrete, slightly scaly,
erythematous plaques with a sharp but irregular or
undulating border (4.5). Hyperkeratosis or crust may
sometimes form, but ulceration is a marker of development
of invasive cancer (4.6). Actinic damage of the surrounding
skin is usually present.

4.5 Intraepithelial carcinomas on the leg. 4.6 IEC developing features of invasion – ulcerating
granulation tissue appearance with hyperkeratosis.
50 Skin tumours

Cutaneous horn Disseminated superficial actinic

porokeratosis
Introduction
Cutaneous horns (cornu cutaneum) are uncommon lesions Introduction
consisting of keratotic material resembling that of an animal Disseminated superficial actinic porokeratosis (DSAP) is an
horn. These may arise from a wide range of benign, uncommon autosomal dominant chronic disorder of
premalignant, or malignant epidermal lesions. keratinization, characterized by multiple superficial
keratotic lesions surrounded by a slightly raised keratotic
Clinical presentation border. SCC development within lesions of porokeratosis
The diagnosis is made clinically. The lesion is a hard yellow- has been described, as has its association with immuno-
brown horn that occurs typically in sun-exposed areas, suppression. Sun exposure and immunosuppression are
particularly the face, ear, nose, forearms, and dorsum of known triggers to the development of these lesions, which
hands (4.7). Even though over 60% of cutaneous horns are are also inherited as an autosomal dominant trait.
benign, the possibility of skin cancer should always be kept
in mind5; inflammation and induration indicate malignant Clinical presentation
transformation. The lesions appear on sun-exposed areas as slightly raised
keratotic rings, which expand outwards, with the skin within
Differential diagnosis the ring being atrophic and hyperpigmented.
The primary diagnosis may be a viral wart, molluscum
contagiosum, keratoacanthoma, actinic or seborrhoeic Differential diagnosis
keratosis. The outward expansion and sharp rim of the lesion
distinguish it from other skin lesions (4.8).
Treatment
Although the underlying disorder may be clinically evident, Management
surgical excision and histopathological analysis are indicated Cryotherapy with liquid nitrogen is the standard treatment
to rule out any malignant transformation. although 5-fluorouracil is also used.

4.7 A cutaneous
horn. The
presence of a
marked shoulder
at the base of the
horn can be a sign
of malignancy.

4.8 Disseminated superficial actinic porokeratoses

on the leg.
 Skin tumours 51

Erythroplasia of Queyrat Radiation-induced keratoses

Introduction Introduction
Erythroplasia of Queyrat is a carcinoma in situ that mainly Chronic diagnostic, therapeutic, or occupational radiation
occurs on the glans penis, the prepuce, or the urethral exposure may result in radiodermatitis, radiation-induced
meatus of elderly males. Up to 30% progress to invasive keratoses, or radiation-induced malignancy. Ionizing
squamous cell carcinoma. The condition usually occurs in radiation used in the treatment of internal malignancies,
fair-skinned individuals but may also occur in dark subjects. cutaneous malignancies, benign skin tumours, or benign
Human papilloma virus infection has been implicated. inflammatory dermatoses may induce radiation keratoses.
Although histologically indistinguishable from Bowen’s The potential for malignant change is proportional to the
disease, clinically and epidemiologically this is a separate radiation dose.
entity.
Clinical presentation
Clinical presentation Chronic radiodermatitis, which usually precedes the
The commonest site of involvement is the glans penis of development of radiation keratoses, produces cutaneous
uncircumcised men, although it may also occur on the shaft features similar to those of chronic sun exposure (4.9).
or scrotum or vulva in females. The lesion is a solitary, Radiation-induced keratosis has morphological and
sharply defined, discrete, nontender, erythematous plaque histopathological similarities to actinic keratosis, although
with erosive or slightly scaly surface (see Chapter 7). elastotic changes and vascular obliteration may be more
marked in radiation keratosis.
Differential diagnosis
Erythroplasia of Queyrat must be differentiated from Management
psoriasis, eczema, lichen planus, Zoon’s balanitis, fixed drug The available treatment options include curettage,
eruption, and extramammary Paget’s disease. electrodessication, and excision.

Management
To prevent functional impairment and mutilation of the
vital structure, treatment modalities of choice include 5-
fluorouracil, imiquimod, and microscopically controlled
surgery (Moh’s). Progression to invasive SCC is the norm in
untreated cases.

4.9 Radiodermatitis.
52 Skin tumours

Arsenical keratoses

Introduction UV radiation is the major aetiological agent in the

These are arsenic-induced corn-like keratoses, most pathogenesis of BCC. However, though exposure to UV is
commonly occurring over the palms and soles. The lesions essential, its relationship with risk is unclear and
may progress to SCC in 5% or less of the patients. Exposure epidemiological studies suggest its quantitative effect is
to arsenicals may be industrial, medicinal, or from modest. Recent studies suggest that intermittent rather than
consumption of contaminated well water. In addition to cumulative exposure is more important7. The relationship
arsenic-related skin diseases including keratosis, Bowen’s between tumour site and exposure to UV is also unclear.
disease, BCC, and SCC, there is also an increased risk of The distribution of lesions does not correlate well with the
some internal malignancies. area of maximum exposure to UV in that BCCs are
common on the eyelids, at the inner canthus, and behind the
Clinical presentation ear, but uncommon on the back of the hand and forearm.
Numerous corn-like areas of hyperkeratosis occur over the Thus, though exposure to UV is critical, patients develop
palmar and/or plantar skin. In addition to these lesions, BCC at sites generally believed to suffer relatively less
patients may have other cutaneous manifestations of chronic exposure. The basis of the different susceptibility of skin at
arsenicosis, including macular hyperpigmentation, multiple different sites to BCC development is not known.
superficial BCC, and Bowen’s disease. Inflammation, The concept of genetic susceptibility to BCC is complex
induration, rapid growth and ulceration signify malignant as genes may influence susceptibility as well as tumour
transformation. numbers, rate of appearance, and site. Candidate genes may
be selected from those involved in DNA repair, defence
Differential diagnosis against oxidative stress, immune modulation, tanning, and
Viral warts, Darier’s disease, lichen planus, and familial other related biochemical activities. Some of the better
punctate palmar/plantar keratosis may cause diagnostic studied genes include p53, cytochrome P450s (CYP),
difficulties. CYP2D6, and glutathione S-transferases (GST) with the
GSTM1 null genotype predisposing to BCC, probably due
Management to its role in defence against UV-induced oxidative stress8,9.
Keratolytic ointments, cryotherapy, curettage, and oral Somatic and germ line mutations in PTCH gene and
acitretin have their advocates. Periodic examination for disrupted expression of the human homologues of Hh (sonic
cutaneous or visceral malignancies should be performed. hedgehog; SHH), Ptc (PTCH and PTCH2), Smo (SMOH),
and Ci (GLI) have been demonstrated in BCC
tumourigenesis.
Basal cell carcinoma
Clinical presentation
Introduction Nodular BCC
This is the most common malignant tumour affecting This is the most common clinical variant, representing
humans. The low malignant and metastatic potential of this approximately 60% of all BCC. The lesion is a translucent,
tumour makes it an underestimated health problem, pink or red, well-defined papule or nodule with surface
although the associated morbidity can be significant. The telangiectasia (4.10). As the lesion enlarges, ulceration may
incidence of BCC continues to rise and the age of onset has occur which may then be diagnosed as nodulo-ulcerative
decreased, owing to habits and lifestyles leading to increased variant, or may slowly progress to reach a large size
sun exposure. The incidence is increasing by ~10%/year destroying the underlying tissue, an appearance that is
worldwide, indicating that the prevalence of this tumour will referred to as ‘rodent ulcer’ (4.11). Even with larger
soon equal that of all other cancers combined6. destructive lesions, the diagnosis can be made by examining
Furthermore, 40–50% of patients with one or more lesions the ulcer edges which are elevated, translucent and
will develop at least one more within 5 years. telangiectatic (4.12). Variable amounts of pigmentation may
be present which may be confused with melanocytic lesion.
 Skin tumours 53

Superficial BCC
This variant is more commonly seen over truncal skin. The indurated feel; the lesion is ivory coloured with the presence
lesion is flat, erythematous or pink, with an irregular outline of superficial telangiectasia (4.14). Ulceration is uncommon
and thread-like margin (4.13). Surface scale, central atrophy and recurrence rate after treatment high.
and pigmentation may be additional features.
Cystic BCC
Morphoeic or sclerodermiform BCC In addition to the above-mentioned common variants of
As suggested in the name, the lesion resembles a plaque of BCC, cystic degeneration of the BCC may occur which may
morphoea. The dense underlying fibrosis gives the lesion its give the lesion its blue-grey cystic appearance (4.15).

4.10 Nodular
BCC.

4.11 A small rodent ulcer (nodulo-ulcerative BCC) on the

lower eyelid.

4.12 A large rodent ulcer of the scalp. 4.13 A superficial BCC on the back.
54 Skin tumours

Squamous cell carcinoma

Introduction
SCC is the second commonest skin cancer after BCC. Early
diagnosis and treatment of SCCs are important to avoid
metastasis and tissue destruction as these cancers are more
invasive and have a higher metastatic spread compared to
BCCs.
Although ultraviolet radiation is the most important risk
factor in the genesis of both SCCs and BCCs, there is a
proportionately greater effect of increasing sun exposure on
the risk of developing SCC. Chronic irritation,
inflammation, and injury to the skin can predispose to
4.14 A morphoeic BCC. malignant SCC. Examples include complicated scars from
frostbite, electrical injury, chronic sinuses or fistulas,
chronic osteomyelitis, chronic stasis dermatitis, and scars
following various cutaneous infections. The most often
reported dermatoses complicated by cancer are discoid
lupus erythematosus, scarring variants of epidermolysis
bullosa, genital lichen sclerosus et atrophicus, its variant
balanitis xerotica obliterans, and lichen planus.
Photochemotherapy (PUVA) increases the risk of
developing SCC and this correlates with the cumulative
dose of ultraviolet A. As discussed above, arsenic is an
important chemical carcinogen implicated in the
development of SCC; patients who have received a renal
transplant have a 50 to 250-fold increased risk of developing
this tumour. Various syndromes are associated with SCC
development, including xeroderma pigmentosum, albinism,
4.15 A BCC with blue-grey cystic degeneration and Muir–Torre syndrome, KID (keratosis, icthyosis, deafness),
telangiectasia. and Werner syndrome.
As with BCC, several candidate susceptibility genes have
been identified in the pathogenesis of SCC. Amongst others
Management these include p53, p63, RAS, CDKN2A, and MC1R.
Various tumour characteristics dictate the choice of therapy. Human papilloma virus infection, immunosuppression, and
These include tumour site, size, clinical subtype, and the DNA repair enzyme defects are other mechanisms which
ability to define tumour margins. Patients’ age, coexisting appear to play an active role in SCC pathogenesis.
medical problems, and previous treatments are also
important. Destructive therapies include curettage and Clinical presentation
cautery, cryotherapy, lasers, surgical excision, and Moh’s SCC usually develops on sun-exposed sites on the
micrographic excision. Moh’s excision is the treatment of background of photodamaged skin; the most common sites
choice for recurrent, morphoeic, large and nodular BCCs are back of hands, upper face, lower lip, and pinna. The skin
with ill-defined margins and for lesions at high-risk sites like around the lesion has signs of photodamage and the lesion
nasolabial folds, nose, and periocular regions. Photo- itself may be a nodule, plaque, or an ulcerated and tumid
dynamic therapy and imiquimod are newer modalities area (4.16–4.18). A common feature of all SCC lesions is
which have been explored in the management of BCC with induration, which is usually the first sign of malignancy. The
promising results. margins of the tumour are ill defined, indicating spread
 Skin tumours 55

beyond the visible limits. Not uncommonly, the lesion is Management

papillomatous with a superficial adherent crust. Ulcerated As with BCCs the choice of treatment depends upon the
or eroded tumour is revealed on removal of the crust. tumour and patient characteristics. Complete excision or
destruction of the primary tumour and prevention of
Differential diagnosis metastasis is the aim of treatment, which for smaller (<1 cm)
Keratoacanthomas (4.19) are self-healing lesions which and slow-growing well-differentiated tumours may be
resemble SCCs clinically and histologically. They are best accomplished using destructive therapies like cryotherapy,
excised, as the diagnosis is often difficult to make. curettage, cauterization, and laser ablation. For larger
lesions (>1cm), surgical excision is the standard treatment.
Moh’s micrographic surgery is the treatment of choice for
high-risk tumours.

4.16 Ulcerating 4.17 SCC of

SCC of the side the scrotum.
of the nose.

4.18 Ulcerating SCC of the shin. 4.19 Keratoacanthoma of the forehead.

56 Skin tumours

MELANOMA AND MELANOMA PRECURSORS

The incidence of melanoma continues to rise, perhaps due to especially large ones, may be asymmetric and irregular, with
the emphasis on early recognition and diagnosis. As the varying pigmentation and may therefore simulate
leading killer skin disease, early diagnosis is critical as it melanoma. The lesions are classified depending upon the
influences survival. For patients with thin (0.75 mm) primary size: those less than 1.5 cm are called small, 1.5–19.9 cm
melanoma, the 5-year survival rate is nearly 100%; 5-year medium, and those 20 cm or more in greatest diameter are
survival for those with advanced disease at diagnosis is known as giant CMNs. Patients with large lesions are at an
extremely poor. Clearly therefore, early diagnosis of this skin increased risk of developing melanomas although the risk
tumour cannot be stressed enough. At present the only avail- varies with size, depth of penetration, surface features, and
able effective tool for early diagnosis of melanoma is clinical homogeneity of the lesions.
evaluation and identification of thin or early melanomas using
the ABCDE system (Asymmetry, Border irregularity, Colour Management
variegation, and Diameter ≥6 mm Enlargement). Most CMNs do not progress to melanomas; therefore,
Most early melanomas have: routine excision of these lesions is not indicated. Treatment
• Asymmetry – the two halves of the lesion are not similar. of these lesions is tailored for the individual patient, with
• Border irregularity – most melanomas have irregular careful consideration of the pros and cons of anaesthesia,
borders. surgery, and postoperative cosmetic considerations.
• Colour variability – variegation in colour within the lesion Prophylactic excision of large lesions with atypical features,
is noted in most melanomas. This however, may not be nodularity, or thickening should be considered.
true in amelanotic melanomas.
• Diameter – most melanomas are identified when they Dysplastic (Clark’s) naevus
reach a diameter of ≥6 mm. Introduction
• Enlargement – malignant tumours continue to grow. Dysplastic naevi are markers of increased risk of
development of malignant melanoma. These are acquired,
Melanomas arise either from pre-existing melanocytic pigmented, clinicopathological entities which develop de
lesions (30%) or normal skin (70%). novo or from CMNs and represent disordered proliferation
of atypical melanocytes. There is increasing evidence that
suggests that families and individuals with multiple
Melanoma precursors dysplastic naevi are prone to developing malignant
melanoma, and that this may be due to a dominantly
Congenital melanocytic naevi (CMN) inherited gene. Several candidate susceptibility genes for
Introduction melanoma and dysplastic naevi have been described
These are pigmented lesions present at birth although a few including tumour suppressor gene p16/cyclin dependent
(tardive) may appear later in life. These lesions may be kinase 2A, oncogene CDK4, and a tumour suppressor gene
precursors of malignant melanoma, regardless of their size. p19. Defective DNA repair systems for UV-induced DNA
The lesions form between the fifth and twenty-fourth week damage and microsatellite instability are other mechanisms
of gestation. The dysregulated growth of melano- thought to be responsible for the genesis of these lesions.
blasts/melanocytes occurs as a result of error in the
neuroectoderm. Also, the melanoblasts’ migration to the Clinical presentation
leptomeninges and integument is dysregulated. The clinical distinction between dysplastic naevus and
malignant melanoma can be very difficult. The lesions are
Clinical presentation round, oval or ellipsoid macules usually ≥5 mm with
CMNs are homogenous brown pigmented lesions with well indistinct margins and are brown, tan, pink, or red in colour
demarcated borders, mammilated surface and, sometimes, with colour variegation (4.23–4.27). Unlike CMNs, these
hypertrichosis (4.20–4.22). Although most congenital develop later in life and do not undergo spontaneous
melanocytic lesions are regular and symmetric, some, resolution.
 Skin tumours 57

Management
This remains challenging and for lesions that are changing histopathological analysis and help in the identification of
in size, colour, shape, and pigmentation pattern, is usually early malignant melanomas. Patients with familial and
excision. Photographs of the lesions and, in cases of multiple sporadic dysplastic naevi should be followed regularly at 3
naevi, the whole body, should be taken for surveillance, and 6 monthly intervals, respectively. Sun avoidance should
which may reduce the need for excision of lesions for be advised and sunscreen use advocated.

4.20 Melanoma developing in a 4.21 Large bathing trunk congenital 4.22 Melanoma and in-transit
congenital melanocytic naevus melanocytic naevus. secondaries in a large CMN.
of the ankle.

4.23 Dysplastic naevus. 4.24 Halo naevus, papillomatous naevus with surrounding
local anaesthetic and 4 junctional naevi on the back.
58 Skin tumours

4.25 Halo naevus. These are benign lesions where the 4.26 Meyerson’s naevus – a benign mole surrounded by
mole disappears leaving a depigmented patch. eczematous inflammation.

4.27 A compound melanocytic naevus. 4.28 An early lentigo maligna.

Lentigo maligna (melanoma in situ)

Introduction
This is the precursor lesion of lentigo maligna melanoma.
The same factors are involved as described for malignant
melanoma and dysplastic naevi.

Clinical presentation
Lesions are always present on sun damaged skin of older
patients, with a slow progression to lentigo maligna
melanoma. The individual lesion is a flat, brown-black
macule of variable size, with irregular but sharply defined
borders, on a background of sun damaged skin (4.28, 4.29).
4.29 A more extensive lentigo maligna.
 Skin tumours 59

Management Malignant melanoma

Factors such as site and size of lesion and patient
comorbidities influence the treatment modality undertaken. Superficial spreading melanoma
Surgical excision is the treatment of choice to obtain clinical The commonest form comprising 70% of all melanomas.
and histological clearance, but many other modalities have This presents as a uniformly elevated dark brown to black
been used with variable success. Moh’s micrographic plaque with marked variegation in colour (4.30–4.32) and
surgery is associated with the lowest recurrence rate at may be associated with regional lymphadenopathy. Usual
4–5%, but conventional surgery, cryotherapy, and sites of occurrence include the upper back and legs.
radiotherapy also yield good results, with recurrence rates in
the order of 7–10%10. Other options include laser ablation
and topically applied imiquimod.

4.30 A superficial spreading melanoma with surface

ulceration.

4.31 Dermatoscopic findings of 4.30.

4.32 Superficial spreading melanoma with regression.

60 Skin tumours

Nodular melanoma Acral lentiginous melanoma

The second most common form of malignant melanoma. These are more common in brown-skinned individuals. It
This form tends to involve the dermis at a relatively early involves the palms, soles, finger or toenail bed, and
stage, in contrast to others that tend to remain confined to mucocutaneous skin of the mouth, genitalia, or anus.
the epidermis. The lesion differs from other variants in being On the palm and sole skin, these appear as irregularly
a uniformly dark blue, brown, or black coloured nodule with pigmented slow growing macules (4.36, 4.37), which later
smooth margins and a rapid progression (4.33, 4.34). develop papules or nodules in the vertical growth phase.
The subungual lesions involve the nail matrix and extend to
Lentigo maligna melanoma cause nail ulceration and eventual destruction as a result of
This lesion develops from lentigo maligna. In contrast to involvement of the nail bed and nail plate (4.38, 4.39).
lentigo maligna, which is a uniformly flat macule, this is a
flat patch or macule with focal areas of papules or nodules
and variegation in colour (4.35).

4.33 An early nodular melanoma. 4.34 A nodular melanoma with a poor prognosis.

4.35 A lentigo maligna melanoma and a coincidental 4.36 An acral lentiginous melanoma.
senile comedone.
 Skin tumours 61

Desmoplastic melanoma Verrucous melanoma

This is an uncommon histological variant of melanoma, Verrucous naevoid malignant melanoma is a recently
with a dermal fibroblastic component and a high incidence described variant of malignant melanoma that may be
of local recurrence and nodal metastases, requiring early confused both clinically and histologically with SCC or
aggressive surgery. It is most commonly seen on sun- benign exophytic lesions11. It is considered as a variant of
damaged skin of the head and neck. The lesions may be superficial spreading melanoma characterized by an
variegated lentiginous macules or a dermal nodule. Absence exophytic papilliferous growth pattern.
of pigmentation commonly leads to a delay in diagnosis.

4.37 A more advanced acral lentiginous melanoma.

4.38 An acral 4.39 An acral

lentiginous lentiginous
melanoma in situ melanoma of the
of the nail bed. thumb with
Hutchinson’s sign
(proximal spread
of pigmentation).
62 Skin tumours

Differential diagnosis Table 4.1 Margins recommended in the excision of

Differential diagnosis of malignant melanoma includes: malignant melanoma lesions
haemangioma, pyogenic granuloma, pigmented seborrhoeic
wart, and senile comedone (4.40–4.43).
Breslow thickness Margin
Management of melanoma In situ 0.2–0.5 cm
Surgical excision with margins based on Breslow thickness <1 mm 1 cm
forms the cornerstone of treatment of malignant melanoma. 1–2 mm 1–2 cm
The British Association of Dermatologists in their published 2.1–4 mm 2–3 cm
guidelines for management of patients with malignant >4 mm 2–3 cm
melanoma12 recommends the margins listed in Table 4.1 to
be included in the excision of malignant melanoma lesions.
At present, sentinel lymph node biopsy is a staging and
prognostic tool. Adjuvant therapy in the form of followed, every 2–3 months for the initial 3 years, for signs
chemotherapy, immunotherapy, or vaccine therapy may be of recurrent disease. Finally, patients should carry out
considered for patients with thick primary tumours and regular skin self-examinations and they should be
positive lymph nodes as these have a high risk of recurrent encouraged to use sunscreens and other sun avoidance
disease. Patients with primary melanomas should be closely measures.

4.40 Thrombosed haemangioma. 4.41 Pyogenic granuloma of the finger tip.

4.42 Benign seborrhoeic keratosis. 4.43 Senile comedone.

 Skin tumours 63

References

1 Glogau RG (2000). The risk of progression to invasive 8 Lear JT, Heagerty AH, Smith A, et al. (1996). Multiple
disease. J Am Acad Dermatol 42:23–24. cutaneous basal cell carcinomas: glutathione S-
2 Lebwohl M (2003). Actinic keratosis: epidemiology and transferase (GSTM1, GSTT1) and cytochrome P450
progression to squamous cell carcinoma. Br J Dermatol (CYP2D6, CYP1A1) polymorphisms influence tumour
149 (Suppl 66):31–33. numbers and accrual. Carcinogenesis 17:1891–1896.
3 Lee PK, Harwell WB, Loven KH, et al. (2005). Long- 9 Lear JT, Smith AG, Heagerty AH, et al. (1997).
term clinical outcomes following treatment of actinic Truncal site and detoxifying enzyme polymorphisms
keratosis with imiquimod 5% cream. Dermatol Surg 6: significantly reduce time to presentation of further
659–664. primary cutaneous basal cell carcinoma. Carcinogenesis
4 Tseng WP, Chu HM, How SW, et al. (1968). 18:1499–1503.
Prevalence of skin cancer in an endemic area of chronic 10 Stevenson O, Ahmed I (2005). Lentigo maligna:
arsenicism in Taiwan. J Natl Cancer Inst 40:453–463. prognosis and treatment options. Am J Clin Dermatol
5 Copcu E, Sivrioglu N, Culhaci N (2004). Cutaneous 6:151–164.
horns: are these lesions as innocent as they seem to be? 11 Blessing K, Evans AT, al-Nafussi A (1993). Verrucous
World J Surg Oncol 2:18. naevoid and keratotic malignant melanoma: a clinico-
6 Karagas MR, Greenberg ER (1995). Unresolved issues pathological study of 20 cases. Histopathology
in the epidemiology of basal cell and squamous cell skin 23:453–458.
cancer. In: Skin Cancer: Mechanisms and Human 12 Roberts DL, Anstey AV, Barlow RJ, et al. (2002).
Relevance. H Mukhtar (ed). CRC Press, Boca Raton, British Association of Dermatologists; Melanoma Study
Florida, pp. 79–86. Group. UK guidelines for the management of cutaneous
7 Kricker A, Armstrong BK, English DR, Heenan PJ melanoma. Br J Dermatol 146:7–17.
(1995). Does intermittent sun exposure cause basal cell
carcinoma? A case-control study in Western Australia.
Int J Cancer 60:489–494.
 Chapter 5 65

Hand and foot dermatoses

John SC English, MRCP

Introduction

The commonest dermatosis of the hands and feet is vesicles, dryness, cracking, and hyperkeratosis? Looking for
dermatitis or eczema (the two terms are synonymous), but signs of skin disease elsewhere is useful especially in
other inflammatory conditions must be differentiated (Table establishing a diagnosis of psoriasis. It could be that the
5.1). As with all other parts of the skin the distribution, patient has a chronic fungal infection of the hands and then
configuration, and morphology of the rash are helpful they are likely to have fungal infection of their feet. The feet
pointers in making a diagnosis. Is the rash all over the hands should always be examined in conjunction with the hands.
or feet, or just on one? Are the lesions confluent or discrete
and what is the morphology of the lesions? Are there
Hand and foot dermatitis

Table 5.1 Conditions affecting the hands and feet Introduction

The patterns of hand dermatitis can be divided into four
groups (Table 5.2). Dermatitis predominantly affects the
• Dermatitis backs of the hands, the fingers, the palms, or the whole
• Psoriasis hand. Hand eczema can be divided into either allergic,
• Pustular psoriasis irritant, or endogenous, or a mixture of all three (5.1).
• Fungal infections
• Infestation
• Other inflammatory dermatoses

Table 5.2 Patterns of hand eczema

Dorsa of hands Fingers Palms Whole hand

ICD ICD ACD ACD
ACD ACD ICD ICD
Endogenous eczema Endogenous eczema Endogenous eczema

ACD, allergic contact dermatitis; ICD, irritant contact dermatitis

66 Hand and foot dermatoses

Clinical presentation
Infection Infection Irritant contact dermatitis (ICD)
Endogenous
Irritant dermatitis of the hands tends to affect the finger
webs and the backs of the hands, but can affect the palmar
Atopic
surface (5.2–5.4). It is due to a direct toxic effect of exposure
to irritant substances. The commonest causes are soaps,
detergents, solvents, and occlusive effect of rubber gloves.
Allergic Irritant
Almost any chemical given enough exposure can be irritant,
even water. Friction can also play a role in causing
dermatitis. It is much more common than allergic contact
dermatitis (ACD). ICD is not so common on the feet, as
shoes are worn and this tends to cause occlusion and
Infection sweating. Juvenile plantar dermatosis of the feet is probably
an irritant effect of drying out of sweaty feet after wearing
5.1 The various causes of hand eczema. occlusive trainers (5.5).

5.2 ICD affecting the finger webs and back of the hand. 5.3 ICD of the palmar aspect of the fingers.

5.5 Juvenile plantar

dermatoses.

5.4 ICD discoid pattern affecting the back of the hand.

 Hand and foot dermatoses 67

Allergic contact dermatitis

The pattern of ACD is variable; predominantly vesicles will rubber (5.11–5.13). However, patients can be allergic to the
usually be present, especially on the palmar surface, and any glues, which often can contain rubber and therefore may get
part of the hand can be affected (5.6–5.10). ACD of the feet a pattern that can affect any part of the foot (5.12).
can affect the dorsal or plantar surface. The dorsal surfaces However, even with careful examination of the hands and
are often associated with leather allergy and the plantar feet it is frequently not possible to tell whether sensitization
surface with rubber allergy, due to the fact that leather on has occurred (5.14) and therefore patch testing is strongly
the insoles of shoes tends to be vegetable tanned and not recommended (see Chapter 1).
chromium tanned, and the soles usually tend to be made of

5.6 ACD from isopropyl phenyl phenylenediamine in

bicycle tyres.
5.7 ACD from epoxy resin paint.

5.8 ACD from epoxy resin. 5.9 ACD from

Notice periungual vesicles methylchloroisothi-
and nail dystrophy (see zolinone in a liquid
Chapter 8). soap.
68 Hand and foot dermatoses

5.10 ACD from thiurams in rubber gloves mimicking ICD 5.11 ACD from chromium-tanned leather.
pattern of dermatitis.

5.12 ACD from mercaptobenzothiazole in a shoe lining.

5.13 ACD from mercaptobenzothiazole in rubber

soles. Notice the weight-bearing area of the foot
is affected.

5.14 ACD from imidazolidinyl urea mimicking endogenous

hyperkeratotic hand eczema.
 Hand and foot dermatoses 69

Endogenous eczema
Endogenous eczema can have any pattern and affect any One variety of endogenous eczema is that of recurrent
part of the hands or feet. It is a diagnosis made on exclusion, pompholyx of the palms and soles, which may well be
with negative patch tests and no history of irritant exposure. associated with bacterial infection (5.15–5.17).

5.16 Infected foot eczema.

5.15 Vesiculo-bullous hand eczema reaction

(id reaction) from infected foot eczema.

5.17 Chronic infected endogenous

hand eczema.
70 Hand and foot dermatoses

Differential diagnosis Prognosis

Table 5.3 highlights the features that help to distinguish The prognosis is not always good with allergen avoidance in
between ICD and ACD. Elicitation of the aetiology of hand ACD patients. Some allergens, especially potassium
dermatitis rests more on a detailed history and the results of dichromate through cement or Compositae plant allergens
patch tests than on the clinical distribution or the pattern of (chrysanthemums and dandelions), can cause a chronic
the hand eczema. dermatitis leading to suffering for many years. Otherwise
exposure elimination will usually ‘cure’ a patient of hand
Management eczema, especially if the allergen is easily avoidable such as
Allergen avoidance is advised if allergens have been epoxy resin (5.7, 5.8). The prognosis for irritant dermatitis
identified through patch testing. If ICD has been diagnosed, can also be bad if exposure reduction cannot be achieved.
then exposure reduction to the irritants is key to the Often patients will have continued exposure to irritants in
management of ICD. With endogenous eczema topical the home, rather than workplace. Once the dermatitis has
steroids and emollients would be the treatment of choice, broken out it is difficult to get it healed. Endogenous eczema
possibly with antibiotics if infection was thought to be can run a protracted course, and sensitization to medica-
playing a part. Emollients and topical steroids would also be ment allergens or other allergens can, of course, occur.
used for ACD and ICD. Treatments other than topical steroids would be hand and
foot PUVA for resistant cases and even systemic immuno-
suppressants such as azathioprine and cyclosporin. Topical
immunomodulators (calcineurin inhibitors) are not
particularly effective as it is difficult for the large active
molecules to penetrate the stratum corneum of the palms
and soles.

Table 5.3 Characteristics of irritant and allergic contact hand dermatitis

ICD ACD
Lesions Oligomorphic with redness, scaling, chapping Polymorphic with redness, papules, vesicles,
crusts, exudation, erosions, lichenification
Demarcation Patchy, relatively clear Diffuse, tendency to spread (face, wrist, axillae,
genitals)
Localization Fingertips, fingerwebs, dorsum of the hand, Interdigital, fingers, palmar and dorsal side
ball of the thumb
Course Chronic, aggravation by climate changes, Relapsing, healing in weekends and holidays
wet work, detergents, gloves
Epidemiology More persons affected in same work One person affected in same work environment
environment
Patch testing Negative, positive – nonrelevant Relevant positive, negative – allergen missed
 Hand and foot dermatoses 71

Psoriasis

Introduction Clinical presentation

Unfortunately patients sometimes develop a hyperkeratotic Psoriasis of the palms or soles (5.20, 5.21) tends to present
condition of the hands (5.18, 5.19), often without signs of with painful cracking rather than itching or bleeding.
psoriasis elsewhere. There is usually no vesiculation and it is Friction is an important cause of koebnerization of psoriasis
mainly a painful cracking of the skin that they complain of. of the palms and soles.
Friction plays an important part in this. Psoriasis can affect
just the palms and soles; however, if one carefully looks
elsewhere, one sometimes finds evidence of psoriasis.

5.18 Palmar 5.19 Palmar

psoriasis. psoriasis.

5.20 Psoriasis of the toes. 5.21 Psoriasis of the instep of the foot.
72 Hand and foot dermatoses

Differential diagnosis Fungus infection

Hyperkeratotic hand dermatitis or tylotic eczema shows
hyperkeratotic plaques, centrally located in both palms, with Introduction
a tendency to painful fissures (5.22). The histopathology Fungus infection of the feet is extremely common; up to
reveals a slight focal parakeratosis and hyperkeratosis, with a 5–10% of the population have fungus infection of the toe
spongiotic dermatitis rather than acanthosis and extended webs, spreading on to their plantar surface and the dorsal
rete ridges. It is a separate entity, which has to be aspect of the feet. Fungus infection of the hands is less
differentiated from psoriasis. It is usually far itchier than common and tends to be more asymmetrical.
palmar psoriasis. Familial palmar keratodermas can present
in adulthood and are differentiated by the family history Clinical presentation
(5.23). Fungal infection of the hands presents with dryness and
scaling, usually unilateral (see Chapter 9, 5.24, 5.25). With
Management fungus infection of the feet the nails will often be involved.
Topical steroids, including potent topical steroids, often A spreading ringworm-like infection to the dorsum of the
under polythene occlusion, are necessary to help palmar foot (5.26), or dry moccasin-form of fungal infection
psoriasis and plantar psoriasis. Use of emollients helps to affecting the soles can be seen.
prevent fissuring.
Differential diagnosis
Prognosis The differential diagnosis includes psoriasis, hyperkeratotic
Psoriasis of the palms and soles does not respond as well as hand eczema, or even ICD. Table 5.4 lists the differences
dermatitis to topical steroids and the prognosis is usually between psoriasis, fungus infection, and eczema of the hand.
worse. Second-line treatment such as oral retinoids or Scrapings of the skin should be sent for mycological
topical PUVA are often necessary. examination and culture.

Management
If fungus infection has been diagnosed, then topical
terbinafine will usually be effective. If it has been a very
chronic problem and also affects the nails, then oral
terbinafine would be needed.

5.22 Hyperkeratotic hand eczema. 5.23 Familial palmar keratoderma.

 Hand and foot dermatoses 73

Prognosis
It is easy to be caught out by fungus infections of the hands;
if there is asymmetrical scaling then a fungus infection must
be thought of and scrapings for mycology taken.
Providing the fungus responds to terbinafine then the
prognosis is good and clearance will occur. However, if it is
a resistant case then further courses of terbinafine will be
needed.

5.24 Fungal infection of the palm.

5.25 Note the unilateral presentation of this rash with nail 5.26 An active edge of fungal infection of the skin of the
involvement. Tinea manum. back of the foot.

Table 5.4 The differences between hand psoriasis, tinea manum and hand eczema

Psoriasis Tinea manum Hyperkeratotic hand eczema

Not usually itchy Can be itchy Itchy
Painful fissuring Sometimes fissuring Painful fissuring
Dry silvery scale Usually dry, scaly Vesicular, scaly
Well-defined lesions Active edge on back of hand More diffuse lesions
Nail and knuckle involvement Nails often involved Nails not involved
Koebner phenomena
74 Hand and foot dermatoses

Palmo-plantar pustulosis Differential diagnosis

Vesicular hand eczema and fungus infection are the
Introduction differential diagnosis. It is sometimes difficult to make the
This is a variant of psoriasis, a localized form of pustular diagnosis of palmo-plantar pustulosis if there is
psoriasis affecting the palms and soles. Probably less than predominantly a vesicular component to it.
10% of patients with palmo-plantar pustular psoriasis will
have signs of psoriasis elsewhere. Management
Potent, or very potent topical steroids under polythene
Clinical presentation occlusion are usually necessary to gain some control.
It presents with localized vesicles and pustules on the palms
and soles which can be very painful; patients often liken it to Prognosis
walking on broken glass (5.27–5.29). In the early phase Prognosis is often poor, with palmo-plantar pustulosis
sometimes the pustules are not so obvious, but they usually running a prolonged course; however, if control can be
fade to leave brown spots. achieved then hopefully, it will remain clear for a long period
of time. Further treatment options include oral retinoids
and local hand/foot PUVA.

5.27 Palmar 5.28 Close-up

pustular psoriasis of 5.27 showing
– not vesicular there are
hand eczema! pustules.

5.29 More obvious plantar pustular psoriasis.

 Hand and foot dermatoses 75

Miscellaneous conditions affecting the

hands and feet

A variety of inflammatory dermatoses can affect the hands. the first place to look when one suspects scabies, as the
The commonest include lichen planus, granuloma annulare burrows are more visible here than elsewhere (see Chapter
(see Chapter 2) and bullous pemphigoid (see Chapter 3) 3). Crusted scabies can cause a diagnostic problem on
(5.30–5.32). Rarer dermatoses such as dermatomyositis and occasion, especially when it is very severe (5.35). Scabies
vasculitis are also seen (5.33, 5.34). Scabies commonly infestation is very easily caught from these patients.
affects the finger webs and hands and feet, and this is often

5.30 Lichen 5.31 Granuloma

planus of the annulare on the
wrist spreading back of the hand
to the palm. mimicking a
Wickam striae fungal infection
can be seen on or ICD.
the wrist lesions.

5.33
Dermatomyositis
(Gottron’s
papules) on the
knuckles and
over the
interphalangeal
joints.

5.32 Vesiculobullous eruption of bullous pemphigoid.

76 Hand and foot dermatoses

5.34 An area of necrosis and haemorrhagic vesicles on

the sole of a foot due to small vessel thrombosis in a
patient with phospholipid syndrome.

5.35 Norwegian scabies in an elderly

patient from a nursing home.

Further reading

Menne T, Maibach H (eds) (2001). Hand Eczema (2nd

edn). CRC Press, Boca Raton, Florida.
English JSC (ed) (1999). A Colour Handbook of
Occupational Dermatology. Manson Publishing, London.
 Chapter 6 77

Facial rashes
Paul Farrant, MRCP and
Russell Emerson, MD, MRCP

Introduction

Facial rashes cause cosmetic embarrassment to patients and • Vesicles/milia/cysts: vesicles are seen with herpetic
are an important source of anxiety. The face is involved in infections. Milia are common but may be a feature of
many different diseases because it contains numerous porphyria. Cysts are common on the face and can occur
sebaceous glands and is constantly exposed to the in isolation (epidermoid, pilar) or as part of an acneiform
environment. This chapter describes the common eruption.
dermatological diseases and an approach to differentiating • Swelling: periorbital swelling is seen with angio-oedema
them from each other. (urticaria), dermatomyositis, and rosacea. Swelling and
redness of one cheek are seen with erysipelas. Acute
contact dermatitis often causes localized itching and
History swelling which becomes dry or scaly, whereas
urticaria/angio-oedema does not.
It is important to take a thorough history of the presenting • Pigmentation: macular pigmentation on the cheeks is
skin complaint and exposure to external factors including suggestive of melasma. The face is also a common site for
ultraviolet light (UV), cosmetic products, prescribed topical simple lentigo, lentigo maligna, and seborrhoeic
creams, and systemic therapies. This should include a keratoses.
medical history and enquiry about other medical symptoms • Atrophy/scarring: discoid lupus is associated with
including muscle weakness, joint pains, and past history of scarring. Atrophoderma vermiculatum, a facial variant of
skin problems. Table 6.1 lists the clinical features of common keratosis pilaris, causes atrophy over the cheeks.
facial rashes.
• Scale: rashes with associated scale suggest psoriasis A stepwise approach to the management of patients with
(silvery-white), seborrhoeic dermatitis (greasy, yellow), erythema/scaling and papules/pustules is seen in 6.1 and
eczema, contact dermatitis, or possibly a fungal infection. 6.2, respectively.
• Pustules and papules: acne, rosacea, perioral dermatitis,
folliculitis and pseudo folliculitis barbae. Multiple small
papules on the cheeks are seen in tuberous sclerosis and
polymorphic light eruption following UV exposure.
78 Facial rashes

Table 6.1 Clinical features of facial rashes

Skin erythema and scaling Vesicles/bullae

• Seborrhoeic dermatitis • Herpes simplex/zoster
• Atopic eczema • Erysipelas
• Tinea • Erythema multiforme
• Psoriasis • Pemphigus
• Keratosis pilaris
Pigmentation
Papulo-pustular • Melasma/chloasma
• Rosacea • Solar lentigines
• Acne • Drug-induced
• Adenoma sebaceum • Lentigo maligna
• Polymorphic light eruption • Poikiloderma of Civatte
• Rare: sarcoidosis, granuloma faciale

Erythema/scaling

No scarring Scarring

Chronic DLE
No photosensitivity Photosensitivity

No systemic Systemic No systemic

symptoms symptoms symptoms

Nasolabial folds or Itchy Systemic LE Muscle Papules,

scalp involved skin Subacute LE weakness pustules

Seborrhoeic Atopic eczema Dermatomyositis Rosacea

dermatitis Contact dermatitis Polymorphic
Psoriasis Fungal infection light eruption
(no pustules)

6.1 Management of erythema and scaling.

 Facial rashes 79

Papules/pustules

Central face Perioral Unilateral

Comedones No comedones Perioral dermatitis Painful

Acne vulgaris Telangiectasia Itchy Herpes simplex or zoster

Rosacea Contact dermatitis

Polymorphic light
eruption

6.2 Management of papules and pustules.

Acne

Introduction
Acne is a disorder affecting the pilosebaceous unit
associated with excess grease production of the skin,
keratinization of the opening of the hair follicle, and
inflammation due to bacterial infection with
Propionibacterium acnes that may result in scarring.

Clinical presentation
Acne typically presents with open comedones (black heads),
closed comedones (white heads), papules, pustules, and
cystic lesions (6.3). The face, upper chest, and upper back
are most commonly affected. Macrocomedones and scarring
(both pitted and hypertrophic) are also features. A particular
variant, acne excoriée, is characterized by marked
excoriations on the face and is typically seen in young
women (6.4).

Histopathology
Perifollicular inflammation with a predominance of 6.3 Inflammatory acne with numerous
neutrophils is seen. The hair follicles are often dilated, and papules, pustules, and comedones.
filled with keratin. Rupture of the follicles can result in a
foreign body reaction.
80 Facial rashes

Differential diagnosis Perioral dermatitis

Folliculitis, rosacea, and perioral dermatitis can all mimic
acne on the face. Acne-like conditions can also be Introduction
precipitated by drugs (e.g. antiepileptics), topical and oral Perioral dermatitis typically affects young women in the
corticosteroids, oils applied to the hair line (pomade acne), 20–35-year-old age group. It is a variant of rosacea and may
and exposure to various chemicals (e.g. chloracne). be precipitated by inappropriate use of moderate/potent
topical corticosteroids.
Management
Most acne will clear spontaneously by the mid twenties. Clinical presentation
Mild acne can be managed by topical agents, applied daily It is characterized by small erythematous papules around the
for 3–6 months. These include benzoyl peroxide (first line, mouth and chin (6.5A). The area immediately adjacent to
good for noninflammatory acne), topical antibiotics the vermillion border is usually spared. There may also be
(erythromycin, clindamycin), and topical retinoid related periorbital involvement. Comedones are not a feature.
drugs (tretinoin and adapalene). Combinations of these
agents can also be used, for example benzoyl peroxide in the Differential diagnosis
morning and a retinoid in the evening. Acne vulgaris, steroid acne, rosacea, and seborrhoeic
Moderate acne is best managed with systemic antibiotics dermatitis are the main differentials.
in addition to topical agents. These again require 3–6
months of treatment to achieve long-term clearance. These Management
include oxytetracycline, lymecycline, erythromycin, and Patients should be advised to stop the application of topical
trimethoprim. corticosteroids and placed on a 2–4 month course of oral
For unresponsive cases or severe acne associated with tetracycline antibiotics (6.5B). Topical tacrolimus and
scarring, specialist referral is indicated. Such patients may pimecrolimus may also be beneficial for flares.
require a 4–6 month course of oral isotretinoin. This
achieves clearance in 85% of patients. Frequent side-effects
include dryness of the lips, mucous membranes, and skin. It Rosacea
should be avoided in pregnancy and patients may require
monitoring of their liver function and lipids. Any change in Introduction
mood or tendency to depression during treatment should Rosacea is a common cause of facial redness in the 25–55-
lead to cessation of therapy. year-old age group, especially women.

Clinical presentation
Many patients have a history of flushing exacerbated by
trigger factors including spicy foods, temperature changes,
and alcohol. Facial redness typically occurs with small
papules and occasional pustules (6.6, 6.7). The
inflammatory changes typically affect the cheeks and naso-
labial folds. Fixed redness may develop associated with
superficial blood vessels (telangiectasia) and rarely
sebaceous hyperplasia leads to an enlarged nose
(rhinophyma) (6.8). Up to 15% of patients may have
associated eye involvement presenting as conjunctivitis,
keratitis, blepharitis, and cyst formation along the eyelid
margin. Comedones are typically absent in rosacea.

6.4 Acne excoriée with typical inflamed scarred lesions

over the forehead.
 Facial rashes 81

A B
6.5 Perioral dermatitis before (A) and after (B) successful treatment with an oral 6.6 Papular lesions on the cheeks,
tetracycline. nose, and chin with no evidence of
comedones is typical of rosacea.

6.8 Rhinophyma
6.7 Severe rosacea of the forehead requires is often
systemic treatment. associated
with rosacea.

Histopathology Management
A mixed lympho-histiocytic perifollicular infiltrate may be Patients should avoid trigger factors. Mild cases can be
present. In addition, there may be a perivascular infiltrate or managed with topical metronidazole gel. More severe
granulomatous response. These changes are nonspecific. cases (6.7) require courses of systemic tetracyclines for
There may also be vascular dilatation, solar elastosis, and 2–4 months. Many patients experience disease relapses and
sebaceous gland hyperplasia indicating solar damage. patients should be informed that it might be a chronic
condition. Severe cases may need a specialist opinion and
Differential diagnosis low-dose oral isotretinoin can be beneficial. Patients with
Rosacea should always be suspected in patients with facial rhinophyma and telangiectasia may benefit from skin
redness and papules. Other causes of flushing and erythema surgery and laser therapy, respectively.
include eczema, seborrhoeic dermatitis, systemic lupus
erythematosus, and the carcinoid syndrome.
82 Facial rashes

Atopic eczema Contact dermatitis

Introduction Introduction
Facial eczema commonly affects adults with severe eczema Facial eczema can develop due to a number of external
and can be a presenting feature of allergic contact allergens including perfume, nail varnish, preservatives in
dermatitis. cosmetic creams, nickel in jewellery, and plants. Typically,
this occurs as a delayed type IV allergy and patients require
Clinical presentation referral to a dermatologist for specialist investigation with
In infants the cheeks are a common site to be involved, with patch testing (see Chapter 1).
an ill-defined, red, scaling rash that is symmetrical. Episodes
of infection are common and weeping and crusting are both Clinical presentation
common in this context. In adults, eczema can be either The sudden onset of facial eczema in a patient with no
generalized (6.9, 6.10), or more localized to specific areas previous history of skin problems should raise suspicion of
such as the skin around the eyes and mouth. Lichenification contact allergy. Contact dermatitis is more frequently seen
of the skin may be present around the eyes (6.11). in individuals with eyelid dermatitis (perfume/nail varnish)
(6.12), localized ear involvement (topical medicaments used
Histopathology for otitis externa/nickel in ear rings), and scalp involvement
See Chapter 3. (hair dyes). A detailed clinical history is useful in
pinpointing the onset of the symptoms, exacerbating factors,
Differential diagnosis and improvement following avoidance, but patch testing is
The main differential diagnosis is contact dermatitis and all usually necessary to identify the cause.
patients with facial eczema should be considered for patch
testing to look for a contact allergen. Seborrhoeic dermatitis Histopathology
and psoriasis may also cause confusion. The pathological features are similar for other types of
eczema. Eosinophils may be more conspicuous and
Management Langerhans cells, when stained with S100, are more
Soap and irritants should be avoided and emollients should numerous.
be applied frequently. Treatment consists of topical steroids
and/or topical calcineurin inhibitors. The skin on the face is Differential diagnosis
particularly susceptible to the side-effects of topical steroids Atopic eczema, seborrhoeic dermatitis, and psoriasis should
and treatment should be carefully monitored. Mild steroids be considered.
(1% hydrocortisone) should be used initially and cream may
be more cosmetically acceptable to patients. Moderate Management
steroids may be necessary but used for limited periods of Patients with suspected contact allergy should be advised to
time (clobetasone butyrate, aclometasone dipropionate). stop all cosmetic products, use unperfumed soaps, and
Steroids should not be used continuously and there should apply regular moisturizers. Topical corticosteroids may be
be regular breaks from their use. They should not be used necessary for disease flares. Specialist referral for patch
on the eyelids. The calcineurin inhibitors, tacrolimus testing is usually indicated to identify the culprit allergen or
ointment and pimecrolimus cream, are very useful on the allergens.
face as they do not cause thinning of the skin.
 Facial rashes 83

6.9 Ill-defined 6.10 Sub-acute

erythema with facial eczema.
lichenification of
the inner canthus
is typical of
chronic atopic
eczema.

6.11 Localized atopic eczema causing lichenification of

the eyelids.

6.12 Contact dermatitis caused by nail varnish often causes

B
a rash on the eyelids (A) and neck (B).
84 Facial rashes

Seborrhoeic dermatitis Psoriasis

Introduction Introduction
Seborrhoeic dermatitis is a chronic condition that typically The face can be involved in patients who have psoriasis, but
produces redness and pronounced scaling around the naso- often this is limited to the hairline.
labial folds and hair-bearing areas of the skin. There is an
association with HIV infection, Parkinson’s disease, and Clinical presentation
stress. The exact aetiology is unknown although Pityro- Psoriasis usually produces isolated red plaques on the
sporum ovale, a skin commensal, is thought to play a role. forehead, outer cheeks, and naso-labial folds. It usually has
a sharply marginated border with a silvery-white scale
Clinical presentation (6.14A). It rarely occurs in the absence of psoriasis at other
Infants present with thick yellow scales on the scalp – ‘cradle body sites and careful examination should be made looking
cap’. In adults, there is an erythematous rash with thick for fine scaling and redness at other sites including the
scale (6.13) that has a predilection for the eyebrows, hairline (6.14B), ears, and elbows. Sometimes patients
nasolabial folds, glabella, and scalp (dandruff and present with a clinical picture of psoriasis and seborrhoeic
erythema). It can occur in the beard and moustache areas. dermatitis – sebo-psoriasis (6.14C).
There may also be involvement of the external auditory
meatus, upper trunk, axillae, and groin. Histopathology
See Chapter 3.
Histopathology
The pathological findings are nonspecific but typically there Differential diagnosis
is spongiosis, hyperkeratosis, parakeratosis associated with Seborrhoeic dermatitis and contact dermatitis should be
the hair follicles, and exocytosis of neutrophils. considered.

Differential diagnosis
Psoriasis can mimic seborrhoeic dermatitis and may even
coexist (sebo-psoriasis). Dermatophyte infection may also
cause a red scaly rash, but tends to be asymmetrical and has
an active scaly border. Skin scrapings may be necessary to
rule out fungal infection if in doubt.

Management
Many patients experience a chronic disease with remission
and relapses. Therapy is aimed at disease suppression and at
reducing yeast overgrowth of the skin, thought to contribute
to the disease process. Topical imidazoles may be used alone
or in combination with mild topical steroids to treat
associated inflammation (1% hydrocortisone). Keto-
conazole/selenium sulphide shampoos may be used in dilute
form to control scalp dandruff and washed gently into
affected areas of the body. More potent steroids may be
required in more resistant cases and pimecrolimus/tacro-
limus are of benefit in persistent disease.

6.13 Localized scaling of the eyebrows and naso-labial

fold with ill-defined erythema is suggestive of seborrhoeic
dermatitis.
 Facial rashes 85

A
6.14 A: Psoriasis often has a sharp border
with prominent silvery-white scale, but
often the only facial involvement is an
extension on to the forehead from the
scalp (B) or overlap with seborrhoeic
dermatitis (C), so called sebo-psoriasis.

Management
Patients should be advised to apply regular emollients, avoid
soaps, and apply topical steroids (1% hydrocortisone and
clobetasone butyrate) on a once/twice daily basis when
disease is active. Tacrolimus and pimecrolimus may be
useful for more chronic persistent disease. Severe cases
(6.15) may benefit from phototherapy or systemic therapy,
particularly if there is more extensive involvement of other
body sites.

6.15 The face is often spared in psoriasis but disease flares

may lead to a severe facial rash.
86 Facial rashes

Melasma

Introduction Management
Melasma is an acquired pigmentation that typically occurs High-factor sunscreens are necessary for all patients
on the cheeks and is associated with oral contraceptives and complaining of melasma and should be applied on a daily
hormone replacement therapy. It can also occur during basis all year round. Spontaneous resolution may be seen in
pregnancy. Extensive sun exposure is a common feature in melasma induced by pregnancy/hormonal therapy.
the patient’s history. Depigmentating creams (containing hydroquinone 2–4%)
may be prescribed for more resistant cases on a twice-daily
Clinical presentation basis for 4–6 months (6.16B).
Melasma presents as a uniform brown macular area of
increased pigmentation usually over the cheeks (6.16). It
often affects both cheeks and is very well demarcated. Lupus erythematosus

Histopathology Introduction
There is an increase in the amount of melanin in Lupus erythematosus is an autoimmune disorder with
keratinocytes, as well as an increase in epidermal frequent involvement of the skin and photosensitivity. There
melanocytes and dermal melanophages. Solar elastosis is is a spectrum of disease, which includes discoid lupus
usually present in the papillary dermis. (DLE), subacute cutaneous lupus (SCLE), and systemic
lupus erythematosus (SLE).
Differential diagnosis
Postinflammatory hyperpigmentation should be considered. Clinical presentation
Patients with cutaneous DLE usually present with well-
defined patches of redness, atrophy, pigmentary disturbance,

A B
6.16 Melasma before (A) and after (B) treatment with hydroquinone.
 Facial rashes 87

and follicular plugging of hair follicles (6.17, 6.18). The Differential diagnosis
most common sites include the cheeks, bridge of the nose, Isolated plaques of DLE may resemble psoriasis,
ears, neck, and scalp. Scalp involvement is frequently seborrhoeic dermatitis, contact dermatitis, tinea (6.21),
observed and a scarring alopecia may develop (see Chapter Jessner’s (6.22), and lupus vulgaris. The facial butterfly rash
8). In other forms of lupus, the patient typically has systemic of SLE is rare and may be confused with rosacea, which is
symptoms including tiredness and joint pains. In systemic common. The majority of patients with systemic or
lupus, the erythema tends to be more widespread on the face subacute lupus feel systemically unwell.
with a typical malar ‘butterfly’ flush (6.19). In subacute
cutaneous lupus, there are multiple erythematous plaque- Management
like lesions, which may be annular and resemble psoriasis Patients with cutaneous lupus require specialist referral and
(6.20). All forms of cutaneous lupus are aggravated by UV management. All patients with lupus should be advised to
light exposure. avoid direct sun exposure and use high factor (>SPF30)
UVA/UVB sunscreens. DLE lesions usually respond to
Histopathology potent topical corticosteroids, which control inflammation
In cutaneous lupus there is intense inflammation of the and reduce the incidence of permanent scarring. More
basal layer of the skin associated with a dermal perivascular severe cases need oral antimalarial therapy with
and perifollicular lymphocytic infiltrate. Basement hydroxychloroquine. In SLE and more resistant cases,
membrane thickening may occur along with pigmentary immunosuppressive drugs may be required.
incontinence. In DLE there may be marked hyperkeratosis,
dilated hair follicles, keratin plugging, and epidermal
atrophy.

6.17 Erythematous
scarring of the ear
with follicular
plugging and
atrophy.

6.18 Chronic scarring DLE of the face.

88 Facial rashes

6.19 Severe facial rash of SCLE. 6.20 Annular scaly erythematous

plaques in SCLE.

6.21 Tinea facei. This should be included 6.22 Jessner’s benign lymphocytic
in the differential for lupus and psoriasis infiltrate affecting the chest. There is
on the face. no scaling and the lesions tend to
disappear after a few weeks.
 Facial rashes 89

Dermatomyositis Tuberous sclerosis

Introduction Introduction
This rare autoimmune disorder can cause a facial rash, This autosomal dominant condition is associated with a
together with papules over the knuckles (Gottron’s papules), number of cutaneous features, one of which occurs on the
and proximal myopathy. A third of adult cases are associated face – adenoma sebaceum. In addition to this, patients may
with underlying internal malignancy. There is no association have periungual fibromas (see Chapter 8), ash leaf macules,
with malignancy in the childhood variant. and a connective tissue naevus known as a ‘shagreen patch’.
Eye and neurological features are also common.
Clinical presentation
The classical appearance on the face is a purple, periorbital, Clinical presentation
oedematous rash, known as the heliotrope rash (6.23). The Multiple, small, skin-coloured papular lesions that coalesce
forehead, cheeks, and neck may also be involved, together to form a cobbled appearance (6.25) occur on the cheeks,
with Gottron’s papules, erythema on the extensor surface of naso-labial folds, and chin from early childhood. 50% will
the arms, nail fold telangiectasia (6.24), and muscle have some angiofibromas by 3 years of age.
weakness (proximal myopathy).
Management
Management Other clinical features of tuberous sclerosis should be
Patients with suspected dermatomyositis should be referred sought and the diagnosis confirmed. Genetic counselling
for a specialist opinion and further investigation. Systemic should be offered to parents planning a family. The facial
therapy with oral prednisolone and other systemic lesions can be removed by a number of surgical means for
immunosuppressive agents is usually required for several cosmetic purposes.
months.

6.23 Periorbital 6.24 Prominent

oedematous vessels of nail
rash of folds in
dermatomyositis dermatomyositis.
(heliotrope rash).

6.25 Erythematous papules associated

with adenoma sebaceum.
90 Facial rashes

Keratosis pilaris Further reading

Introduction Ashton R, Leppard B (2004). Differential Diagnosis in

Keratosis pilaris is a common disorder of keratinization Dermatology. Radcliffe Publishing, Oxford.
affecting the hair follicles of Caucasian children and young Cunliffe WJ, Strauss J, Gollnick H, Lucky AW (2001).
adults. It most commonly affects the outer aspect of the Acne: Diagnosis and Management. Taylor & Francis,
arms (6.26) but has two forms that can affect the face, London.
ulerythema ophryogenes and atrophoderma vermiculatum. Du Vivier A (2002). Atlas of Clinical Dermatology. Churchill
Livingstone, Oxford.
Clinical presentation Lowe NJ (2003). Psoriasis: A Patient’s Guide. Taylor &
In ulerythema ophryogenes there is involvement of the Francis, London.
eyebrows, with redness, hairloss and prominent keratin at Mckee PH, Calonje E, Granter SR (2005). Pathology of the
the site of hair follicles. Skin. Mosby, Philadelphia.
Atrophoderma vermiculatum is a rare variant of keratosis Wolff K, Johnson R, Suurmond R (2005). Fitzpatrick’s
pilaris, affecting the cheeks (6.27), causing a honeycomb, Colour Atlas and Clinical Synopsis of Dermatology.
atrophic appearance, with prominent keratotic papules and McGraw-Hill, New York.
a background erythema.

6.26 Keratosis pilaris typically affects the outer 6.27 Keratosis pilaris on the outer cheeks.
aspects of the arms.
 Chapter 7 91

Genital and oral problems

Sheelagh M Littlewood, MBChB, FRCP

Introduction Lichen sclerosus

Genital and oral disease is often regarded as a difficult Introduction

subspeciality. There are several reasons for this. Firstly, the Lichen sclerosus (LS) is a chronic inflammatory condition
appearance of dermatoses on genital skin may be very which tends to produce scarring that preferentially affects
‘nonspecific’ and the characteristics of disease seen the genital area. It is 6–10-fold more prevalent in women.
elsewhere may be absent in this area. It is important, The aetiology is unknown, but a strong association with
therefore, to search for clues to diagnoses of diseases of oral autoimmune disease is recognized. Occasionally, the disease
and genital skin on nonmucosal surfaces. can be asymptomatic and found purely by chance. However,
Many diseases of the genital area result in scarring that the vast majority of patients complain of pruritis and
would not be expected to occur in nongenital disease. This soreness. In men, the condition only affects the
results in a ‘common end-stage’ appearance of shiny, uncircumcised. It can be asymptomatic but tends to
smooth, featureless scarred tissue with little evidence of the produce not only itching and burning, but also bleeding,
original underlying disease, but could equally represent, for blistering, sexual dysfunction, and difficulties with urination
example, lichen sclerosus or lichen planus. when the urethral meatus is involved.
As the area is moist, occluded and subjected to friction
and chronic irritation from urine and faeces, it is an Clinical presentation
excellent environment for infection and this often In either situation the classical features are pallor and
complicates other disease processes. It is important to atrophy as demonstrated by a wrinkling of the skin and
remember that patients often attribute disease in the genital textural change, plus an element of purpura, erosions,
area to poor hygiene and as a result overwash the area, fissuring, telangiectasia, hyperkeratosis, bullae, or
adding an irritant dimension to an already complex picture. hyperpigmentation. Atrophy results in loss of the labia
Many doctors and most patients are not familiar with the minora and burying of the clitoris, and pseudocysts of the
normal variation in the anatomy of this area and have little, clitoral hood from adhesions can occur.
or no, experience of normal appearances in an The introitus can be significantly reduced and perineal
asymptomatic patient. This can result in misdiagnosis and involvement produces a classic figure-of-8 shape, extending
unwarranted anxiety. around the anus (7.1–7.4). The histopathology can be very
distinctive and can be useful in differentiating the condition
from lichen planus, lichen simplex, and cicatricial
pemphigoid. Typical findings are epidermal atrophy,
hydropic degeneration of the basal layer, hyperkeratosis with
follicular plugging, oedema, and homogenization of collagen
in the upper dermis with an inflammatory infiltrate below.
The dermis shows sparse elastic fibres with swollen collagen
92 Genital and oral problems

fibres, dilatation of blood vessels, and extravasation of red Management

blood cells. There is often localized or diffuse squamous First-line treatment is now recognized as ultra-potent
hyperplasia which may be the result of chronic scratching, topical steroids, 0.05% clobetasol propionate, for 3 months
but equally can indicate malignant transformation. There initially. It is important to advise on avoiding irritants, and
should be a low threshold for biopsy, sometimes repeatedly, the use of bland emollients and soap substitutes. Previous
of hyperkeratotic suspicious areas to exclude squamous cell treatments such as topical testosterone have been shown to
carcinoma (SCC). be ineffective. Surgery is not indicated for uncomplicated
disease but is useful for complications such as introital
narrowing and removal of pseudocysts. The disease runs a
chronic course and the development of SCC is well
recognized, with an incidence of 4–5%. Topical tacrolimus
has also been used but its place has yet to be fully
determined.

7.1 Perianal LS.

7.2 Juvenile LS. 7.3 Nongenital LS on the leg. 7.4 Extensive LS with petechiae and
marked scarring.
 Genital and oral problems 93

Lichen planus

Introduction The latter two are typically very painful and run a chronic
Lichen planus (LP) is an inflammatory dermatosis that is relapsing course. More than one type can exist at any time
believed to account for 1% of new cases seen in dermatology and can affect the buccal mucosa, lateral border of the
outpatients. Typical skin lesions are violaceous, itchy, flat- tongue, and gingiva.
topped papules (7.5). The aetiology of LP is unknown, but
it is believed to be an autoimmune disease. It can affect the Genital LP
skin or mucous membranes or both simultaneously. LP can affect the perigenital skin with a classic presentation
of violaceous flat-topped papules (7.7). It can also affect the
Clinical presentation mucosal side of the labia, where it typically produces a
Oral LP glazed erythema, which bleeds easily on touch and tends to
Oral LP is one of the commoner conditions seen in oral erode, hence the term ‘erosive LP’. The early glazed
medicine clinics. The prevalence ranges from 0.5% to 2.2% erythema is very nonspecific and is difficult to diagnose
with a slightly higher prevalence in women. correctly as it can resemble a number of other inflammatory
There are three classes of clinical disease: diseases. However, LS tends to affect the outer aspect of the
• Reticular, which is a net or plaque-like area which is often labia minora, as opposed to LP, which affects the inner. In a
painless and is seen in about 20% of patients with typical typical case of mucosal LP, the erythema is bordered by a
cutaneous lichen planus (7.6). white, occasionally violaceous border, which can be an
• Erosive/atrophic, in which erythematous areas of thinned important diagnostic clue. If present then this is the ideal
but unbroken epithelium occur. This includes the place to biopsy. However, it is often absent resulting in
gingival condition of desquamative gingivitis. diagnostic difficulty. One should always examine the mouth
• Ulcerative lesions, in which the epithelium is broken. and other cutaneous sites, and look for evidence of vaginal
disease, as this can be very helpful in making the diagnosis.

7.5 Polygonal flat-topped papules of 7.6 Lace-like Wickham striae of the 7.7 Chronic LP of the anogenital area
LP on the wrist. Wickham striae are buccal mucosa. with hyperpigmentation and gross
easily seen. scarring.
94 Genital and oral problems

The erosive form of genital LP can be associated with a Zoon’s balanitis

similar condition in the mouth, the vulvo-vaginal-oral
syndrome. Introduction
In males, LP tends to present with classical itchy, Zoon’s balanitis is a condition affecting middle-aged and
violaceous papules, but has a particular tendency to produce older uncircumcised men. It is believed to be an irritant
annular lesions (7.8). Occasionally an erosive form is seen in mucinitis produced by the particular environment
males, with mucosal lesions and red erosive changes on the associated with the presence of a ‘dysfunctional foreskin’.
glans and shaft. This can result in a scarring process similar
to that in the vulva, resulting in a phimosis. The differential Clinical presentation
diagnosis would include psoriasis, Zoon’s balanitis, LS, and It presents as an indolent, asymptomatic, well-demarcated,
erythroplasia of Queyrat. glistening, shiny red or orangey patch on the glans or
The classical histology consists of basal epidermal mucosal prepuce (7.9). There is no involvement of the
damage, colloid bodies, pigmentary incontinence, epidermal penile shaft or foreskin. There is often purpura and
acanthosis, hypergranulosis, and a dense band-like haemosiderin resulting in so-called cayenne pepper spots.
lymphocytic infiltrate below a saw toothing of the rete The lesions can be solitary or multiple. Histology is that of
ridges. However, the mucosal erosive form loses many of epidermal attenuation, diamond- or lozenge-shaped basal
these characteristics and in contrast tends just to show an cell keratinocytes, and spongiosis. There may be ulceration
attenuated thinned epidermis, parakeratosis, and large or erosion and a band of plasma cells in the dermis. It is
numbers of plasma cells. sometimes called plasma cell balanitis, but the presence of
plasma cells is not diagnostic as they can be present in many
Management mucosal conditions. The differential diagnosis includes LP,
Treatment is with an ultra-potent topical steroid. Erosive psoriasis, fixed drug eruption, secondary syphilis,
disease tends to run a chronic course, although occasional erythroplasia of Queyrat, and a Kaposi sarcoma.
patients go into remission. Other treatment options include
systemic steroids, methotrexate, hydroxychloroquine, and Management
oral retinoids, particularly in hypertrophic cases. There does Attention to hygiene, topical steroids, with or without
seem to be an increased risk of malignancy although the antibiotics, should be the first line of treatment. However, if
degree of this is uncertain. the condition persists or relapses then circumcision is the
treatment of choice.

7.8 Annular LP
of penis.

7.9 Zoon’s balanitis.

 Genital and oral problems 95

Zoon’s vulvitis Autoimmune bullous diseases

Introduction Introduction
A similar condition affecting the vulva has been described, Pemphigoid, cicatricial pemphigoid, and pemphigus can
but is a much rarer entity in women and there is doubt as to affect the oral and genital areas (7.11, 7.12).
its existence. Typically, the lesions resemble those in males
with well-circumscribed, glistening, orangey erythema, Clinical presentation
sometimes with cayenne pepper spots, which can affect any Bullous pemphigoid mainly affects the elderly; occasionally
area of the vulva (7.10). The symptoms vary and the children have genital involvement. Typically, it presents
histology is similar to that in the male. Many cases are with tense bullae which can arise from normal or
thought to represent LP. erythematous skin. Histology shows subepidermal bullae
and direct immunofluorescence IgG at the basement
membrane.
7.10 Zoon’s In cicatricial pemphigoid the changes on histology and
vulvitis. immunofluorescence are identical to pemphigoid, but the
clinical presentation varies, in that it tends to affect mucous
membranes more frequently with resultant scarring.
Pemphigus shows an intraepidermal blister on histology
with IgG in the intracellular spaces. It affects younger
patients and pemphigus vulgaris often presents with oral
lesions in the form of extensive ulceration.
In the mucosal areas, intact blisters are seldom seen. In
the absence of blisters elsewhere, or a history of blistering,
the diagnosis can be difficult to make. The clinical
presentation tends to be painful erosions and scarring, and
in the mouth erythema and erosion of the gingiva. The
differential diagnosis lies between all the bullous diseases as
well as LP and LS and requires biopsy for histology as well
as normal skin for immunofluorescence.

7.11 Perianal cicatricial pemphigoid. 7.12 Oral ulceration due to cicatricial pemphigoid.
96 Genital and oral problems

Malignant lesions

Introduction Clinical presentation

Dysplasia affecting the vulva is referred to as vulval VIN lesions can vary from skin coloured, red or white
intraepithelial neoplasia (VIN), and on the penis, penile papules and plaques to hyperpigmented lesions which are
intraepithelial neoplasia (PIN). VIN is further divided into commonly multiple and multifocal (7.13). The larger single
categories I–III, depending on the degree of involvement of plaques can be pink, scaly, or eroded. Any nonhealing
the epidermis. However, most of the information and work persistently eroded lesion on the genitalia should be
refer to full thickness dysplasia, or VIN III. biopsied.
In the past, there have been many terms used to describe In men, there can be a similar pink or reddish plaque, or
varying clinical appearances for what is now all regarded as eroded patches. A rarer form developing on the glans has a
VIN III. Other than as a clinical description there is no slow-growing, skin-coloured plaque which is scaly and may
justification for this. The incidence of VIN has increased eventually involve the entire glans penis, becoming thick and
markedly in the last 25 years, mainly in younger women and crusted. This has been termed pseudoepitheliomatous
it is strongly associated with sexually transmitted disease, keratotic and micaceous balanitis. Over time this may
smoking, and the presence of cervical intraepithelial develop into a frank low-grade SCC (7.14).
neoplasia (CIN). There is a clear association between VIN
and human papilloma virus (HPV), type 16 in particular. Management
There is a subset of patients with VIN in whom HPV testing Treatment of PIN and VIN may involve local destruction or
is negative. The HPV type tend to be younger patients and excision of solitary lesions, but for multifocal extensive
the disease multicentric and multifocal. The non-HPV type lesions treatment is much more difficult. In many patients
is found in older women and is more commonly unifocal observation is often appropriate. Extensive surgery for
and unicentric. The risk of progression to invasive multifocal disease is mutilating and unlikely to be curative.
carcinoma is low and has been estimated to be 3–4%. Laser, cryotherapy, topical 5-fluorouracil, or immiquimod
However, the risk for the older group of patients with for extensive areas have all been used but complete
solitary disease is almost certainly much higher, and in clearance is uncommon and recurrence frequent. Patients
elderly women it is frequently associated with LS. should be encouraged to stop smoking, as this is associated
with progression to frank squamous carcinoma.

7.13 LS and VIN.

7.14 Intraepithelial squamous carcinoma of the glans.

 Genital and oral problems 97

Eczematous conditions

Introduction Contact dermatitis, both irritant and allergic, often

Eczematous rashes in the vulva are common. Atopic eczema complicates the picture. This is not surprising as many
can affect the genital area either acutely or chronically when, patients self-medicate and aggressively over-cleanse the
as the result of chronic scratching and rubbing, thickened area. Vulval skin reacts more readily to irritants than other
erythematous scaly plaques develop often with overlying areas, and the barrier function is often substantially weaker.
excoriation and fissuring (7.15). Examination reveals varying degrees of redness, swelling,
and scaling, sometimes with ulceration. In chronic cases,
Clinical presentation lichenification and excoriation, together with abnormalities
This appearance is termed ‘lichen simplex’. It can be of pigmentation, become prominent. Secondary infection is
bilateral or unilateral and the labia majora are the most not uncommon.
frequently affected sites, although the labia minora,
vestibule, mons pubis, and inner thighs can all be affected.
In both men and women, the perianal area is a site of
predilection and, in men, the scrotum is a frequently
involved site (7.16). The diagnosis is usually simple to make
on the basis of lichenification and excoriation (7.17).

Management
The treatment involves breaking of the ‘itch-scratch cycle’,
replacing irritants with bland emollients and soap
substitutes, topical steroids of medium to high potency,
occasionally systemic steroids, sedating antihistamines for
night-time itch and, sometimes, selective serotonin reuptake
inhibitors for daytime itching.
7.15 Perianal eczema.

7.16 Lichen
simplex of the
scrotum.

7.17 Vulval eczema.

98 Genital and oral problems

Allergic contact dermatitis can be difficult to distinguish secondary infection underlying dermatological disease, and
from irritant dermatitis and they do sometimes overlap. The previously administered therapy (7.18). One should not
most common allergens are fragrances, preservatives, topical guess at the aetiology of an ulcer and initiate treatment
medications, rubber products, nail polish, and nickel. The before appropriate investigations have been done. For acute
presentation can be acute, subacute, or chronic and, in the ulcers this includes bacterial, viral, and sometimes fungal
acute phase, vesiculation, swelling, and spread beyond the cultures. Even if bacterial or candidal infection is
site of contact are seen. In more chronic cases, the changes demonstrated, these may not be the primary cause of the
can be indistinguishable from those seen in an irritant ulcer. Any chronic ulcer necessitates a biopsy to exclude
dermatitis. The diagnosis is made from history and patch malignancy.
testing, and one should have a low threshold for patch
testing of patients with vulval disease.
Further reading

Vulval ulceration Black M, McKay M (2002). Obstetric and Gynaecological

Dermatology, 2nd edn. Mosby, Philadelphia.
Introduction Bunker CB (2004). Male Genital Skin Disease. Saunders,
Vulval ulcers can broadly be classified as infectious, Edinburgh.
noninfectious, and malignant (Table 7.1). Although acute Ridley CM, Neill S (eds) (2002). The Vulva (2nd edn).
ulcers tend to be infectious in origin, the natural history Blackwell Scientific, Oxford.
depends on many factors including immune status,

Table 7.1 Aetiology of vulval ulcers

Infectious ulcers
• Syphilis
• Herpes simplex
• Herpes zoster
• Candida
• Chancroid

Noninfectious ulcers
• Pyoderma gangrenosum
• Urethral caruncle
• Trauma
• Behçet’s syndrome
• Apthae
• Epstein–Barr virus

Malignant ulcers
• BCC
• SCC
• Malignant melanoma 7.18 Perivulval ulcer.
• Extramammary Paget’s disease
 Chapter 8 99

Scalp and nail disorders

Stuart N Cohen, BMedSci, MRCP

Introduction DISORDERS OF THE SCALP AND HAIR

Disorders of the scalp are common and may be intensely Alopecia areata
symptomatic. Hair loss, in particular, is frequently
associated with a high degree of distress. Uncertainty Introduction
regarding diagnosis makes counselling such patients even This is a nonscarring alopecia with a prevalence of
more difficult, so accurate diagnosis is especially important. approximately 0.1%. It is associated with other organ-
Although scalp involvement may be a feature of several of specific autoimmune diseases, such as thyroid disease and
the most common inflammatory dermatoses, including vitiligo. Atopy also appears to be linked. In monozygotic
psoriasis, atopic dermatitis, and seborrhoeic dermatitis, the twins, a concordance rate of 55% has been found, suggesting
focus of this section is on diseases with a predilection for the that both genetic and environmental factors are relevant.
scalp, those that are scalp specific, and on disorders of hair.
This latter group often leads to diagnostic difficulty. The Clinical presentation
value of simple blood tests should not be forgotten, as Alopecia areata usually presents with well-defined, circular
biochemical abnormalities such as iron deficiency patches of complete hair loss, with no evidence of scarring
commonly lead to hair loss and are easily correctable. (8.1). Exclamation mark hairs (where the proximal shaft is
Many abnormalities of the nail unit result from general narrower than the distal shaft) are often seen around the
skin conditions, most typically psoriasis, but also atopic periphery of the patches. Other patterns include alopecia
eczema, lichen planus, and others. In some cases, disease is totalis (where the scalp is completely bald), alopecia
restricted to the nails. Where the cause of a rash is unclear, universalis (where all body hair is lost), and ophiasis, in
specific nail changes may help to confirm the diagnosis. The which there is hair loss over the temporo-parietal and
nails may also give clues to systemic disease, with features of occipital scalp. In diffuse alopecia areata, there is
Beau’s lines, leuconychia, yellow nail syndrome, and so on. widespread thinning, rather than the usual well-defined
Unfortunately, many conditions affecting the nail unit are patches (8.2). Several nail abnormalities may be associated.
difficult to manage, but care should be taken not to overlook
a treatable problem such as onychomycosis. Histopathology
A lymphocytic infiltrate is seen in the peribulbar and
perivascular areas, the external root sheath, and invading the
follicular streamers. Langerhans cells are also present.

Differential diagnosis
Localized hair loss is seen with trichotillomania, tinea
capitis, traction alopecia, and pseudopelade of Brocque.
History and clinical findings will differentiate the vast
100 Scalp and nail disorders

majority of cases. Diffuse alopecia areata is more Clinical presentation

challenging, as telogen effluvium, iron deficiency-related Onset is most commonly in childhood. The scalp is the most
hair loss, and androgenetic alopecia may look similar. common site, resulting in localized or patchy alopecia (8.3).
The affected areas tend to have irregular borders and often
Management contain broken hairs of varying lengths. Even in extensive
If there is doubt about the diagnosis, hair microscopy and cases, the occiput is usually spared.
serum ferritin may exclude other possibilities. A biopsy is
only rarely required. Treatment options include potent or Histopathology
very potent topical steroid applications, or intralesional Biopsy is rarely needed, though follicular plugging, melanin
steroid injection. For more extensive disease, contact casts, trichomalacia, haemorrhage, and increased numbers
sensitization with diphencyprone, PUVA, systemic of catagen follicles may be seen.
corticosteroids, and ciclosporin have been used, but
response rates are disappointing. Differential diagnosis
The disease may spontaneously remit, though some Alopecia areata and tinea capitis are the main differentials.
patients have regrowth in some areas at the same time as The former usually results in better defined areas of
new hair loss in others. Regrowing hairs are often not alopecia.
pigmented. Ophiasis pattern, extensive disease, and
associated atopy carry a worse prognosis. Management
Diagnosis is usually clinical, though mycological
examination of plucked hairs and histology are helpful if
Trichotillomania there is doubt. Some cases, particularly in childhood, will
spontaneously resolve. Treatments have included cognitive
Introduction behavioural therapy and antidepressants.
This is characterized by the plucking of hairs in a habitual
manner. It does not necessarily reflect significant
psychopathology, though it may be a sign of impulse control
disorders, personality disorder, or psychosis.

8.1 Localized alopecia areata with 8.2 Diffuse alopecia areata. 8.3 Trichotillomania. In this case,
some fine downy regrowth, a good the majority of short hairs are the
prognostic sign. same length.
 Scalp and nail disorders 101

Tinea capitis

Introduction Management
Dermatophyte infection of the scalp occurs frequently in The diagnosis should be confirmed by mycological studies.
children, but rarely in adults. Trichophyton tonsurans and Samples may be obtained through skin scrapings and
Microsporum canis are the commonest causative organisms. brushings, or from plucked hairs. Microscopy with
potassium hydroxide will reveal the fungus, which may be
Clinical presentation cultured. If the diagnosis is suspected and these tests are
Tinea capitis most commonly presents with discrete patches negative, fungal staining of a biopsy specimen will identify
of alopecia, with or without scaling. Diffuse scaling may hyphae or spores.
occur. Posterior cervical and posterior auricular Tinea capitis always requires systemic therapy.
lymphadenopathy is often present. Alopecia is usually Griseofulvin 10–20 mg/kg/day for 8–12 weeks or terbinafine
reversed on treatment, but may be permanent after severe or 62.5 mg daily (10–20 kg), 125 mg daily (20–40 kg), 250 mg
long-standing infection. daily (>40 kg) may be used. For kerion, in addition to this,
An exaggerated host response may result in formation of antibiotics for superadded infection may be necessary and
a kerion (8.4). This is a boggy, purulent plaque with abscess topical steroids may be used to suppress inflammation.
formation and may give rise to systemic upset.

Differential diagnosis
Where scaling is prominent, the condition may mimic
seborrhoeic dermatitis or psoriasis (such as in pityriasis
amiantacea, 8.5). The alopecia may be mistaken for alopecia
areata or trichotillomania. Other causes of scarring alopecia
may be considered if scarring is a feature. Kerion is
frequently misdiagnosed as bacterial infection.

8.4 Scalp ring worm (kerion). (Courtesy of 8.5 Pityriasis amiantacea describes build-up of thick,
Dr Andrew Affleck.) adherent scaling; it is usually in the context of psoriasis,
but may also result from seborrhoeic dermatitis or
tinea capitis.
102 Scalp and nail disorders

Folliculitis decalvans Dissecting cellulitis of the scalp

Introduction Introduction
This is a form of painful, recurrent, patchy scalp folliculitis, This condition is uncommon, usually affecting young, black
which results in scarring and thus hair loss. It is thought to men. Follicular hyperkeratosis is thought to represent the
result from an abnormal response to Staphylococcus aureus primary cause, though bacterial superinfection is frequent.
toxins.
Clinical presentation
Clinical presentation Multiple painful inflammatory nodules and fluctuant
There is patchy, scarring alopecia, with crusting and abscesses occur, giving a ‘boggy’ feel to the affected areas
pustules (8.6). There may be tufting of hairs (more than one (8.7). It is most common over the occiput. As lesions settle
hair erupting from a single follicle). with scarring, alopecia occurs.

Histopathology Histopathology
Histology shows hyperkeratosis, follicular plugging, and Biopsy reveals neutrophilic folliculitis, granulomatous
perifollicular inflammation. response to keratinous debris, and fibrosis.

Differential diagnosis Differential diagnosis

Other causes of scarring alopecia may look similar, including In advanced, or burnt-out disease, the boggy feeling may be
discoid lupus, lichen planopilaris, or pseudopelade of lost, and the appearance may be similar to other causes of
Brocque. scarring alopecia such as folliculitis decalvans, discoid lupus,
and pseudopelade.
Management
Treatment options include topical or oral antibiotics, Management
including combination treatment such as clindamycin and Oral antibiotics, intralesional steroid injection to inflam-
rifampicin, or oral isotretinoin. Small areas of scarring matory nodules, oral isotretinoin, incision and drainage, and
alopecia may be excised. local excision of discrete areas have been used.

8.7 Scarring
alopecia due
to dissecting
cellulitis of
the scalp.
(Courtesy of
Dr Andrew
Affleck.)

8.6 Scarring alopecia due to long-standing folliculitis

decalvans. (Courtesy of Dr Andrew Affleck.)
 Scalp and nail disorders 103

Acne keloidalis nuchae Lichen planopilaris

Introduction Introduction
This occurs mainly in black men. The precise cause is This is lichen planus (LP) of the scalp. The cause of the
unclear. condition is unknown.

Clinical presentation Clinical presentation

It usually begins on the nape of the neck with formation of There is patchy hair loss, perifollicular erythema, and
small follicular papules (8.8). These then become firmer and scarring alopecia. There may also be evidence of LP at other
more numerous, before coalescing into plaques. There is sites, including nails and mucous membranes (8.9).
alopecia over the affected area and sometimes tufting of
hairs, similar to that in folliculitis decalvans. Advanced Histopathology
disease may be associated with abscesses and sinuses. As in LP at other sites, biopsy shows hyperkeratosis,
irregular acanthosis, basal layer liquefaction, Civatte bodies,
Histopathology and a band-like lymphocytic infiltrate at the dermo-
Various types of inflammatory infiltrate may be seen, epidermal junction; pigment incontinence may be marked.
particularly in the upper third of the follicle. Hair fragments
with surrounding granulomata may be seen, with scarring. Differential diagnosis
True keloid changes are only seen later. Appearances may be similar to other causes of scarring
alopecia, but the violaceous rim around active areas is
Differential diagnosis characteristic. Burnt-out lichen planopilaris may be
Lesions may be similar to other types of folliculitis or acne. indistinguishable from pseudopelade of Brocque.
Advanced disease may mimic folliculitis decalvans, though
the site is usually characteristic. Management
The diagnosis may be confirmed histologically. Treatment
Management options start with topical steroids; intralesional or systemic
Early disease may respond well to topical treatment with steroids may be tried, or other agents such as oral retinoids
potent or very potent steroids, or retinoids. Antibiotics may and immunosuppressants. Some cases will resolve
be used to settle active folliculitis. More advanced disease spontaneously.
may be improved with intralesional steroid or surgical
intervention.

8.8 Acne keloidalis nuchae. 8.9 Lichen planopilaris.

104 Scalp and nail disorders

Discoid lupus erythematosus

Introduction Management
Lupus is more common in blacks than whites. Discoid lupus Topical treatment consists of steroid applications;
is the commonest form seen in dermatology clinics. Lesions intralesional steroids may be used. Systemic options include
are most often seen on the face and scalp. Most patients hydroxychloroquine and methotrexate. High-factor sun-
have disease localized to the skin, with no detectable screen (SPF >30) should also be advised.
autoantibodies, but a small proportion (5–10%) may later
develop systemic lupus erythematosus.
Pseudopelade of Brocque
Clinical presentation
There is erythema, follicular plugging, sometimes indura- Patchy scarring alopecia, with no active inflammation and
tion, scarring alopecia, and commonly dyspigmentation, no diagnosis evident on histology, is known as pseudopelade
especially hypopigmentation (8.10). Disease is often photo- of Brocque (8.11). This may represent the end-stage of
aggravated. several other recognized conditions. Treatment is
unsatisfactory, although excision of the affected areas is
Histopathology effective where practical.
Biopsy shows hyperkeratosis and damaged keratinocytes;
there is often thickening of the dermo-epidermal and
follicular basement membrane zones; in the dermis, there is Naevus sebaceus
often a pronounced lymphohistiocytic interface, and peri-
vascular and periadnexal cellular infiltrate. Follicular This congenital lesion presents in early childhood as an oval
plugging is seen, or follicular structures may be atrophic or or linear yellow-orange plaque, commonly on the head or
absent. neck (see Chapter 2). Alopecia is typical in scalp lesions.
The lesion may become more verrucous with age and darker
Differential diagnosis in colour. Not uncommonly, neoplasms develop within
On the scalp, discoid lupus may appear similar to lichen naevus sebaceus, many benign, but also basal cell
planopilaris or tinea capitis. The scaling is different from carcinomata. Treatment consists merely of observation or
that seen in psoriasis and, in established cases, alopecia is excision.
more prominent.

8.10 Chronic discoid lupus erythematosus of the scalp. 8.11 Pseudopelade of Brocque or ‘footprints in the snow’.
 Scalp and nail disorders 105

Diffuse hair loss Traction alopecia

Introduction Introduction
From the normal scalp, up to 150 hairs are shed per day. In Excessive tension put on hair may lead to hair loss. It tends
telogen effluvium, a greater than normal proportion of hairs to occur when a ponytail is aggressively pulled back, but also
enter the telogen phase of the hair cycle, leading to increased around tight braids (8.12). Regular hair straightening is
shedding. Iron deficiency and thyroid dysfunction should be another cause.
excluded in all cases of diffuse hair loss. Various
chemotherapeutic agents and some other drugs also cause Clinical presentation
hair loss. If caused by a ponytail, hair loss is seen in the temporal
regions. The scalp appears normal.
Clinical presentation
Telogen effluvium classically presents 2–4 months after a Histopathology
high fever, other severe illness, or pregnancy with increased Biopsy is not usually required and is nonspecific or normal.
shedding and diffuse hair loss. In other patients, particularly
middle-aged women, it may be chronic. Here it is more Differential diagnosis
difficult to distinguish from other causes of diffuse thinning. Diagnosis is usually clear from the distribution matching a
history of putting hair under tension. Frontal fibrosing
Differential diagnosis alopecia, which causes slowly progressive temporal and
Diffuse thinning may result from androgenetic alopecia, frontal recession, and loss of eyebrow hair, may appear
although this is usually most marked over the crown. There similar. If this diagnosis is suspected, histology is helpful.
may be a family history. Iron deficiency and thyroid disease
should be excluded biochemically. Chronic telogen Management
effluvium and diffuse alopecia areata should be considered. Hair should be kept in a relaxed style, though hair loss may
In the former, increased numbers of telogen hairs (‘club be permanent.
hairs’) are seen on hair microscopy; in the latter,
exclamation mark hairs may be seen and histology is
characteristic.

Management
Correction of biochemical abnormalities, such as iron
deficiency, may lead to resolution. Telogen effluvium,
especially where acute, usually resolves spontaneously after
several months. Antiandrogens have been used in
androgenetic alopecia, as has topical minoxidil. Stopping
the latter may cause any benefits of treatment to be lost.

8.12 Traction alopecia.

106 Scalp and nail disorders

DISORDERS OF NAILS

Onychomycosis Histopathology
This is rarely necessary, though it may be helpful where there
Introduction is diagnostic doubt, or suspected dual pathology. Fungal
Fungal nail infection is common, with prevalence rates of stains will confirm the presence of causative organisms.
2–13%. Several factors predispose to onychomycosis,
including local trauma, orthopaedic problems, affected close Differential diagnosis
contacts, previous history, and tinea pedis. Infection may be Psoriasis may look identical. Pitting and onycholysis may be
due to dermatophytes or yeasts. Common organisms diagnostic of this, though it should be remembered that
include Trichophyton rubrum, T. interdigitale, Candida psoriatic nails may be colonized by fungus. Yellow nail
albicans, and Fusarium spp. syndrome usually affects all nails, hyperkeratosis is lacking,
and there is typically associated lymphoedema.
Clinical presentation
Apart from abnormal appearance, there is sometimes Management
associated pain. Toenails are far more commonly affected Diagnosis should be confirmed by mycological study of nail
than fingernails (8.13, 8.14). In distal and lateral subungual clippings. Recurrent tinea pedis should be treated
onychomycosis (DLSO), the lateral nailfolds may be scaly aggressively. Topical treatment of onychomycosis with
and the nail is opaque or discoloured (8.15). There may be amorolfine 5% lacquer as monotherapy is often ineffective,
thickening and crumbling as well as nailbed hyperkeratosis. except in superficial nail plate infection. It may render
Superficial white onychomycosis produces chalky white systemic therapy more effective when used in combination.
patches on the surface of the nail, which may coalesce. The systemic agent of choice is terbinafine 250 mg once
Where there is loss of the cuticle due to proximal nailfold daily, for 6 weeks in fingernail infections and 12 weeks in
disease, fungi may enter, causing proximal subungual toenail infection. Alternatives include pulsed itraconazole
onychomycosis. Total dystrophic onychomycosis is usually a 200 mg once daily for 1 week in 3 consecutive months or
result of DLSO, but may occur with other subtypes. The griseofulvin 500–2000 mg per day, continued until 1 month
entire nail is thickened, with a rough surface and mixed after clinical resolution. Griseofulvin has many interactions,
colours. as it induces hepatic enzymes.

8.13 Fungal infection of the toenails and skin of feet. 8.14 Superficial white onychomycosis of the toenails.
 Scalp and nail disorders 107

8.15 Distal and Psoriasis

lateral subungual
onychomycosis. Introduction
Psoriasis is common, with worldwide prevalence figures of
1–3%. Most patients with psoriasis will, at some point, have
signs of nail involvement.

Clinical presentation
Pits are the most common change seen in psoriasis (8.16).
These are punctate depressions, seen as a result of proximal
matrix disease. They may be seen also in other
dermatological conditions. Toenail disease often leads to
discoloration, which may mimic onychomycosis. Subungual
hyperkeratosis may lead to marked thickening of the nail
plate. Focal parakeratosis produces an ‘oil spot’ or ‘salmon
patch’; if this extends to a free margin, onycholysis or
separation of the nail plate from the nailbed results. Other
abnormalities include splitting of the nail plate and
paronychia. A variant of psoriasis, acropustulosis continua
of Hallopeau, gives rise to sterile pustules around the nail
unit (8.17). The nail may be completely lifted off (8.18).

Histopathology
Nail unit biopsy is often unnecessary, but shows acanthosis,
neutrophil exocytosis, and parakeratosis; microabscesses or
pustules may be seen and there may be a granular layer,
usually absent from a healthy nail plate. Fungal hyphae may
be seen indicating either infection or merely colonization.
8.16 Psoriatic pitting and distal onycholysis of the
fingernails.

8.17 Acropustulosis of
Hallopeau.

8.18 Acropustulosis of Hallopeau of the big toenail.

108 Scalp and nail disorders

Differential diagnosis Clinical presentation

Other features of psoriasis should be sought to confirm the A wide variety of changes may be seen including thickening,
diagnosis. The presence of an oil spot is highly suggestive of pits, and transverse ridges (8.19). Nailbed disease gives rise
psoriasis. Differential diagnoses include onychomycosis; to subungual hyperkeratosis and onycholysis. Often, but not
other causes of pitting include atopic disease, alopecia areata always, there will be eczema around the nail units (8.20).
and LP; nail thickening may be seen in Darier’s disease,
pityriasis rubra pilaris, and pachyonychia congenita; Reiter’s Histopathology
syndrome may be indistinguishable from psoriasis, though As with the skin, histology shows spongiosis and a
associated features of keratoderma blenorrhagica, urethritis, predominately lymphocytic infiltrate. As in psoriasis of the
and uveitis should indicate the correct diagnosis. nail, a granular layer is seen.

Management Differential diagnosis

General hand care is important, including frequent use of The diagnosis is usually obvious from the cutaneous
emollients, keeping nails short, and protecting the hands findings. Hand dermatitis may be difficult to distinguish
from wet work and irritants. Very potent topical steroid from psoriasis and exogenous factors should be considered
application around the nail folds may help; injection of as possible causes or exacerbating factors.
triamcinolone is possible, but requires ring block. The nails
may improve with PUVA and oral treatment may be given Management
in the form of the retinoid acitretin. Methotrexate or As with psoriasis, scrupulous hand care is advised, involving
ciclosporin may also help. frequent use of emollients and soap substitute, and avoiding
allergens, irritants, and wet work. Patch testing should be
considered. Treatment involves emollients, and topical
Eczema steroids may be applied to the nail folds. Infection should be
treated with topical or systemic antibiotics. PUVA may be
Introduction helpful.
Hand eczema commonly leads to disruption of the nail unit,
though changes such as pitting may be a feature of a general
atopic tendency. The nails may be exposed to a variety of
allergens and irritants, and a combination of these may play
a role in eczematous nail disease.

8.19 Nail dystrophy due to chronic periungual eczema 8.20 Eczematous nail dystrophy.
showing thickening, pits, and transverse ridges.
 Scalp and nail disorders 109

Lichen planus 8.21 LP of the

nail showing
Introduction splitting of the
There are many different forms of LP. Typically, it manifests nail and
as a cutaneous, pruritic papular eruption, but may also affect brittleness.
the nails and mucosal surfaces. Nail disease is present in
about 10% of cases. The cause is unknown.

Clinical presentation
LP nail disease may be the sole manifestation of the disease,
or it may be accompanied by one of the other types. A
variety of changes may be seen in the nail. These include
superficial splitting of the nail (onychorrhexis), brittleness,
subungual hyperkeratosis, and onycholysis (8.21, 8.22).
A sandpapered effect (trachyonychia) may result. Where
all nails are affected, it is known as ‘twenty nail
dystrophy’ (8.23).

Histopathology
The skin shows basal cell liquefaction with a band-like
inflammatory infiltrate. In addition, there is marked
spongiosis on nail histology.

Differential diagnosis
Examination of skin and mucous membranes may confirm
the diagnosis. Isolated nail disease is more challenging.
Onycholysis is commonly associated with psoriasis but may
be due to various infectious, inflammatory or physical
insults. Trachyonychia may also be seen associated with
alopecia areata, psoriasis, ichthyosis, or ectodermal 8.22 Subungual hyperkeratosis and onycholysis in LP
dysplasia. LP-like changes are also seen in graft-versus-host nail dystrophy.
disease.

Management
Scarring nail changes will be permanent, but other effects
may resolve spontaneously, especially in children. Potent or
very potent topical steroids may be applied to the nail folds;
triamcinolone may be injected into the nail unit under ring
block anaesthesia.

8.23 Trachyonychia in twenty nail dystrophy.

110 Scalp and nail disorders

Alopecia areata Yellow nail syndrome

Introduction Classically associated with lymphoedema and respiratory

This usually presents with patchy hair loss (see above), but disease, the nails show yellow-green discoloration,
nail changes are seen in a substantial proportion of those decreased growth rate, thickening and hardening of the nail
affected. These may occur synchronously with, or precede plate, and loss of the cuticle (8.24). The cause is unknown
the hair loss. and the condition may resolve spontaneously.

Clinical presentation
One to twenty nails may be affected. There may be shallow Onychogryphosis
pits; nails may be thickened and brown, appear sandpapered
(trachyonychia, see above), or be thin, shiny, and fragile. This is characterized by overgrowth and increased curvature
Superficial splits, spoon-shaped nails (koilonychia), of the nail plate. It is most common in the elderly (8.25).
thinning, or thickening may be seen. Although mainly attributable to neglect, vascular and
mechanical factors, and local skin disease may contribute.
Histopathology Treatment may include trimming, chemical destruction
The nail matrix shows spongiosis. There may be a with 40% urea paste, or total ablation through phenol
lymphocytic infiltrate; PAS-positive inclusions may be seen application.
in the nail plate. The parakeratosis seen in psoriatic pits is
lacking.
Pincer nail
Differential diagnosis
The typical pattern of hair loss usually suggests the Pincer nail is usually an isolated familial abnormality of the
diagnosis. If this is lacking, appearances may be confused big toe or thumb nails which develops in adulthood (8.26).
with psoriasis, LP, or onychomycosis. The sides of the nail become ingrown and are very painful
because of recurrent infections and associated swelling.
Management Total ablation of the nail is often required to stop ingrowing
Potent or very potent topical steroids, or injected steroids of the sides of the nail and recurring infections.
may be effective. Systemic immunosuppressives may also
reverse the nail changes.

8.24 Yellow nail

syndrome.

8.25 Onychogryphosis.
 Scalp and nail disorders 111

8.26 Pincer nail. Median nail dystrophy

Median nail dystrophy or washboard nail is due to repetitive

disruption of the cuticle, often due to a nervous habit. There
is a lower threshold for the development of this in patients
with psoriasis (8.27, 8.28).

Tumours of the nail unit

Any tumour of the nail unit, benign or malignant, may give

rise to abnormalities of the nail plate. Such a diagnosis
should be considered particularly where a single nail is
affected. Differential diagnosis includes skin cancers (see
Chapter 4), or benign lesions, such as glomus tumour,
myxoid cyst (8.29), neurofibroma, periungual fibroma
8.27 Median nail (8.30), and viral wart. Exostosis of the distal phalanx may
dystrophy in a also present similarly. Radiography and biopsy should be
patient with considered.
psoriasis.

8.28 More common form of median nail dystrophy.

8.29 Myxoid cyst. 8.30 Periungual fibromas in a patient with tuberose

sclerosis.
112 Scalp and nail disorders

Further reading

Bolognia JL, Jorizzo JL, Rapini RP (eds) (2003). Sinclair RD, Banfield CC, Dawber RPR (1999). Handbook
Dermatology. Mosby, London. of Diseases of the Hair and Scalp. Blackwell Sciences,
de Berker DAR, Baran R, Dawber RPR (1995). Handbook Oxford.
of Diseases of the Nails and their Management. Blackwell Tosti A, Iorizzo M, Piraccini BM, Starace M (2006). The
Sciences, Oxford. Nail in Systemic Diseases. Dermatol Clin 24(3):341–347.
Holzberg M (2006). Common nail disorders. Dermatol Clin
24(3):349–354.
 Chapter 9 113

Skin infections and

infestations
Neill C Hepburn, MD, FRCP

Introduction BACTERIAL INFECTIONS

Skin infections can be divided into bacterial, viral, or fungal Impetigo

whereas infestation will be with either an insect or a worm.
The distribution, configuration, and morphology of the rash Introduction
are important in helping to make the diagnosis but the A common, highly contagious, bacterial infection with
history, including travel, will also be key. Often dermatitis streptococci and/or staphylococci.
becomes secondarily infected and can even at times be
caused by infection (see Chapters 2 and 3). The use of Clinical presentation
swabs, tissue culture, histology, mycological studies, and Patients present with erythematous areas, which start in one
serological tests will often be necessary to make or confirm area, but can rapidly spread and become numerous. They
the diagnosis. may form small bullae with breakdown (9.1A), or just moist
crusty areas (9.1B). There is usually a peripheral collar of
scale or crust but little surrounding erythema.

A B
9.1 A, B: Impetigo. Note eroded areas with collarette of scale/crust.
114 Skin infections and infestations

Differential diagnosis Clinical presentation

Infected eczema may look similar and, of course, those with Patients present with sudden onset of malaise and, within a
eczema are predisposed to impetigo. few hours, the skin becomes erythematous, warm,
oedematous, and painful. In cellulitis that involves the
Management deeper layer, there is no clear distinction between involved
The lesions should be swabbed to identify the infecting and uninvolved skin. The skin may form bullae, which
bacterium and its sensitivity. The area should be treated rupture (9.2). In erysipelas, which tends to involve the more
topically with fucidic acid or systemically with flucloxacillin superficial layers and cutaneous lymphatics, there is a clear
or clarithromycin. line of demarcation between involved and uninvolved skin
(9.3), and there is prominent streaking of the draining
Prognosis lymphatics.
Recurrence is common. Swabs should be taken from the
nares of the patient and family members. Differential diagnosis
Secondarily infected eczema is common around leg ulcers
but the skin is not warm to the touch. In necrotizing fasciitis,
Cellulitis infection of the subcutaneous tissues results in destruction
of fat and fascia with pain out of proportion to the clinical
Introduction signs, and often only a mild fever but with diffuse swelling
Cellulitis and erysipelas are bacterial infections involving the and pain (9.4). Urgent surgical debridement is needed.
dermis and subcutaneous tissues. Common pathogens are
group A streptococci or Staphylococcus aureus in adults and Management
Haemophilus influenzae type B in children. Breaks in the skin It is usually not possible to identify the infecting organism
such as surgical wounds, abrasions, ulcers, or tinea pedis from blood cultures or skin swabs. Needle aspiration from
predispose to cellulitis by providing a portal of entry for the the subcutaneous tissues and blood cultures can be helpful.
bacteria. Previous episodes of cellulitis, lymph node Oral phenoxymethyl penicillin and flucloxacillin or
resections, and radiation therapy, which damage the erythromycin should be given. In patients who are allergic to
lymphatics, also predispose to cellulitis. penicillin, ciprofloxacin can be used. If the patient is toxic,
antibiotics should be given intravenously initially.

9.3 Erysipelas.
Note the sharply
demarcated
areas of
erythema.

9.2 Streptoccocal cellulitis. Note the well-defined red area

and the formation of bullae, one of which has ruptured.
 Skin infections and infestations 115

Prognosis Pitted keratolysis

Recurrence after antibiotic treatment occurs in about 25%
of cases and may be spontaneous or initiated by quite minor Introduction
trauma. Recurrent cases may require long-term prophylactic This is a common superficial bacterial infection occurring
treatment with low-dose penicillin or erythromycin. on the soles of the feet. It usually occurs in those with sweaty
feet, or those who wear occlusive footwear, such as work
boots or trainers.

Clinical presentation
The skin over the weight-bearing areas appears moist and
oedematous with punched out circular pits and furrows,
resembling the surface of the moon (9.5). The feet usually
have an offensive smell. Several species of bacteria have
been implicated including Corynebacterium, Dermatophilus,
and Micrococcus spp. These bacteria excrete enzymes that
degrade keratin and thereby produce the characteristic
pitted surface.

Differential diagnosis
The appearance (and smell) are characteristic; however, it is
sometimes mistaken for a fungal infection.

Management
The bacterial infection responds to topical antibiotics such
as fusidic acid cream, or acne medications such as
9.4 Necrotizing fasciitis with necrotic muscle. clindamycin solution.

Prognosis
It is important to dry the skin of the feet to prevent
recurrences. Options include 20% aluminium chloride
(Drichlor) or 10% formaldehyde soaks.

9.5 Pitted keratolysis. Note the punched out circular pits

and furrows, resembling the surface of the moon, over
the weight-bearing areas.
116 Skin infections and infestations

Erythrasma Atypical mycobacterium infection

Introduction Introduction
Erythrasma is an indolent skin infection usually of the Fish tank, or swimming pool, granuloma is an infection with
axillae, groin, or toe webs caused by the bacterium Mycobacterium marinum – an atypical mycobacterium which
Corynebacterium minutissimum. Hot, humid environmental grows in culture at 30°C. It is most commonly seen in
conditions encourage this infection. keepers of tropical fish (the infected fish usually die). It can
also be contracted from swimming pools.
Clinical presentation
There are sharply marginated, reddy-brown patches in the Clinical presentation
axillae or groin (9.6), which develop often over many years. The lesions usually develop following an abrasion after an
Sometimes patients complain of irritation but usually they incubation period of 2–3 weeks. A nodule develops that may
are asymptomatic. then break down to form an ulcer or remain as a warty
plaque (9.7). Lesions are frequently multiple and nodules
Differential diagnosis may form along the line of the draining lymphatics, known
The coral red fluorescence is typical of erythrasma but as sporotrichoid spread (9.8).
pityriasis versicolor and tinea infections can have a similar
appearance. Histopathology
The pathology varies from nonspecific inflammation to well
Management formed tuberculoid granulomas. Intracellular acid-fast
Patients respond well to a range of topical antimicrobials bacilli are only identified in 10% of cases.
such as fusidic acid, miconazole, or erythromycin (oral or
topical). Differential diagnosis
The main differential in the UK is bacterial pyoderma. In
Prognosis those returning from the tropics, leishmaniasis and sporo-
Without treatment the condition persists indefinitely. If trichosis are alternatives as is a tuberculous chancre (9.9).
treated, it will relapse if climatic conditions are adverse or
personal hygiene is poor. Management
A skin biopsy should be sent for culture at 30°C but it will
take a month for the colonies to grow. Although self-
limiting, with spontaneous healing occurring within 6
months, several treatments are advocated, but the optimum
treatment has not been established.

Prognosis
Commonly advocated treatment regimens include:
minocycline 100–200 mg daily for 6–12 weeks, rifampicin
600 mg and ethambutol 1.2 g daily for 3–6 months, and co-
trimoxazole 2–3 tablets twice daily for 6 weeks. Public
health authorities should be notified.
 Skin infections and infestations 117

A B
9.6 A, B: Erythrasma. Sharply marginated lesions in the axillae and groin.

9.7 Atypical mycobacterial infection due to M. marinum in 9.8 Sporotrichoid spread in atypical mycobacterial
a tropical fish keeper, clinically similar to warty infection.
tuberculosis.

9.9 Tuberculous chancre in a patient from Pakistan.

118 Skin infections and infestations

Anthrax Clinical presentation

The lesions are typical, once recognized, and present as
Introduction small vesicles with a red halo, which become haemorrhagic
Anthrax is an extremely rare, but often fatal, infection pustules (9.12). They occur in crops or three to four lesions
caused by Bacillus anthracis. It has recently become scattered over the limbs and heal after a few days.
important because of its use, by terrorists, as a biological
weapon. Natural infection occurs after contact with infected Differential diagnosis
animal hides that have usually been imported from Africa or Septicaemia and vasculitis from other causes.
the Indian subcontinent.
Management
Clinical presentation Patients should be referred to a genitourinary medicine
Patients present with a vesicle or bulla that enlarges over a department as coexisting sexually transmitted diseases are
week or so, to become haemorrhagic and necrotic, leading common; antibiotic-resistant strains are very frequent.
to the formation of an adherent back eschar (9.10). It is
sometimes surrounded by satellite vesicles and is a striking Prognosis
brawny oedema that is surprisingly painless. The lymph The prognosis is good providing it is treated adequately.
glands enlarge and the patient becomes unwell with a low- Contact tracing is advisable.
grade fever.

Histopathology Secondary syphilis

The bacilli can be seen on Gram staining of the exudate.
Culture, polymerase chain reaction (PCR), and serology are Introduction
helpful. There is an epidemic of syphilis currently in Europe and
probably worldwide. After many decades of syphilis being a
Differential diagnosis rare disease in dermatology clinics, dermatologists in the
Acute pyoderma is usually painful and the systemic upset is UK are now beginning to see patients presenting with
greater in anthrax. Cowpox is very similar in appearance and secondary syphilis.
clinical course but is benign and self-limiting (9.11).
Clinical presentation
Management The cutaneous presentations of secondary syphilis are
Ciprofloxacin 500 mg bd, initially intravenously, for 14 variable, but the commonest to present to the dermatologist
days. is a widespread pityriasis rosea-like rash (roseola) with
palmar lesions (9.13, 9.14).
Prognosis
In 80% of cases the lesion heals over 2–4 weeks and the Differential diagnosis
patient recovers with little scarring. In 20% a bacteraemia These include pityriasis rosea, psoriasis, and urticaria.
occurs followed by a haemorrhagic meningitis and death.
Antibiotic treatment does not change the course of the Management
primary lesion and the eschar still forms, but it reduces the Patients should be referred to a genitourinary medicine
bacteraemia and the consequent mortality. department as coexisting sexually transmitted diseases are
common. Resistance to antibiotics has not occurred.
Treponema pallidum still responds to penicillin or
Gonococcal septicaemia doxycycline.

Introduction Prognosis
Gonorrhoea can on rare occasions present to the The prognosis is good providing it is treated adequately.
dermatologist with one or two pustules with arthritis of one Contact tracing is advisable.
or more joints.
 Skin infections and infestations 119

9.11 Cowpox. It is
similar to anthrax
but self-limiting
and benign.
Contact with cows
or cats should be
investigated.

9.10 Cutaneous anthrax. Note black eschar, surrounding

erythema and oedema.

9.12 Haemorrhagic gonococcal pustules on the fingers.

9.13 Roseolar rash of secondary syphilis showing

symmetrical, coppery-red, round and oval spots of no
substance. On the back, the lesions follow the lines of
cleavage resembling pityriasis rosea.

9.14 Psoriasisform papules of the palms or soles help

make the diagnosis of secondary syphilis.
120 Skin infections and infestations

VIRAL INFECTIONS Clinical presentation

A prodromal pain, sometimes associated with fever or
Herpes simplex malaise, occurs 4–5 days before the lesions appear. Red,
oedematous plaques appear that spread to cover the
Introduction dermatome. Then clusters of vesicles appear on the surface
Herpes simplex is a common viral infection with two phases. becoming pustules that may rupture to form a crust (9.17,
After the primary infection, the virus lies dormant in the 9.18). Lesions generally heal in 3 weeks.
nerve ganglion. The secondary infections occur when the
virus comes out from the reservoir in the nerve. Many Differential diagnosis
primary infections are asymptomatic. It is spread by direct It is frequently impossible to make the diagnosis accurately
contact. during the prodromal phase.

Clinical presentation Management

Symptoms start about 3–7 days after contact, starting with a The aim is to suppress the inflammation with potassium
prodromal pain followed by the appearance of vesicles on an permanganate compresses, to treat the pain with analgesics,
erythematous base. They are more scattered in the primary and to treat the infection with antivirals such as aciclovir.
infection than in recurrences (9.15). The primary lesions
heal in about 2–3 weeks. Prognosis
7% of patients have severe pain lasting 3 months or longer.
Histopathology
The diagnosis is established by electron microscopy and
viral culture. Molluscum contagiosum

Differential diagnosis Introduction

These include Stevens–Johnson syndrome. Patients with This is a common poxvirus infection, most commonly seen
eczema are predisposed to develop a widespread infection in children and is spread by direct contact.
(eczema herpeticum), which requires aggressive antiviral
treatment (9.16). Clinical presentation
Patients present with small (2–5 mm) shiny papules with a
Management central pit, often occurring in groups (9.19, 9.20). They are
Symptomatic treatment with cold compresses of potassium frequently inflamed, following scratching.
permanganate is helpful. Oral antiviral agents, such as
aciclovir, decrease the duration of viral excretion and new Differential diagnosis
lesion formation, and promote more rapid healing, but need When the lesions are inflamed, the secondary eczema may
to be started early. disguise the underlying mollusca. Isolated lesions may
resemble intradermal naevi or basal cell carcinomas.
Prognosis
Recurrences average 2 or 3 per year, but can be more Management
frequent and require suppressive antivirals. Simply squeezing the lesions with forceps is usually followed
by an inflammatory reaction and resolution. Vioform-
hydrocortisone ointment can be applied to reduce the
Herpes zoster reaction. Alternatives include cryotherapy or curettage of
individual lesions, or the application of salicylic acid or
Introduction imiquimod cream.
Herpes zoster results from reactivation of the varicella virus
that has been dormant in the cutaneous nerves following an Prognosis
earlier infection with chickenpox. Mollusca are self-limiting, usually clearing in 9 months but
occasionally persisting for as long as 4 years. Often the best
treatment is to do nothing.
 Skin infections and infestations 121

9.15 Herpes simplex. Note scattered lesions of a primary 9.16 Eczema herpeticum. Note the large number of
infection with eroded crusted areas arising on an lesions.
erythematous base.

9.18 Herpes
zoster. Note the
principal lesions
along the
dermatome but
with additional
satellite lesions.

9.17 Herpes zoster. Note the unilateral distribution along

the dermatome.

9.19 Molluscum
contagiosum. Note
pearly papules with
central pit and
surrounding
eczema.

9.20 Molluscum contagiosum. Genital area is a common

site in adults.
122 Skin infections and infestations

Viral warts Orf

Introduction Introduction
Warts are caused by the human papilloma virus (HPV), of Orf is a poxvirus infection, which is widespread in sheep,
which there are over 100 types. It is transmitted by direct mainly affecting young lambs. It is spread by direct
contact with infected skin scales; subclinical infection is inoculation so it is most commonly seen on the fingers of
common. farmers.

Clinical presentation Clinical presentation

The appearance varies with the site of the infection. Most A firm reddish-blue papule appears after an incubation
commonly a flesh coloured papule appears which then period of 5–6 days. It enlarges to form a haemorrhagic
develops a hyperkeratotic surface with back dots, pustule or bulla 2–3 cm in diameter. It may then form a
representing thrombosed capillaries which are most easily crust in the centre. It is tender and usually solitary (9.22).
seen on paring the wart down with a scalpel (9.21).
Management
Differential diagnosis Treatment is only needed to prevent or treat a secondary
The clinical appearance is usually diagnostic. Periungual infection.
warts may mimic periungual fibromas. Verrucas may mimic
corns or rare appendageal tumours. Prognosis
Spontaneous recovery occurs in 3–6 weeks, but second
Management attacks are quite common.
There is no treatment to eradicate HPV. Treatment de-
bulks the wart and stimulates an inflammatory reaction to
trigger the immune response required.

Prognosis
Options include simple occlusion with duct tape, salicylic
acid wart paints, cryotherapy, and curettage. Warts resolve
spontaneously in 40% of cases over 6 months.

9.21 Periungual
warts.

9.22 Orf on the finger of a shepherdess. Note the large

bluish pustule.
 Skin infections and infestations 123

FUNGAL AND YEAST INFECTIONS

Introduction Differential diagnosis

Superficial fungal infections (tinea) are common. The Eczema and psoriasis cause confusion, especially on the
fungus only invades the top layer of skin but may stimulate hands (beware the one-handed rash! 9.24). Pyoderma can
a cell-mediated immune response that varies according to mimic fungal infection of the scalp.
the species of fungus. Common ringworm fungi belong to
the groups Trichophyton, Microsporum, and Epidermo- Management
phyton and may be contacted from another person, either Scrapings taken from the active edge reveal fungus on
directly or indirectly, or from animals. microscopy and should be cultured to determine the
infecting species. Most superficial infections respond well to
Clinical presentation terbinafine 1% cream. Deeper infections and those with a
Clinical presentation is variable, depending on the site and marked inflammatory reaction are best treated systemically.
the immune response. There is usually scaling on the
surface, and erythema is most marked at the ‘active edge’ Prognosis
(9.23). If the inflammatory reaction is marked there is Most infections respond well. It is often necessary to treat
pustule formation and, if severe, it can transform into a the inflammatory reaction with a weak topical steroid.
boggy swelling. Relapses are common.

Histopathology
Fungus can be seen in the top layer of skin along with
neutrophils in a PAS-stained section.

9.23 Tinea infection of the arm due to T. canis. Note the

ring of active inflammation.
9.24 Tinea infection of the left hand due to T. rubrum.
Note unilateral distribution.
124 Skin infections and infestations

Pityriasis versicolor INFESTATIONS

Introduction Cutaneous larva migrans

Pityriasis versicolor (PV) is a chronic superficial fungal
infection of the trunk causing pigmentary changes. It is Introduction
caused by an overgrowth of the mycelial form of the Creeping eruption is the most common tropical skin disease
commensal yeast Pityrosporum orbiculare and is particularly seen in returning travellers. Hookworm larvae migrating
common in hot or humid environments. Patients often through the skin cause the tracts. Most commonly it is
present following a holiday in a hot climate. It is commonest Ancylostoma braziliense, the dog hookworm, which is
in young adults and can be spread by physical contact. contracted on tropical beaches from dog faeces.

Clinical presentation Clinical presentation

The condition presents as brown or pinkish, oval or round, Most patients give a history of tropical travel where they
slightly scaly lesions on the trunk, upper arms and thighs have spent time on beaches. After about 3 weeks an
(9.25). In tanned or dark skin, hypopigmented patches intensely itchy reddish-blue tract appears which grows by
occur due to inhibition of melanogenesis by carboxylic acids about 1 cm daily (9.26, 9.27). The hookworm itself is
released by the organism. invisible and lies about 1 cm ahead of the advancing edge of
the tract.
Histopathology
Lesional scrapings treated with potassium hydroxide show Differential diagnosis
the classical ‘spaghetti and meatballs’ appearance of the There is really nothing quite like it!
spores and hyphae.
Management
Differential diagnosis Albendazole 400 mg daily for 3–5 days or ivermectin 12 mg
The commonest differential diagnosis is that of vitiligo, but single dose is effective.
in PV a fine scale can be demonstrated if the lesional skin is
stretched. Pityriasis rosea, secondary syphilis, and tinea Prognosis
corporis must also be considered. Untreated the larvae live for about 6 weeks but occasionally
for up to 1 year. Travellers should be advised not to walk
Management barefoot on beaches.
Topical selenium sulphide or ketoconazole shampoos
applied to affected areas and left on overnight, repeated
twice at weekly intervals, is effective in most cases.

Prognosis
Infections can frequently recur so repeated treatments with
selenium sulphide or ketoconazole shampoos are often
necessary. Resistant cases will respond to itraconazole 200
mg daily for 7–14 days.

9.25 Pityriasis versicolor affecting the trunk.

 Skin infections and infestations 125

Tungiasis

Introduction Management
Tungiasis is caused by the jigger, or sand flea found in South The flea is removed by curettage and cautery of the cavity
America and Africa. Larvae develop in dry sandy soil. The performed.
impregnated female burrows into the skin producing a 1 cm
nodule, then extrudes its eggs. Prognosis
Left untreated the flea dies in 2 weeks.
Clinical presentation
An intensely itchy nodule, usually on the soles of the feet,
appears with a central punctum. Secondary infection is
common (9.28).

9.27 Cutaneous
larva migrans on
the abdomen
after lying on a
tropical beach
where locals
exercised their
dogs.

9.26 Cutaneous larva migrans on the foot. Note the

advancing tracts.

9.28 Tungiasis. Note the white nodule with a central

punctum in a typical location on the sole of the foot.
126 Skin infections and infestations

Leishmaniasis

Introduction Prognosis
Leishmaniasis occurs in South and Central America (the Old World cutaneous leishmaniasis usually heals
New World), in the Middle East, Asia, Afghanistan, and spontaneously within 1 year. If treatment is needed, simple
around the Mediterranean (the Old World). It is caused by options such as cryotherapy, itraconazole, or intralesional
a protozoon and transmitted by the bite of an infected sodium stibogluconate are best. Those contracted in the
sandfly. Depending on the infecting species, it may produce New World run a more prolonged course lasting many years
a localized skin lesion or a systemic illness, kala-azar. and occasionally develop into the mucocutaneous form
‘espundia’ with destruction of the nasopharynx. These cases
Clinical presentation require systemic sodium stibogluconate.
Patients present with a chronic ulcer, usually on an exposed
site, with an infiltrated raised edge and a necrotic base (9.29,
9.30).

Histopathology
It is a granulomatous inflammation. In early lesions,
intracellular amastigotes may be visible (9.31).

Differential diagnosis
Any chronic tropical ulcer may mimic leishmaniasis.

Management
A skin biopsy from the edge of the lesion should be sent for
histology and culture. PCR is also useful.

9.29 Leishmaniasis from the Middle East. Note the

infiltrated margin and dry base.

9.30 Leishmaniasis from Belize. Note the exposed site, 9.31 Cutaneous leishmaniasis from Belize. Note the
the multiple lesions, and the raised edge. granuloma formation with giant cells and plasma cells.
 Skin infections and infestations 127

Cutaneous myiasis

Introduction Management
Myiasis is the development of fly larvae in living tissue. It is The punctum should be covered with petroleum jelly and
seen in Africa (tumbu fly) and South and Central America the larva expressed manually once its spiracle appears
(botfly). The fly captures a flying blood-sucking insect, such (9.33). Alternatively, the larva can be excised under local
as a mosquito, and lays its eggs on the abdomen. The eggs anaesthetic (9.34).
fall off the carrier insect during feeding, and the larvae crawl
through the hole into the skin where they develop. Prognosis
If left alone the larva would pupate and extrude itself
Clinical presentation through the punctum, fall to the ground, then develop into
A furuncle with a large punctum oozing blood stained fluid a fly.
(9.32) occurs. The spiracle may be seen protruding from the
hole from time to time. The patient is aware of the larva
wriggling around to enlarge the hole.

9.32 Botfly. Note the punctum with larva along the site. 9.33 Botfly larva being expressed manually.

9.34 Botfly larva in the base of an excision.

128 Skin infections and infestations

Further reading

Tyring SK, Lupi O, Hengge UE (2006). Tropical

Dermatology. Elsevier Churchill Livingstone,
Philadelphia.
Habif TP (2004). Cinical Dermatology, 4th edn. Mosby,
Philadelphia.
Savin JA, Hunter JAA, Hepburn NC (1997). Skin Signs in
Clinical Medicine. Mosby-Wolfe, London.
 Chapter 10 129

Leg ulcers and

wound healing
Anna Rich, RN (Dip BSc Hons) and
John SC English, FRCP

Introduction

Leg ulceration is a common and often debilitating problem. standing occupations, limb trauma, or multiple pregnancies
A leg ulcer can be defined as a loss of skin below the knee may be suggestive of venous disease. Obesity is an increasing
on the leg or foot, which takes more than 6 weeks to heal1. cause of venous incompetence.
They affect 1–2% of the population and are more prevalent • Ulcer site: ulcer is most likely to occur around the medial
in females2. Venous leg ulceration is the most common or lateral aspect of the gaiter area of the lower limb (10.1,
aetiology (70–90%), followed by arterial (5–20%), and 10.2).
mixed venous and arterial ulceration (10–15%)3. These • Ulcer appearance: venous leg ulcers tend to be shallow in
ulcers can also be affected by other underlying (e.g. appearance (10.3).
diabetes) and unusual aetiologies (e.g. pyoderma • Pain: patients may complain of localized pain or a
gangrenosum), which may occur simultaneously and may generalized aching/heaviness in their legs.
also occur in isolation; they account for 5–10% of ulcers. • Limb appearance/skin changes:
The key to successful management of leg ulceration relies – Haemosiderin staining: brown/red pigmentation of the
upon thorough assessment, establishment of a diagnosis, skin of the lower limb occurs as a result of the release of
and treating the underlying pathology4. haemosiderin (a breakdown product of haemoglobin). It
This section on leg ulceration discusses the important is released owing to distension of vessel walls and leakage
factors involved in assessment and investigations to be of red blood cells into interstitial space (10.4).
considered. Aetiology of the more common types of leg – Varicose eczema: eczema of the lower limb associated
ulceration will be presented as well as consideration for with venous hypertension; can be aggravated by allergic
differing diagnosis. The main principles of leg ulcer and contact dermatitis from the medicaments used (10.5).
wound management and common therapies will also be – Ankle flare: chronic venous hypertension can result in the
discussed. distension of tiny veins on the medial aspect of the
foot/ankle (10.6).
– Atrophy blanche: areas of white skin, stippled with red
Clinical presentation dots of dilated capillary loops (10.7).
– Varicose veins: distended veins, a sign of chronic venous
Venous disease hypertension usually due to damaged valves in the leg
Venous leg ulceration arising from venous disease usually veins, which become dilated, lengthened, and tortuous
occurs as a result of incompetent valves in the deep and (10.8).
perforating veins. Incompetence of these valves results in a – Dermatoliposclerosis: ‘woody’ induration of tissues and
backflow of blood from the deep to the superficial veins, fat, replaced by fibrosis (10.9).
leading to chronic venous hypertension. Predisposing – Oedema: oedema tends to be generalized and worsens as
factors such as a previous medical history of deep vein legs are dependent as the day goes on; reduction in
thrombosis (DVT), lower limb fractures, varicose veins, oedema is reported upon elevation of the limb(s) or after
phlebitis, pulmonary embolism, previous venous ulceration spending the night in bed (10.10).
or a family history of leg ulceration or thrombosis, as well as
130 Leg ulcers and wound healing

10.2 Venous
ulceration with
pseudomonas
overgrowth. Note
the surrounding
dermatolipo-
sclerosis.

10.1 Venous ulceration.

10.3 Venous ulceration and severe maceration from ulcer

exudate. A potent topical steroid in addition to the
compression will help healing in this situation.

A B
10.4 Haemosiderin deposition over the medial malleolus. 10.5 Allergy to hydrocortisone (A) and 2 weeks after
stopping the preparation (B).
 Leg ulcers and wound healing 131

10.6 Distension of superficial veins on the medial aspect 10.7 Atrophy blanche scarring surrounding an ulcer on the
of the foot. sole of the foot.

10.8 Obvious
varicose veins
and stasis
eczema.

10.9 Dermatoliposclerosis surrounding an ulcer.

10.10 Oedema and stasis eczema.

132 Leg ulcers and wound healing

Arterial disease
Poor arterial supply as a result of narrowing or occlusion of • Limb appearance/skin changes:
the vessels may lead to tissue ischaemia and necrosis. – Poor tissue perfusion and reduced capillary refill; absent
Predisposing factors such as a previous medical history of or difficult-to-locate pedal pulses.
myocardial infarction, transient ischaemic attacks, cerebral – Loss of hair on the lower leg and the skin may appear
vascular attack, hypertension, diabetes, rheumatoid atrophic and shiny, with trophic changes in the nails.
arthritis, peripheral neuropathy or diabetes, or a history of – Muscle wastage in the calf.
being a smoker may be suggestive of arterial disease. – The limb/foot may be cool to the touch with colour
• Ulcer site: ulcers may be sited anywhere around the lower changes evident, pale when raised and dusky pink when
limb or foot. dependent (10.13).
• Ulcer appearance: arterial ulcers tend to be deeper and
more punched out in appearance (10.11, 10.12). Mixed vessel
• Pain: patients may complain of severe pain, worse at Patients may present with a mixed vessel disease and may be
night or on elevation of the limb. They may also complain suffering from both venous and arterial disease (10.14).
of intermittent claudication, cramp-like pain in the calf
muscles brought on by walking a certain distance and
relieved upon rest.

10.12 Arterial
ulceration causing
the tendon to
protrude.

10.11 Arterial ulceration.

10.14 Severe
ulceration in
mixed vessel
disease. This
ulcer responded
very well to larva
therapy.

10.13 Gangrene of the toes in severe ischaemia.

 Leg ulcers and wound healing 133

Assessment and investigations

The key to successful leg ulcer management relies upon a an ABPI of 1.3 or above is obtained, as it may be a falsely
thorough and accurate assessment. To determine the high reading and indicative of arterial calcification.
underlying cause of the ulceration a number of factors
should be taken into consideration: Foot pulses
• Cause and history of current ulceration. The presence of palpable pulses can be checked; however,
• Current treatment and management strategies. their presence does not exclude significant arterial disease.
• Any previous history of ulceration.
• Current medication. Duplex scan
• Pain. Colour flow duplex ultrasonography can be used to obtain
• Current and previous medical history. more detailed anatomical and functional parameters, both
• Any drug allergies. on venous and arterial disease.
• Any known or suspected contact allergies.
• Attention paid to any previous leg problems.
• Site and appearance of the ulcer. Differential diagnosis
• Levels of wound exudate and any odour.
• Any local problems at the wound site that may complicate There are a number of differentials for arterial/venous causes
or delay healing. of ulcer. Varicose eczema (gravitational/stasis eczema/derma-
• Appearance of the limb and the skin surrounding the titis) is an eczematous eruption as a consequence of venous
ulcer. hypertension. It characteristically originates around the
• Social circumstances, paying particular attention to gaiter area of the lower leg; ulceration is not necessary for its
smoking history, diet, mobility, lifestyle, occupation, development. Its symptoms may include pain, erythema,
ability to sleep in bed, and duration of elevation. weeping, maceration, burning, itching, dryness, and scaling
(10.8, 10.15). Treatment involves the management of the
Simple investigations such as capillary refill, measure- venous hypertension combined with the application of
ment of the ankle and calf circumferences, wound mapping, emollients and topical steroids.
and photography of the wound and limb can be performed
easily.
10.15 Severe
Doppler ultrasound varicose eczema is
Doppler is a test carried out to establish the blood supply to often misdiagnosed
the lower limb and calculates the ankle brachial pressure as cellulitis and does
index (ABPI). This test should be carried out by a suitably not respond to
trained and experienced professional and the results should systemic antibiotics.
not be considered in isolation but as part of a holistic
assessment. This test involves recording a systolic pressure
with a hand-held Doppler machine at the foot, usually taken
at the dorsalis pedis and posterior tibial pulse, but it may
also be recorded at the peroneal and the anterior tibial
pulses, and also at the brachial artery. The foot pulse rate is
then divided by the brachial pulse rate to obtain a ratio, the
ABPI. In a limb with a normal blood supply, an ABPI of
around 1.0 can be expected; an ABPI of 0.8–1.0 suggests
some arterial involvement, an ABPI <0.79 is likely to
indicate significant arterial disease, while an ABPI <0.5
signifies severe arterial disease. Caution should be taken if
134 Leg ulcers and wound healing

Table 10.1 Allergen patch testing in leg Chronic oedema/lymphoedema is tissue swelling due to
ulcer patients failure of lymph drainage, further complicated by limb
dependency. Patients may present with primary
lymphoedema as a consequence of genetic abnormalities or
Allergen % positive Source
absent lymphatics. Secondary lymphoedema may occur as a
Lanolin 18 In emollients result of cancer or its subsequent treatment, trauma or
Fragrances 18 Soaps, body lotions injury to the lymphatic system, or secondary to venous
Neomycin 15 Topical antibiotic disease or prolonged dependency of a limb (10.16, 10.17).
Thiuram 14 Rubber accelerator Management relies upon elevation of the limb, external
found in bandages support, and manual lymph drainage.
Laceration, burns, radiation injuries, and other such
Colophony 11 Adhesive in
trauma can result in ulcers (10.18, 10.19). Where the
hydrocolloid dressings
patient has underlying venous/arterial problems, minor
Formaldehyde 7 Foam baths, some trauma can lead to intractable ulcer.
moisturizers Iatrogenic causes such as over-tight bandage and ill-
Hydrocortisone 3 Topical steroid fitting plaster cast can cause ulcers. This is a problem
particularly when arterial disease has failed to be recognized.
Self-inflicted ulcers can be secondary to IV drug use or
Contact allergy/irritation to components found in topical caused for psychological reasons in dermatitis artefacta.
skin and wound preparations is a common phenomenon in Asteatotic eczema occurs in older people with a dry,
patients with leg ulceration (10.5). Statistics vary, but ‘crazy-paving’ pattern, particularly on the legs. It is
between 20% and 50% of patients with chronic leg exacerbated by cold weather, central heating, and over
ulceration suffer from contact allergy. The commonest washing, and is treated with emollients (10.20).
culprits depend upon which products the local healthcare Pyoderma gangrenosum (10.21–10.23) causes painful
community apply to their patients. In the Nottingham area, ulceration on any area of the skin, the commonest sites
thiuram, lanolin, and hydrocortisone are the commonest being the legs then trunk. When on the lower aspect of the
allergens found on patch testing (Table 10.1). leg, it can be distinguished from venous ulceration by the

10.16 Weeping stasis 10.17 Chronic

eczema and cellulitis. lymphoedema due to
elephantiasis (worm
infestation of the
lymphatics).
 Leg ulcers and wound healing 135

10.18 Venous ulceration in an IV drug user. The deep and 10.19 Chronic thermal burns from sitting too close to
superficial veins are often thrombosed in this group of the fire. Signs of erythema ab igne are visible around
patients. the erythema.

10.20 Asteatotic eczema. 10.21 Pyoderma gangrenosum on the leg.

10.22 Pyoderma 10.23 Low-grade

gangrenosum on pyoderma
the back in a gangrenosum,
Crohn’s patient. which took
3 years to
diagnose.
136 Leg ulcers and wound healing

clinical appearance of a dusky, cyanotic edge to the ulcer, returning from the tropics (see Chapter 9).
rapid onset, and severe pain. However, sometimes it is a Various malignancies including squamous cell carcinoma
difficult diagnosis to make and low-grade pyoderma (SCC), basal cell carcinoma, malignant melanoma, and
gangrenosum is easily missed. Kaposi’s sarcoma can cause ulceration. Malignancy is an
Vasculitis (inflammation of cutaneous blood vessels) will uncommon cause of ulceration, but the possibility of
lead to leakage of blood (purpura) and skin necrosis if severe malignancy should not be overlooked in ulcers failing to
enough (10.24, 10.25). Blood disorders such as poly- respond to treatment. An SCC can develop in a chronic
cythaemia, sickle cell, and thalassaemia can cause ulcera- venous leg ulcer (Marjolin’s ulcer); it is rare but should be
tion. Infections including tuberculosis, leprosy, syphilis, and considered if the ulcer has an unusual appearance,
fungal infections should be considered. However, these are particularly overgrowth of tissue at the base or wound
rare causes in the UK, but may be seen in people living in or margin (10.26–10.28).

10.24 Haemorrhagic vasculitis. 10.25 Vasculitis that has ulcerated.

10.26 Basal cell carcinoma on the dorsum of the foot

(which looks like SCC).
10.27 Hyperplastic granulation tissue mimicking
squamous cell carcinomatous change. A biopsy is
essential in ruling out malignant change.
 Leg ulcers and wound healing 137

In diabetics, ulceration may be due to neuropathy or venous return due to ankle immobility, and the debilitating
impaired blood supply. Neuropathic ulcers occur as a result effect of prolonged steroid therapy.
of pressure exerted on the feet that they are unaware of Decubitus ulceration occurs at the site of pressure usually
because of loss of sensation due to diabetes. Ischaemic associated with immobility (10.30–10.32). An unconscious
ulcers occur due to damage to arterial circulation as a result patient will develop pressure sores within hours on the
of the disease process (10.29). Diabetes also delays wound sacrum or heel if not frequently turned. Prevention is the
healing. People with rheumatoid arthritis are thought to best treatment. Otherwise, dressings that enhance wound
develop ulcers due to a combination of local vasculitis, poor healing and pressure care are the best management.

10.28 Calcium deposits can occur in chronic ulcers. 10.29 Diabetic foot.

10.30 Nicorandil- 10.31 A pressure

induced perianal sore in a patient
ulceration. This is with a foot
probably due to deformity.
pressure and
irritant effects of
the bowel
contents.
138 Leg ulcers and wound healing

history of the wound occurrence, as well as the identification

and management of the underlying cause and the
appropriateness of care provision.
Graduated compression therapy can be applied in the
form of varying bandaging systems or compression hosiery.
Graduated external compression helps to reverse venous
hypertension and reduce oedema by forcing fluid from the
interstitial space back into the vascular and lymphatic
compartments, and by improving venous function. The
bandages or hosiery aim to provide graduation of the
compression by applying the highest compression (35–40
mmHg) at the ankle and reducing to approximately 17
mmHg just below the knee. By applying the bandages at the
10.32 A typical site for a decubitus ulcer in an same tension all the way up the limb the natural shape of
immobile patient. most legs facilitates graduated compression, as the
circumference of the limb increases as it gets towards the
knee.
There is a vast amount and variety of wound dressings
available; however, appropriate dressing selection relies
upon the skilled practitioner, with an appropriate dressing
Management leading to the provision of the optimum wound healing
environment.
The priority in the treatment of leg ulceration is Paste bandages may be applied on their own or can be
management of the underlying cause, i.e. improving the applied underneath graduated compression bandages and
venous or arterial circulation, and to create an optimum are particularly useful for acute flares of eczema,
wound healing environment4. It is also essential to address excoriation, and inflammation. They are also used for
any wider issues that may affect wound healing and work softening lichenified skin and act as an occlusive barrier to
towards preventing complications. protect the skin and to help prevent scratching. Zinc paste
The aim when managing venous disease is to reverse bandages are often the first paste bandage of choice but may
venous hypertension and aid venous return. This can be be impregnated with calamine, coal tar, or calamine and
achieved through the application of graduated external clioquinol or ichthammol. Choice will depend upon the
compression (see below) and through elevation and simple desired effect.
exercise of the limb. Management of arterial disease relies The skin on limbs occluded underneath bandages can
upon any feasible surgical intervention and the management become dehydrated. Emollients provide a surface lipid film,
of any wound and symptom relief such as pain and exudate which prevents water loss from the epidermis, and are most
control. effective when applied after washing when the water content
Wound healing depends upon the provision of the of the skin is at its greatest. Emollients used in the
optimum temperature, moisture, and pH for cells involved management of leg ulceration should be kept simple and
in the healing process. It is also essential that any foreign bland to minimize the risk of contact sensitivity.
bodies are removed, as is any devitalized tissue, thick Topical steroid therapy is the first-line treatment for the
slough, or pus. The wound should be protected from any management of eczema, and the lower leg is no exception.
avoidable trauma and the entry of any potentially However, it is important to consider the fact that the
pathogenic microorganisms, and any clinical infection potency of the steroid will be increased if applied
should be managed. It is important to consider other factors underneath an occlusive bandage or dressing. It is important
that may delay wound healing such as general health and also to consider whether the frequency of dressing change
any illnesses or diseases the patient may have, age, nutrition, may need to be increased to deal with an acute flare of
certain drug therapies, social environment, infection, the eczema on the lower leg.
 Leg ulcers and wound healing 139

Elevation of the limb when at rest is advantageous, References

provided there is adequate arterial supply to the limb. For
patients with venous disease sitting with the legs elevated 1 Dale J, Callam M, Ruckley C, Harper D, Berrey PN
above the level of the hips helps to reduce oedema by aiding (1983). Chronic ulcers of the leg: a study of prevalence
venous return. in a Scottish community. Health Bulletin 41:310–314.
Gentle exercise is important for all patients as it aids 2 Gawkrodger D (1997). Dermatology: An Illustrated Colour
venous return by activating the calf muscle pump, as well as Text (2nd edn). Churchill Livingstone, London.
helping to prevent other complications associated with 3 Cullum N (1994). Leg ulcers: a review of research in
prolonged immobility. nursing management in the community. Bandolier
www.jr2.ox.ac.uk/bandolier/band10/b10-2.html.
4 Falanga V, Phillips TJ, Harding KG, Moy RL, Peerson
LJ (eds) (2000). Text Atlas of Wound Management.
Martin Dunitz, London.
 141

Index

Note: page numbers in italic comedone, senile 60, 62 eczema (continued) granulation tissue, hyperplastic
refer to tables in the text compression therapy 138 nail dystrophy 108 136
contact dermatitis varicose/stasis 129, 131, 133, granuloma
ABCDE criteria 9–10 allergic (ACD) 2, 8, 67–8, 134 fish tank/swimming pool 116,
acne 6, 79–80 70, 70, 98 eczema herpeticum 120, 121 117
infantile 26, 27 facial 82, 83 elephantiasis 134 pyogenic 20
acne excoriée 79, 80 genital area 97 epidermis 1–2 granuloma annulare 22, 75
acne keloidalis nuchae 103 irritant (ICD) 66, 70, 70 epidermolysis bullosa 26, 27
acropustulosis of Hallopeau 107 wound preparations 134 epoxy resin allergy 67 haemangioma
actinic keratosis 48 cowpox 118, 119 erysipelas 114 infantile (strawberry naevus)
actinic porokeratosis, Coyrnebacterium spp. 115, 116 erythema 7 14, 15
disseminated superficial crust 7, 8 toxic 28, 29 thrombose 62
(DSAP) 50 cutaneous horn 50 erythema ab igne 135 Haemophilus influenzae type B
adenoma sebaceum 89 erythema multiforme 44, 45 114
alopecia Darier’s sign 20 erythrasma 116, 117 haemosiderin deposition 5, 129,
diffuse 105 DCM mnemonic 8–9 erythroderma 35–6, 41 130
scarring 87, 102, 103 decubitus ulceration 137–8 erythroplasia of Queyrat 51 hair follicles 2–4
traction 105 dermatitis, perioral 80, 81 ‘espundia’ 126 hyperkeratosis 90, 102
alopecia areata 99–100, 110 see also contact dermatitis; examination, skin 5–10 plugging 87
Ancyclostoma braziliense 124 eczema excoriated lesions 7 hair loss
angio-oedema 33, 34 dermatitis herpetiformis 8, 30, diffuse 105
ankle brachial pressure index 31 facial rashes trichotillomania 100
(ABPI) 133 dermatofibroma 47 history and clinical features see also alopecia
anthrax 118, 119 dermatoliposclerosis 131 77, 78 hands
aplasia cutis 18, 19 dermatomyositis 75, 89 management 78, 79 dermatomyositis 75, 89
apocrine glands 3, 4 dermatophyte infections 101, see also named conditions eczema 65–70, 72, 73, 108
arsenical keratoses 52 123 feet fungal infections 72–3
atrophoderma vermiculatum 90 see also tinea dermatitis 66–70 palmar pustulosis 74
atrophy blanche 129, 131 dermis 2 fungal infections 72–3 psoriasis 71–2, 73
autoimmune bullous disease 95 dermographism 33, 36 plantar pustulosis 74 see also nails
diabetes mellitus 137 scabies 75, 76 ‘heliotrope’ rash 89
bacterial infections 113–19 disseminated superficial actinic tungiasis 125 Henoch–Schönlein purpura 28,
basal cell carcinoma (BCC) porokeratosis (DSAP) 50 see also nails 29
52–4, 136 Doppler ultrasound 133 fibroma, periungual 111 herpes simplex 9, 44, 120, 121
biopsies 10 drug reactions 6, 20, 28, 34, 36, fish tank granuloma 116, 117 herpes zoster 120, 121
birthmarks 14–19 40, 44 flea bites 34, 35 herpetiform lesions 8
Bowen’s disease (intraepithelial drug use, IV 134, 135 fly larvae 127 history taking 4, 77
carcinoma) 49 duplex ultrasonography, colour follicular hyperkeratosis 90, 102 hookworm, dog 124, 125
bulla 5 flow 133 follicular plugging 87 human papilloma virus 51, 96
bullous disease dysplasia, genitalia 96 folliculitis decalvans 102 Hutchinson’s sign 61
chronic of childhood 30, 31 fungal infections 123–4 hyperpigmentation 6, 7
impetigo 44, 45 ecchymosis 7 hands and feet 72–3 hyperplastic granulation tissue
pemphigoid 44, 45, 75, 95 eccrine sweat glands 3, 4 nails 106, 107 136
burns, thermal 135 eczema see also tinea hypopigmentation 7, 30
‘butterfly’ rash 87, 88 asteatotic 134, 135
atopic 36, 82, 83 genetic factors icthyosis 26, 27
café au lait macule 16, 17 atopic in infancy 24, 25, 26 basal cell carcinoma 52 immunosuppressive agents 41–2
Candida infection 24 discoid 38 melanoma/dysplastic naevi 56 impetigo 7, 8, 113–14
cayenne pepper spots 94, 95 endogenous 69, 70 squamous cell carcinoma 54 bullous 44, 45
cellulitis 114–15 genital area 97–8 genital disease insect bites 34, 35
dissecting of the scalp 102 hand and foot 65–70, 108 diagnosis 91 insect infestations 125, 127
cervical intraepithelial neoplasia hyperkeratotic hand (tylotic) see also named conditions intraepithelial carcinoma
(CIN) 96 72, 73 gonococcal septicaemia 118, 119 (IEC/Bowen’s disease) 49
Clark’s (dysplastic) naevus 56–8 impetiginized 7, 8 Gottron’s papules 75, 89 investigations 10–11
142 Index

Jessner’s benign lymphocytic melasma 86 paste bandages 138 seborrhoeic dermatitis 84

infiltrate 88 Merkel cells 2 patch 5 infantile 24
juvenile plantar dermatosis 32, Microcossus spp. 115 patch testing 10, 10, 11, 67, 98 seborrhoeic keratosis 62
66 Microsporum canis 101 pemphigoid 75 ‘shagreen patch’ 89
milaria 23 bullous 44, 45, 95 skin anatomy and physiology
kala-azar 126 molluscum contagiosum 120, cicatricial 95 1–4
keloid 6 121 pemphigus 95 skin prick tests 10, 11
keratin layer 1, 2 Mongolian blue spot 18, 19 penile intraepithelial neoplasia skin scrapings 10
keratoacanthoma 55 Mycobacterium marinum 116, 96 smoking 96
keratolysis, pitted 115 117 petechia 7 spider naevus 22
keratosis Mycoplasma pneumoniae 44 phospholipid syndrome 76 sporotrichosis 116, 117
arsenical 52 mycosis fungoides 35, 36 pigmentation 2, 7 squamous cell carcinoma 54–5,
seborrhoeic 62 myiasis 127 pilomatricoma 20, 21 92, 96, 136
keratosis pilaris 30, 31, 90 myxoid cyst 111 Pincer nail 110, 111 in situ (intraepithelial
kerion 101 pityriasis alba 30, 31 carcinoma) 49
Koebner’s phenomenon 40 naevus pityriasis amiantacea 101 staphylococcal scalded skin
compound melanocytic 58 pityriasis rosea 28, 29 syndrome 28, 29
Langerhans cell histiocytosis 24, congenital melanocytic 16, 17 pityriasis versicolor 124 Staphylococcus aureus 38, 43,
25 dysplastic 56–8 Pityrosporum orbiculare 124 102, 114
Langerhans cells 2, 99 epidermal 18, 19 Pityrosporum ovale 84 striae 32
larva migrans, cutaneous 124, halo 57, 58 plantar dermatosis, juvenile 32, syphilis, secondary 118, 119
125 intradermal 6 66
leather allergy 67, 68 junctional 57 plaque 5, 6 target lesions 44, 45
leg ulcers Meyerson’s 58 pompholyx, recurrent of telangiectasia, nail-fold 89
arterial disease 132 papillomatous 57 palms/soles 69 telogen effluvium 105
assessment and investigations sebaceous 18, 19 port wine stain 16, 17 tinea infections 123
133 spider 22 pressure sores 137–8 tinea capitis 101
differential diagnosis 133–8 strawberry 14, 15 ‘prickle cell’ layer 1–2 tinea corporis 38
management 138–9 naevus depigmentosum 30 Propionibacterium acnes 79 tinea facei 87, 88
mixed vessel disease 132 naevus flammeus (salmon patch) pseudopelade of Brocque 104 tinea manum 73, 123
venous disease 129–31 15 psoriasis 6, 8, 39–42 tinea pedis 106
leishmaniasis 116, 126 naevus sebaceus 104 arthropathy 40, 42 trachyonychia 109
lentigo maligna 58–9 nail folds, telangiectasia 89 clinical features/differential Treponema pallidum 118
lentigo maligna melanoma 60 nails diagnoses 41 Trichophyton tonsurans 101
lichen aureus 5 alopecia areata 99, 110 erythrodermic 35, 41 trichotillomania 100
lichen planopilaris 103 eczematous dystrophy 108 facial 84, 85 tuberculous chancre 116, 117
lichen planus 75, 93–4, 109 lichen planus 109 hands and feet 71–2, 73 tuberous sclerosis 89, 111
lichen sclerosus 91–2 median dystrophy 111 in infancy 26, 27 tungiasis 125
lichen simplex 97 neoplasia 60, 61, 111 nail involvement 107–8 ‘twenty nail dystrophy’ 109
lichen striatus 9 onychogryphosis 110 palmo-plantar pustular 41, 74
lichenification 36, 37, 82, 83 onychomycosis 106, 107 with seborrhoeic dermatitis ultraviolet (UV) radiation 41,
lupus erythematosus 44, 86–8 Pincer 110, 111 84, 85 48, 49, 52, 54
discoid 77, 86–7, 104 psoriasis 41, 107–8 psychological factors 4, 100 urticaria 2, 33–5
subacute cutaneous (SCLE) yellow nail syndrome 110 punch biopsy 10 urticaria pigmentosum 20, 21
86, 88 nappy area 14, 23, 24, 26, 27 purpura 7
lymphangioma circumscriptum necrotizing fasciitis 114, 115 pyoderma gangrenosum 134–6 varicose veins 129, 131
16, 17 neonatal rashes 23–7 pyogenic granuloma 20, 62 vasculitis 7, 75, 76, 136
lymphoedema, chronic 134 neurofibromatosis 16 vesicle 5
lymphoma, cutaneous (mycosis nickel 8 radiation-induced keratoses 51 viral infections 9, 44, 120–2
fungoides) 35, 36 nodules 5, 6 rheumatoid arthritis 137 vitiligo 30, 31
rhinophyma 81 vulval eczema 97
macule 5 oedema, lower limb 129, 131, ringworm 101, 123 vulval intraepithelial neoplasia
Marjolin’s ulcer 136 134 ‘rodent ulcer’ 52, 53 96
mastocytoma 20 onychogryphosis 110 rosacea 80–1 vulval ulceration 98
medical history 4 onychomycosis 106, 107 rubber allergy 67, 68 vulvo-vaginal-oral syndrome 94
melanocytes 2 oral disease
melanoma, malignant 9–10 bullous autoimmune 95 salmon patch (naevus flammeus) warts, viral 122
acral lentiginous 60, 61 diagnostic difficulties 91 15 wound preparations 134, 138
desmoplastic 61 lichen planus 93 sand flea (jigger) infestation 125
differential diagnosis 62 malignant lesions 96 scabies 42–3, 75, 76 xanthogranuloma 20, 21
early diagnosis 56 orf 122 scalp disorders 99–105
lentigo maligna 60 aplasia cutis 18, 19 yellow nail syndrome 110
management 62 paediatric dermatoses 13 basal cell carcinoma 53
nodular 47, 60 rashes 14, 23–32 psoriasis 39, 41 Zoon’s balanitis 94
precursor lesions 56–9 skin lesions 13, 14–22 sebaceous glands 3, 4 Zoon’s vulvitis 95
superficial spreading 59 palmo-plantar pustulosis 41, 74 sebaceous naevus 18, 19
verrucous 61 papular lesions 5, 6 sebo-psoriasis 84, 85