Dermatology Handbook

Dermatology
A handbook for medical students & junior doctors
British Association of Dermatologists
Dermatology: Handbook for medical students & junior doctors
This publication is supported by the British Association of Dermatologists.
First edition 2009

Revised first edition 2009
Second edition 2014
For comments and feedback, please contact the author at [email protected].
Dermatology
A handbook for medical students & junior doctors
Dr Nicole Yi Zhen Chiang MBChB (Hons), MRCP (UK)

Specialty Registrar in Dermatology
Salford Royal NHS Foundation Trust
Manchester M6 8HD
Professor Julian Verbov MD FRCP FRCPCH CBiol FSB FLS

Professor of Dermatology
Consultant Paediatric Dermatologist
Alder Hey Childrens Hospital
Liverpool L12 2AP
Contents
Preface
Foreword
What is dermatology?
Essential Clinical Skills
Taking a dermatological history

Examining the skin
Communicating examination findings
8
9
10
Background Knowledge
23
Functions of normal skin

Structure of normal skin and the skin appendages
Principles of wound healing
23
23
27
Emergency Dermatology
28
Urticaria, Angioedema and Anaphylaxis

Erythema nodosum
Erythema multiforme, Stevens-Johnson syndrome, Toxic epidermal necrolysis
Acute meningococcaemia
Erythroderma
Eczema herpeticum
Necrotizing fasciitis
Skin Infections / Infestations
29
30
31
32
33
34
35
36
Erysipelas and cellulitis

Staphylococcal scalded skin syndrome
Superficial fungal skin infections
37
38
39
Skin Cancer
41
Basal cell carcinoma

Squamous cell carcinoma
Malignant melanoma
42
43
44
Inflammatory Skin Conditions
46
Atopic eczema
Acne vulgaris
Psoriasis
47
49
50
Blistering Disorders
52
Bullous pemphigoid
Pemphigus vulgaris
53
54
Common Important Problems
55
Chronic leg ulcers

Itchy eruption
A changing pigmented lesion
Purpuric eruption
A red swollen leg
56
58
60
62
64
Management
65
Emollients
Topical/Oral steroids
Oral aciclovir
Oral antihistamines
Topical/Oral antibiotics
Topical antiseptics
Oral retinoids
66
66
66
66
67
67
67
Practical Skills
68
Patient education
Written communication
Prescribing skills
Clinical examination and investigations
71
69
70
70
71
Acknowledgements
72
Preface
This Handbook of Dermatology is intended for senior medical students and newly qualified
doctors.
For many reasons, including modern medical curriculum structure and a lack of suitable
patients to provide adequate clinical material, most UK medical schools provide inadequate
exposure to the specialty for the undergraduate. A basic readable and understandable text
with illustrations has become a necessity.
This text is available online and in print and should become essential reading. Dr Chiang is to
be congratulated for her exceptional industry and enthusiasm in converting an idea into a
reality.
Julian Verbov
Liverpool 2009
Preface to the 2nd edition

Nicole and I are gratifed by the response to this Handbook which clearly fulfils its purpose.
The positive feedback we have received has encouraged us to slightly expand the text and
allowed us to update where necessary. I should like to thank the BAD for its continued
support.
Julian Verbov
Liverpool 2014
Foreword to First edition

There is a real need for appropriate information to meet the educational needs of doctors at
all levels. The hard work of those who produce the curricula on which teaching is based can
be undermined if the available teaching and learning materials are not of a standard that
matches the developed content. I am delighted to associate the BAD with this excellent
handbook, designed and developed by the very people at whom it is aimed, and matching
the medical student and junior doctor curriculum directly. Any handbook must meet the
challenges of being comprehensive, but brief, well illustrated, and focused to clinical
presentations as well as disease groups. This book does just that, and is accessible and easily
used. It may be read straight through, or dipped into for specific clinical problems. It has
valuable sections on clinical method, and useful tips on practical procedures. It should find a
home in the pocket of students and doctors in training, and will be rapidly worn out. I wish it
had been available when I was in need, I am sure that you will all use it well in the pursuit of
excellent clinical dermatology!
Dr Mark Goodfield
President of the British Association of Dermatologists
What is dermatology?
Dermatology is the study of both normal and abnormal skin and associated
structures such as hair, nails, and oral and genital mucous membranes.
Why is dermatology important?
Skin diseases are very common, affecting up to a third of the population at any one
time.
Skin diseases have serious impacts on life. They can cause physical damage,
embarrassment, and social and occupational restrictions. Chronic skin diseases may
cause financial constraints with repeated sick leave. Some skin conditions can be
life-threatening.
In 2006-07, the total NHS health expenditure for skin diseases was estimated to be
around 97 million (approximately 2% of the total NHS health expenditure).
What is this handbook about?
The British Association of Dermatologists outlined the essential and important

learning outcomes that should be achieved by all medical undergraduates for the
competent assessment of patients presenting with skin disorders (available on:
http://www.bad.org.uk/Portals/_Bad/Education/Undergraduate%20Edu
cation/(Link2)%20Core%20curriculum.pdf).
This handbook addresses these learning outcomes and aims to equip you with the
knowledge and skills to practise competently and safely as a junior doctor.
Essential Clinical Skills
Detailed history taking and examination provide important diagnostic clues in the
assessment of skin problems.
Learning outcomes:
1. Ability to take a dermatological history
2. Ability to explore a patients concerns and expectations
3. Ability to interact sensitively with people with skin disease
4. Ability to examine skin, hair, nails and mucous membranes systematically
showing respect for the patient
5. Ability to describe physical signs in skin, hair, nails and mucosa
6. Ability to record findings accurately in patients records
Taking a dermatological history
Using the standard structure of history taking, below are the important points to
consider when taking a history from a patient with a skin problem (Table 1).
For dark lesions or moles, pay attention to questions marked with an asterisk (*).
Table 1. Taking a dermatological history

Main headings
Key questions
Presenting complaint
Nature, site and duration of problem
History of presenting complaint
Initial appearance and evolution of lesion*

Symptoms (particularly itch and pain)*
Aggravating and relieving factors
Previous and current treatments (effective or not)
Recent contact, stressful events, illness and travel
History of sunburn and use of tanning machines*
Skin type (see page 70)*
Past medical history
History of atopy i.e. asthma, allergic rhinitis, eczema

History of skin cancer and suspicious skin lesions
Family history
Family history of skin disease*
Social history
Occupation (including skin contacts at work)

Improvement of lesions when away from work
Medication and allergies
Regular, recent and over-the-counter medications
Impact on quality of life
Impact of skin condition and concerns
Essential Clinical Skills Taking a dermatological history
Essential Clinical Skills Examining the skin
Examining the skin
There are four important principles in performing a good examination of the skin:
INSPECT, DESCRIBE, PALPATE and SYSTEMATIC CHECK (Table 2).
Table 2. Examining the skin

Main principles
Key features
INSPECT in general
General observation
Site and number of lesion(s)
If multiple, pattern of distribution and configuration
DESCRIBE the individual lesion
SCAM
Size (the widest diameter), Shape
Colour
Associated secondary change
Morphology, Margin (border)
*If the lesion is pigmented, remember ABCD

(the presence of any of these features increase the likelihood of melanoma):
Asymmetry (lack of mirror image in any of the
four quadrants)
Irregular Border
Two or more Colours within the lesion
Diameter > 6mm
PALPATE the individual lesion
Surface
Consistency
Mobility
Tenderness
Temperature
SYSTEMATIC CHECK
Examine the nails, scalp, hair & mucous membranes

General examination of all systems
Communicating examination findings
In order to describe, record and communicate examination findings accurately, it is

important to learn the appropriate terminology (Tables 3-10).
Table 3. General terms

Terms
Meaning
Pruritus
Itching
Lesion
An area of altered skin
Rash
An eruption
Naevus
A localised malformation of tissue structures

Example: (Picture Source: D@nderm)
Pigmented melanocytic naevus (mole)
Comedone
A plug in a sebaceous follicle containing altered sebum, bacteria and

cellular debris; can present as either open (blackheads) or closed
(whiteheads)
Example:
Open comedones (left) and closed comedones (right) in acne
10
Essential Clinical Skills Communicating examination findings
Table 4. Distribution (the pattern of spread of lesions)

Terms
Meaning
Generalised
All over the body
Widespread
Extensive
Localised
Restricted to one area of skin only
Flexural
Body folds i.e. groin, neck, behind ears, popliteal and antecubital fossa
Extensor
Knees, elbows, shins
Pressure areas Sacrum, buttocks, ankles, heels

Dermatome
An area of skin supplied by a single spinal nerve
Photosensitive Affects sun-exposed areas such as face, neck and back of hands
Example:
Sunburn
Kebner
A linear eruption arising at site of trauma
phenomenon Example:
Psoriasis
11
Table 5. Configuration (the pattern or shape of grouped lesions)

Terms
Meaning
Discrete
Individual lesions separated from each other
Confluent
Lesions merging together
Linear
In a line
Target
Concentric rings (like a dartboard)

Example:
Erythema multiforme
Annular
Like a circle or ring

Example:
Tinea corporis
(ringworm)
Discoid /
A coin-shaped/round lesion
Nummular
Example:
Discoid eczema
12
Table 6. Colour
Terms
Meaning
Erythema
Redness (due to inflammation and vasodilatation) which blanches on

pressure
Example:
Palmar erythema
Purpura
Red or purple colour (due to bleeding into the skin or mucous membrane)
which does not blanch on pressure petechiae (small pinpoint macules) and
ecchymoses (larger bruise-like patches)
Example:
Henoch-Schnlein purpura
(palpable small vessel vasculitis)
13
Hypo-
Area(s) of paler skin
pigmentation Example:
Pityriasis versicolor
(a superficial fungus infection)
De-
White skin due to absence of melanin
Vitiligo
(loss of skin melanocytes)
Hyper-
Darker skin which may be due to various causes (e.g. post-inflammatory)
Melasma
(increased melanin pigmentation)
14
Table 7. Morphology (the structure of a lesion) Primary lesions

Terms
Meaning
Macule
A flat area of altered colour

Example:
Freckles
Patch
Larger flat area of altered colour or texture

Example:
Vascular malformation
(naevus flammeus / port wine stain)
Papule
Solid raised lesion < 0.5cm in diameter

Example:
Xanthomata
15
Nodule
Solid raised lesion >0.5cm in diameter with a deeper component

Example: (Picture source: D@nderm)
Pyogenic granuloma
(granuloma telangiectaticum)
Plaque
Palpable scaling raised lesion >0.5cm in diameter

Example:
Psoriasis
Vesicle
Raised, clear fluid-filled lesion <0.5cm in diameter
(small blister) Example:
Acute hand eczema

(pompholyx)
Bulla
Raised, clear fluid-filled lesion >0.5cm in diameter
(large blister) Example:
Reaction to insect bites
16
Pustule
Pus-containing lesion <0.5cm in diameter

Example:
Acne
Abscess
Localised accumulation of pus in the dermis or subcutaneous tissues

Example:
Periungual abscess
(acute paronychia)
W(h)eal
Transient raised lesion due to dermal oedema

Example:
Urticaria
Boil/Furuncle Staphylococcal infection around or within a hair follicle
Carbuncle
Staphylococcal infection of adjacent hair follicles (multiple boils/furuncles)
17
Table 8. Morphology - Secondary lesions (lesions that evolve from primary lesions)
Terms
Meaning
Excoriation
Loss of epidermis following trauma

Example:
Excoriations in eczema
Lichenification Well-defined roughening of skin with accentuation of skin markings

Example:
Lichenification due to chronic rubbing in eczema
Scales
Flakes of stratum corneum

Example:
Psoriasis (showing silvery scales)
18
Crust
Rough surface consisting of dried serum, blood, bacteria and cellular debris
that has exuded through an eroded epidermis (e.g. from a burst blister)
Example:
Impetigo
Scar
New fibrous tissue which occurs post-wound healing, and may be atrophic
(thinning), hypertrophic (hyperproliferation within wound boundary), or
keloidal (hyperproliferation beyond wound boundary)
Example:
Keloid scars
Ulcer
Loss of epidermis and dermis (heals with scarring)

Example:
Leg ulcers
19
Fissure
An epidermal crack often due to excess dryness

Example:
Eczema
Striae
Linear areas which progress from purple to pink to white, with the
histopathological appearance of a scar (associated with excessive steroid
usage and glucocorticoid production, growth spurts and pregnancy)
Example:
Striae
20
Table 9. Hair
Terms
Meaning
Alopecia
Loss of hair
Example:
Alopecia areata
(well-defined patch of complete hair loss)
Hirsutism
Androgen-dependent hair growth in a female

Example:
Hirsutism
Hypertrichosis Non-androgen dependent pattern of excessive hair growth

(e.g. in pigmented naevi)
Example:
Hypertrichosis
21
Table 10. Nails

Terms
Meaning
Clubbing
Loss of angle between the posterior nail fold and nail plate
(associations include suppurative lung disease, cyanotic heart disease,
inflammatory bowel disease and idiopathic)
Clubbing
Koilonychia
Spoon-shaped depression of the nail plate

(associations include iron-deficiency anaemia, congenital and idiopathic)
Koilonychia
Onycholysis
Separation of the distal end of the nail plate from nail bed
(associations include trauma, psoriasis, fungal nail infection and
hyperthyroidism)
Onycholysis
Pitting
Punctate depressions of the nail plate

(associations include psoriasis, eczema and alopecia areata)
Pitting
22
Background Knowledge Functions
This section covers the basic knowledge of normal skin structure and function
required to help understand how skin diseases occur.
Learning outcomes:
1. Ability to describe the functions of normal skin
of normal skin
2. Ability to describe the structure of normal skin

3. Ability to describe the principles of wound healing
4. Ability to describe the difficulties, physical and psychological, that may be
experienced by people with chronic skin disease
Functions of normal skin
These include:
i)
Protective barrier against environmental insults
ii)
Temperature regulation
iii)
Sensation
iv)
Vitamin D synthesis
v)
Immunosurveillance
vi)
Appearance/cosmesis
The skin is the largest organ in the human body. It is composed of the epidermis and
dermis overlying subcutaneous tissue. The skin appendages (structures formed by
skin-derived cells) are hair, nails, sebaceous glands and sweat glands.
Epidermis
The epidermis is composed of 4 major cell types, each with specific functions (Table
11).
23
Table 11. Main functions of each cell type in the epidermis

Main functions
Keratinocytes
Produce keratin as a protective barrier
Langerhans cells
Present antigens and activate T-lymphocytes for immune protection
Melanocytes
Produce melanin, which gives pigment to the skin and protects the
cell nuclei from ultraviolet (UV) radiation-induced DNA damage
Merkel cells
Contain specialised nerve endings for sensation
There are 4 layers in the epidermis (Table 12), each representing a different stage of
maturation of the keratinocytes. The average epidermal turnover time (migration of
cells from the basal cell layer to the horny layer) is about 30 days.
Table 12. Composition of each epidermal layer

Epidermal layers
Composition
Stratum basale
Actively dividing cells, deepest layer
(Basal cell layer)

Stratum spinosum
Differentiating cells
(Prickle cell layer)

Stratum granulosum
So-called because cells lose their nuclei and contain
(Granular cell layer)
granules of keratohyaline. They secrete lipid into the

intercellular spaces.
Stratum corneum
Layer of keratin, most superficial layer
(Horny layer)
In areas of thick skin such as the sole, there is a fifth layer, stratum lucidum, beneath
the stratum corneum. This consists of paler, compact keratin.
Pathology of the epidermis may involve:

a) changes in epidermal turnover time - e.g. psoriasis (reduced epidermal
turnover time)
b) changes in the surface of the skin or loss of epidermis - e.g. scales,
crusting, exudate, ulcer
c) changes in pigmentation of the skin - e.g. hypo- or hyper-pigmented skin
24
Cell types
Dermis
The dermis is made up of collagen (mainly), elastin and glycosaminoglycans, which

are synthesised by fibroblasts. Collectively, they provide the dermis with strength
and elasticity.
The dermis also contains immune cells, nerves, skin appendages as well as lymphatic
and blood vessels.
Pathology of the dermis may involve:

a) changes in the contour of the skin or loss of dermis e.g. formation of
papules, nodules, skin atrophy and ulcers
b) disorders of skin appendages e.g. disorders of hair, acne (disorder of
sebaceous glands)
c) changes related to lymphatic and blood vessels e.g. erythema
(vasodilatation), urticaria (increased permeability of capillaries and small
venules), purpura (capillary leakage)
Hair
There are 3 main types of hair:

a) lanugo hair (fine long hair in fetus)
b) vellus hair (fine short hair on all body surfaces)
c) terminal hair (coarse long hair on the scalp, eyebrows, eyelashes and
pubic areas)
Each hair consists of modified keratin and is divided into the hair shaft (a keratinized
tube) and hair bulb (actively dividing cells, and melanocytes which give pigment to
the hair).
Each hair follicle enters its own growth cycle. This occurs in 3 main phases:
a) anagen (long growing phase)
b) catagen (short regressing phase)
c) telogen (resting/shedding phase)
Pathology of the hair may involve:

a) reduced or absent melanin pigment production e.g. grey or white hair
b) changes in duration of the growth cycle e.g. hair loss (premature entry of
hair follicles into the telogen phase)
c) shaft abnormalities
25
Nails
The nail is made up of a nail plate (hard keratin) which arises from the nail matrix at
the posterior nail fold, and rests on the nail bed.
The nail bed contains blood capillaries which gives the pink colour of the nails.
Pathology of the nail may involve:

a) abnormalities of the nail matrix e.g. pits and ridges
b) abnormalities of the nail bed e.g. splinter haemorrhage
c) abnormalities of the nail plate e.g. discoloured nails, thickening of nails
Sebaceous glands
Sebaceous glands produce sebum via hair follicles (collectively called a

pilosebaceous unit). They secrete sebum onto the skin surface which lubricates and
waterproofs the skin.
Sebaceous glands are stimulated by the conversion of androgens to

dihydrotestosterone and therefore become active at puberty.
Pathology of sebaceous glands may involve:

a) increased sebum production and bacterial colonisation e.g. acne
b) sebaceous gland hyperplasia
Sweat glands
Sweat glands regulate body temperature and are innervated by the sympathetic
nervous system.
They are divided into two types: eccrine and apocrine sweat glands.
Eccrine sweat glands are universally distributed in the skin.
Apocrine sweat glands are found in the axillae, areolae, genitalia and anus, and
modified glands are found in the external auditory canal. They only function from
puberty onwards and action of bacteria on the sweat produces body odour.
Pathology of sweat glands may involve:

a) inflammation/infection of apocrine glands e.g. hidradenitis suppurativa
b) overactivity of eccrine glands e.g. hyperhidrosis
26
Background Knowledge Structure of normal skin and the skin appendages
Background Knowledge Principles of wound healing
Principles of wound healing
Wound healing occurs in 4 phases: haemostasis, inflammation, proliferation and

remodelling (Table 13).
Table 13. Stages of wound healing

Stages of wound healing
Mechanisms
Haemostasis
Vasoconstriction and platelet aggregation

Clot formation
Inflammation
Vasodilatation
Migration of neutrophils and macrophages
Phagocytosis of cellular debris and invading
bacteria
Proliferation
Granulation tissue formation (synthesised by
fibroblasts) and angiogenesis

Re-epithelialisation (epidermal cell proliferation
and migration)
Remodelling
Collagen fibre re-organisation

Scar maturation
27
These are rapidly progressive skin conditions and some are potentially lifethreatening. Early recognition is important to implement prompt supportive care
and therapy.
Some are drug reactions and the offending drug should be withdrawn.
The essential management for all dermatological emergencies, like any emergency,
consists of:
i)
full supportive care - ABC of resuscitation
ii)
withdrawal of precipitating agents
iii)
management of associated complications
iv)
specific treatment (highlighted below under each condition)
Learning outcomes:
1. Ability to recognise and describe these skin reactions:
- urticaria
- erythema nodosum
- erythema multiforme
2. Ability to recognise these emergency presentations, discuss the causes,

potential complications and provide first contact care in these emergencies:
- anaphylaxis and angioedema
- toxic epidermal necrolysis
- Stevens-Johnson syndrome
- acute meningococcaemia
- erythroderma
- eczema herpeticum
- necrotising fasciitis
28
Emergency Dermatology Urticaria, Angioedema and Anaphylaxis
Urticaria, Angioedema and Anaphylaxis
Causes
Idiopathic, food (e.g. nuts, sesame seeds, shellfish, dairy
products), drugs (e.g. penicillin, contrast media, non-steroidal antiinflammatory drugs (NSAIDs), morphine, angiotensin-converting
enzyme inhibitors (ACE-i)), insect bites, contact (e.g. latex), viral or
parasitic infections, autoimmune, and hereditary (in some cases of
angioedema)
Description
Urticaria is due to a local increase in permeability of capillaries
and small venules. A large number of inflammatory mediators

(including prostaglandins, leukotrienes, and chemotactic factors)
play a role but histamine derived from skin mast cells appears to
be the major mediator. Local mediator release from mast cells can
be induced by immunological or non-immunological mechanisms.
Presentation
Urticaria (swelling involving the superficial dermis, raising the
epidermis): itchy wheals

Angioedema (deeper swelling involving the dermis and
subcutaneous tissues): swelling of tongue and lips

Anaphylaxis (also known as anaphylactic shock): bronchospasm,
facial and laryngeal oedema, hypotension; can present initially

with urticaria and angioedema
Management
Antihistamines for urticaria

Corticosteroids for severe acute urticaria and angioedema
Adrenaline, corticosteroids and antihistamines for anaphylaxis
Complications
Urticaria is normally uncomplicated

Angioedema and anaphylaxis can lead to asphyxia, cardiac arrest
and death
Urticaria
Angioedema
29
Erythema nodosum
Description
A hypersensitivity response to a variety of stimuli
Causes
Group A beta-haemolytic streptococcus, primary tuberculosis,
pregnancy, malignancy, sarcoidosis, inflammatory bowel disease

(IBD), chlamydia and leprosy
Presentation
Discrete tender nodules which may become confluent

Lesions continue to appear for 1-2 weeks and leave bruise-like
discolouration as they resolve

Lesions do not ulcerate and resolve without atrophy or scarring
The shins are the most common site
Erythema nodosum
30
Emergency Dermatology Erythema nodosum
Emergency Dermatology Erythema multiforme, Stevens-Johnson syndrome and Toxic epidermal necrolysis
Erythema multiforme, Stevens-Johnson syndrome and Toxic epidermal necrolysis
Description
Erythema multiforme, often of unknown cause, is an acute self-
limiting inflammatory condition with herpes simplex virus being

the main precipitating factor. Other infections and drugs are also
causes. Mucosal involvement is absent or limited to only one
mucosal surface.
Stevens-Johnson syndrome is characterised by
mucocutaneous necrosis with at least two mucosal sites involved.

Skin involvement may be limited or extensive. Drugs or
combinations of infections or drugs are the main associations.
Epithelial necrosis with few inflammatory cells is seen on
histopathology. The extensive necrosis distinguishes StevensJohnson syndrome from erythema multiforme. Stevens-Johnson
syndrome may have features overlapping with toxic epidermal
necrolysis including a prodromal illness.
Toxic epidermal necrosis which is usually drug-induced, is
an acute severe similar disease characterised by extensive skin and

mucosal necrosis accompanied by systemic toxicity. On
histopathology there is full thickness epidermal necrosis with
subepidermal detachment.
Management
Early recognition and call for help
Full supportive care to maintain haemodynamic equilibrium

Complications
Mortality rates are 5-12% with SJS and >30% with TEN with
death often due to sepsis, electrolyte imbalance or multi-system
organ failure
Erythema multiforme
Stevens-Johnson syndrome
31
Acute meningococcaemia
Description
A serious communicable infection transmitted via respiratory
secretions; bacteria get into the circulating blood

Cause
Gram negative diplococcus Neisseria meningitides
Presentation
Features of meningitis (e.g. headache, fever, neck stiffness),
septicaemia (e.g. hypotension, fever, myalgia) and a typical rash

Non-blanching purpuric rash on the trunk and extremities, which
may be preceded by a blanching maculopapular rash, and can

rapidly progress to ecchymoses, haemorrhagic bullae and tissue
necrosis
Management
Antibiotics (e.g. benzylpenicillin)

Prophylactic antibiotics (e.g. rifampicin) for close contacts (ideally
within 14 days of exposure)

Complications
Septicaemic shock, disseminated intravascular coagulation, multi-
organ failure and death
Further reading: Hart CA, Thomson APJ. Meningococcal disease and its management in children.
BMJ 2006;333:685-690 (http://www.bmj.com/cgi/content/full/333/7570/685)
32
Emergency Dermatology Acute meningococcaemia
Emergency Dermatology Erythroderma
Erythroderma (red skin)
Description
Exfoliative dermatitis involving at least 90% of the skin surface
Causes
Previous skin disease (e.g. eczema, psoriasis), lymphoma, drugs
(e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol,

captopril) and idiopathic
Presentation
Skin appears inflamed, oedematous and scaly

Systemically unwell with lymphadenopathy and malaise
Management
Treat the underlying cause, where known

Emollients and wet-wraps to maintain skin moisture
Topical steroids may help to relieve inflammation
Complications
Secondary infection, fluid loss and electrolyte imbalance,
hypothermia, high-output cardiac failure and capillary leak

syndrome (most severe)
Prognosis
Largely depends on the underlying cause

Overall mortality rate ranges from 20 to 40%
Erythroderma
33
Eczema herpeticum (Kaposis varicelliform eruption)
Description
Widespread eruption - serious complication of atopic eczema or
less commonly other skin conditions

Cause
Herpes simplex virus
Presentation
Extensive crusted papules, blisters and erosions

Systemically unwell with fever and malaise
Management
Antivirals (e.g. aciclovir)

Antibiotics for bacterial secondary infection
Complications
Herpes hepatitis, encephalitis, disseminated intravascular
coagulation (DIC) and rarely, death
Eczema herpeticum
34
Emergency Dermatology Eczema herpeticum
Emergency Dermatology Necrotising fasciitis
Necrotising fasciitis
Description
A rapidly spreading infection of the deep fascia with secondary
tissue necrosis
Causes
Group A haemolytic streptococcus, or a mixture of anaerobic and
aerobic bacteria
Risk factors include abdominal surgery and medical co-morbidities
(e.g. diabetes, malignancy)

50% of cases occur in previously healthy individuals
Presentation
Severe pain
Erythematous, blistering, and necrotic skin
Systemically unwell with fever and tachycardia
Presence of crepitus (subcutaneous emphysema)
X-ray may show soft tissue gas (absence should not exclude the
diagnosis)
Management
Urgent referral for extensive surgical debridement

Intravenous antibiotics
Prognosis
Mortality up to 76%
Further reading: Hasham S, Matteucci P, Stanley PRW, Hart NB. Necrotising fasciitis. BMJ 2005;330:830-833
(http://www.bmj.com/cgi/content/full/330/7495/830)
35
The normal skin microflora and antimicrobial peptides protect the skin against
infection. However, when there is skin damage, microorganisms can penetrate
resulting in infection.
There are 3 main types of skin infections according to their sources: bacterial (e.g.
staphylococcal and streptococcal), viral (e.g. human papilloma virus, herpes simplex
(see page 34) and herpes zoster (see below)), and fungal (e.g. tinea (see page 39 &
40), candida (see page 39 & 40) and yeasts). Infestations (e.g. scabies (see page 58 &
59), cutaneous leishmaniasis) can also occur.
Herpes zoster (shingles) infection due to varicella-zoster virus affecting the

distribution of the ophthalmic division of the fifth cranial (trigeminal) nerve
Note: Examination for eye involvement is important
Learning outcomes:
Ability to describe the presentation, investigation and management of:
- cellulitis and erysipelas
- staphylococcal scalded skin syndrome
- superficial fungal infections
36
Skin Infections and Infestations Erysipelas and Cellulitis
Erysipelas and Cellulitis
Description
Spreading bacterial infection of the skin

Cellulitis involves the deep subcutaneous tissue
Erysipelas is an acute superficial form of cellulitis and involves
the dermis and upper subcutaneous tissue

Streptococcus pyogenes and Staphylococcus aureus
Causes
Risk factors include immunosuppression, wounds, leg ulcers,
toeweb intertrigo, and minor skin injury

Presentation
Most common in the lower limbs

Local signs of inflammation swelling (tumor), erythema (rubor),
warmth (calor), pain (dolor); may be associated with lymphangitis

Systemically unwell with fever, malaise or rigors, particularly with
erysipelas
Erysipelas is distinguished from cellulitis by a well-defined, red
raised border
Management
Antibiotics (e.g. flucloxacillin or benzylpenicillin)

Supportive care including rest, leg elevation, sterile dressings and
analgesia
Complications
Local necrosis, abscess and septicaemia
Cellulitis with elephantiasis of the penis
37
Erysipelas
Description
Commonly seen in infancy and early childhood
Cause
Production of a circulating epidermolytic toxin from phage group
II, benzylpenicillin-resistant (coagulase positive) staphylococci

Presentation
Develops within a few hours to a few days, and may be worse over
the face, neck, axillae or groins

A scald-like skin appearance is followed by large flaccid bulla
Perioral crusting is typical
There is intraepidermal blistering in this condition
Lesions are very painful
Sometimes the eruption is more localised
Recovery is usually within 5-7 days
Management
Antibiotics (e.g. a systemic penicillinase-resistant penicillin,
fusidic acid, erythromycin or appropriate cephalosporin)

Analgesia
38
Skin Infections and Infestations Staphylococcal scalded skin syndrome
Superficial fungal infections
Description
A common and mild infection of the superficial layers of the skin,
nails and hair, but can be severe in immunocompromised

individuals
Cause
Three main groups: dermatophytes (tinea/ringworm), yeasts (e.g.
candidiasis, malassezia), moulds (e.g. aspergillus)

Presentation
Varies with the site of infection; usually unilateral and itchy

Tinea corporis (tinea infection of the trunk and limbs) - Itchy,
circular or annular lesions with a clearly defined, raised and scaly

edge is typical
Tinea cruris (tinea infection of the groin and natal cleft) very
itchy, similar to tinea corporis

Tinea pedis (athletes foot) moist scaling and fissuring in
toewebs, spreading to the sole and dorsal aspect of the foot

Tinea manuum (tinea infection of the hand) scaling and dryness
in the palmar creases

Tinea capitis (scalp ringworm) patches of broken hair, scaling
and inflammation
Tinea unguium (tinea infection of the nail) yellow discolouration,
thickened and crumbly nail

Tinea incognito (inappropriate treatment of tinea infection with
topical or systemic corticosteroids) Ill-defined and less scaly

lesions
Candidiasis (candidal skin infection) white plaques on mucosal
areas, erythema with satellite lesions in flexures

Pityriasis/Tinea versicolor (infection with Malassezia furfur) scaly
pale brown patches on upper trunk that fail to tan on sun

exposure, usually asymptomatic
Management
Establish the correct diagnosis by skin scrapings, hair or nail
clippings (for dermatophytes); skin swabs (for yeasts)

General measures: treat known precipitating factors (e.g.
underlying immunosuppressive condition, moist environment)
39
Topical antifungal agents (e.g. terbinafine cream)

Oral antifungal agents (e.g. itraconazole) for severe, widespread,
or nail infections
Avoid the use of topical steroids can lead to tinea incognito
Correct predisposing factors where possible (e.g. moist
environment, underlying immunosuppression)
Tinea corporis
Tinea capitis
Tinea manuum (right hand)
Tinea pedis with associated tinea unguium
Candidiasis (right axilla)
Pityriasis versicolor
40
Skin Cancer
Skin Cancer
Skin cancer is one of the most common cancers.
In general, skin cancer can be divided into: non-melanoma (basal cell carcinoma and
squamous cell carcinoma) and melanoma (malignant melanoma).
Malignant melanoma is the most life-threatening type of skin cancer and is one of
the few cancers affecting the younger population.
Sun exposure is the single most preventable risk factor for skin cancer.
Learning outcomes:
Ability to recognise:
- basal cell carcinoma
- squamous cell carcinoma
- malignant melanoma
41
Basal cell carcinoma
Description
A slow-growing, locally invasive malignant tumour of the
epidermal keratinocytes normally in older individuals, only rarely

metastasises
Most common malignant skin tumour
Causes
Risk factors include UV exposure, history of frequent or severe
sunburn in childhood, skin type I (always burns, never tans),

increasing age, male sex, immunosuppression, previous history of
skin cancer, and genetic predisposition
Presentation
Various morphological types including nodular (most common),
superficial (plaque-like), cystic, morphoeic (sclerosing), keratotic

and pigmented
Nodular basal cell carcinoma is a small, skin-coloured papule or
nodule with surface telangiectasia, and a pearly rolled edge; the

lesion may have a necrotic or ulcerated centre (rodent ulcer)
Most common over the head and neck
Management
Surgical excision - treatment of choice as it allows histological
examination of the tumour and margins

Mohs micrographic surgery (i.e. excision of the lesion and tissue
borders are progressively excised until specimens are

microscopically free of tumour) - for high risk, recurrent tumours
Radiotherapy - when surgery is not appropriate
Other e.g. cryotherapy, curettage and cautery, topical
photodynamic therapy, and topical treatment (e.g. imiquimod

cream) - for small and low-risk lesions
Complications
Local tissue invasion and destruction
Prognosis
Depends on tumour size, site, type, growth pattern/histological
subtype, failure of previous treatment/recurrence, and

immunosuppression
Basal cell carcinoma nodular type
42
Skin Cancer Basal cell carcinoma
Skin Cancer Squamous cell carcinoma
Squamous cell carcinoma
A locally invasive malignant tumour of the epidermal
Description
keratinocytes or its appendages, which has the potential to

metastasise
Risk factors include excessive UV exposure, pre-malignant skin
Causes
conditions (e.g. actinic keratoses), chronic inflammation (e.g. leg

ulcers, wound scars), immunosuppression and genetic
predisposition
Presentation
Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate
Management
Surgical excision - treatment of choice

Mohs micrographic surgery may be necessary for ill-defined,
large, recurrent tumours

Radiotherapy - for large, non-resectable tumours
Prognosis
Depends on tumour size, site, histological pattern, depth
of invasion, perineural involvement, and immunosuppression
Squamous cell carcinoma adjacent to ear (left) and glans penis (right)
43
Malignant melanoma
Description
An invasive malignant tumour of the epidermal melanocytes,
which has the potential to metastasise

Causes
Risk factors include excessive UV exposure, skin type I (always
burns, never tans), history of multiple moles or atypical moles, and

family history or previous history of melanoma
Presentation
The ABCDE Symptoms rule (*major suspicious features):
Asymmetrical shape*
Border irregularity
Colour irregularity*
Diameter > 6mm
Evolution of lesion (e.g. change in size and/or shape)*
Symptoms (e.g. bleeding, itching)
More common on the legs in women and trunk in men
Types
Superficial spreading melanoma common on the lower limbs,
in young and middle-aged adults; related to intermittent highintensity UV exposure

Nodular melanoma - common on the trunk, in young and middle-
aged adults; related to intermittent high-intensity UV exposure

Lentigo maligna melanoma - common on the face, in elderly
population; related to long-term cumulative UV exposure

Acral lentiginous melanoma - common on the palms, soles and nail
beds, in elderly population; no clear relation with UV exposure

Management
Surgical excision - definitive treatment

Radiotherapy may sometimes be useful
Chemotherapy for metastatic disease
Prognosis
Recurrence of melanoma based on Breslow thickness (thickness of
tumour): <0.76mm thick low risk, 0.76mm-1.5mm thick

medium risk, >1.5mm thick high risk
5-year survival rates based on the TNM classification (primary
Tumour, regional Nodes, Metastases): stage 1 (T <2mm thick, N0,

M0) - 90%, stage 2 (T>2mm thick, N0, M0) 80%, stage 3 (N1,
M0) 40- 50%, and stage 4 (M 1) 20-30%
44
Skin Cancer Malignant melanoma
Skin Cancer Malignant melanoma
Superficial spreading melanoma
Nodular melanoma
Lentigo maligna melanoma
Acral lentiginous melanoma
45
Eczema, acne and psoriasis are chronic inflammatory skin disorders that follow a
relapsing and remitting course. There are many types of eczema but we shall just
consider atopic eczema here.
These skin disorders are not infectious.
Management is aimed at achieving control and not providing a cure.
Complications are mainly due to the psychological and social effects.
Patient education is important in these chronic skin conditions and should

concentrate on providing information about the nature of condition, aims of
treatment and the available treatment options.
Learning outcomes:
Ability to describe the presentation, demonstrate assessment, formulate a
differential diagnosis, instigate investigation and discuss how to provide
continuing care of:
- atopic eczema
- acne
- psoriasis
46
Inflammatory Skin Conditions Atopic eczema
Atopic eczema
Description
Eczema (or dermatitis) is characterized by papules and vesicles on
an erythematous base
Atopic eczema is the most common type - usually develops by
early childhood and resolves during teenage years (but may recur)
Epidemiology
20% prevalence in <12 years old in the UK
Causes
Not fully understood, but a positive family history of atopy (i.e.
eczema, asthma, allergic rhinitis) is often present

A primary genetic defect in skin barrier function (loss of function
variants of the protein filaggrin) appears to underlie atopic eczema

Exacerbating factors such as infections, allergens (e.g. chemicals,
food, dust, pet fur), sweating, heat and severe stress

Presentation
Commonly present as itchy, erythematous dry scaly patches

More common on the face and extensor aspects of limbs in
infants, and the flexor aspects in children and adults

Acute lesions are erythematous, vesicular and weepy (exudative)
Chronic scratching/rubbing can lead to excoriations and
lichenification
May show nail pitting and ridging of the nails
Management
General measures - avoid known exacerbating agents, frequent
emollients +/- bandages and bath oil/soap substitute

Topical therapies topical steroids for flare-ups; topical
immunomodulators (e.g. tacrolimus, pimecrolimus) can be

used as steroid-sparing agents
Oral therapies - antihistamines for symptomatic relief, antibiotics
(e.g. flucloxacillin) for secondary bacterial infections, and

antivirals (e.g. aciclovir) for secondary herpes infection
Phototherapy and immunosuppressants (e.g. oral prednisolone,
azathioprine, ciclosporin) for severe non- responsive cases

Complications
Secondary bacterial infection (crusted weepy lesions)

Secondary viral infection - molluscum contagiosum (pearly
papules with central umbilication), viral warts and eczema

herpeticum (see page 34)
47
Atopic eczema
Further reading: NICE guidelines. Atopic eczema in children, Dec 2007. http://www.nice.org.uk/Guidance/CG57
48
Inflammatory Skin Conditions Atopic eczema
Inflammatory Skin Conditions Acne vulgaris
Acne vulgaris
Description
An inflammatory disease of the pilosebaceous follicle
Epidemiology
Over 80% of teenagers aged 13- 18 years
Causes
Hormonal (androgen)
Contributing factors include increased sebum production,
abnormal follicular keratinization, bacterial colonization

(Propionibacterium acnes) and inflammation
Presentation
Non-inflammatory lesions (mild acne) - open and closed
comedones (blackheads and whiteheads)

Inflammatory lesions (moderate and severe acne) - papules,
pustules, nodules, and cysts

Commonly affects the face, chest and upper back
Management
General measures - no specific food has been identified to cause
acne, treatment needs to be continued for at least 6 weeks to

produce effect
Topical therapies (for mild acne) - benzoyl peroxide and topical
antibiotics (antimicrobial properties), and topical retinoids

(comedolytic and anti-inflammatory properties)
Oral therapies (for moderate to severe acne) - oral antibiotics, and
anti-androgens (in females)

Oral retinoids (for severe acne)
Complications
Post-inflammatory hyperpigmentation, scarring, deformity,
psychological and social effects
Comedones
Papules and nodules
49
Psoriasis
Description
A chronic inflammatory skin disease due to hyperproliferation of
keratinocytes and inflammatory cell infiltration

Types
Chronic plaque psoriasis is the most common type

Other types include guttate (raindrop lesions), seborrhoeic
(naso-labial and retro-auricular), flexural (body folds), pustular

(palmar-plantar), and erythrodermic (total body redness)
Epidemiology
Affects about 2% of the population in the UK
Causes
Complex interaction between genetic, immunological and
environmental factors
Precipitating factors include trauma (which may produce a
Kebner phenomenon), infection (e.g. tonsillitis), drugs, stress,

and alcohol
Presentation
Well-demarcated erythematous scaly plaques

Lesions can sometimes be itchy, burning or painful
Common on the extensor surfaces of the body and over scalp
Auspitz sign (scratch and gentle removal of scales cause capillary
bleeding)
50% have associated nail changes (e.g. pitting, onycholysis)
5-8% suffer from associated psoriatic arthropathy - symmetrical
polyarthritis, asymmetrical oligomonoarthritis, lone distal

interphalangeal disease, psoriatic spondylosis, and arthritis
mutilans (flexion deformity of distal interphalangeal joints)
Management
General measures - avoid known precipitating factors, emollients
to reduce scales
Topical therapies (for localised and mild psoriasis) - vitamin D
analogues, topical corticosteroids, coal tar preparations,

dithranol, topical retinoids, keratolytics and scalp preparations
Phototherapy (for extensive disease) - phototherapy i.e. UVB and
photochemotherapy i.e. psoralen+UVA

Oral therapies (for extensive and severe psoriasis, or psoriasis
with systemic involvement) - methotrexate, retinoids,

ciclosporin, mycophenolate mofetil, fumaric acid esters,
50
Inflammatory Skin Conditions Psoriasis
Inflammatory Skin Conditions Psoriasis
and biological agents (e.g. infliximab, etanercept, efalizumab)

Complications
Erythroderma (see page 33), psychological and social effects
Kebner phenomenon
Plaque psoriasis
Nail changes and arthropathy
Scalp involvement
51
In general, blistering skin disorders can be divided into: immunobullous diseases

(e.g. bullous pemphigoid, pemphigus vulgaris), blistering skin infections (e.g. herpes
simplex) and other (e.g. porphyria cutanea tarda).
The fragility of blisters depends on the level of split within the skin an intraepidermal split (a split within the epidermis) causes blisters to rupture easily;
whereas a sub-epidermal split (a split between the epidermis and dermis) causes
blisters to be less fragile.
The common causes of blisters are impetigo (see below), insect bites, herpes simplex
infection (see page 34), herpes zoster infection (see page 36), acute contact
dermatitis, pompholyx (vesicular eczema of the hands and feet, see below) and
burns.
Bullous pemphigoid (see page 53) and pemphigus vulgaris (see page 54) are
uncommon conditions due to immune reaction within the skin.
Bullous impetigo in a new tattoo
Pompholyx
Learning outcomes:
1. Ability to recognise common causes of blisters
2. Ability to recognise:
- Bullous pemphigoid
- Pemphigus vulgaris
52
Blistering Disorders Bullous pemphigoid
Bullous pemphigoid
Description
A blistering skin disorder which usually affects the elderly
Cause
Autoantibodies against antigens between the epidermis and
dermis causing a sub-epidermal split in the skin

Presentation
Tense, fluid-filled blisters on an erythematous base

Lesions are often itchy
May be preceded by a non-specific itchy rash
Usually affects the trunk and limbs (mucosal involvement less
common)
Management
General measures wound dressings where required, monitor
for signs of infection

Topical therapies for localised disease - topical steroids
Oral therapies for widespread disease oral steroids, combination
of oral tetracycline and nicotinamide, immunosuppressive agents

(e.g. azathioprine, mycophenolate mofetil, methotrexate, and
other)
Bullous pemphigoid
53
Pemphigus vulgaris
Description
A blistering skin disorder which usually affects the middle-aged
Cause
Autoantibodies against antigens within the epidermis causing an
intra-epidermal split in the skin

Presentation
Flaccid, easily ruptured blisters forming erosions and crusts

Lesions are often painful
Usually affects the mucosal areas (can precede skin involvement)
Management
General measures wound dressings where required, monitor for
signs of infection, good oral care (if oral mucosa is involved)

Oral therapies high-dose oral steroids, immunosuppressive
agents (e.g. methotrexate, azathioprine, cyclophosphamide,

mycophenolate mofetil, and other)
Pemphigus vulgaris
Pemphigus vulgaris affecting the oral mucosa
54
Blistering Disorders Pemphigus vulgaris
There are several commonly-encountered skin problems in clinical practice. Below

are some of the important differential diagnoses for each of these presentations.
Clinical exposure is the key to achieve competence in diagnosing, investigating and

managing these skin problems.
Learning objectives:
Ability to formulate a differential diagnosis, describe the investigation and
discuss the management in patients with:
- chronic leg ulcers
- itchy eruption
- a changing pigmented lesion
- purpuric eruption
- a red swollen leg
55
56
Venous ulcer
56
Arterial ulcer
In clinical practice, there can be mixture of arterial, venous and/or neuropathic components in an ulcer.
carcinoma in long-standing non-healing ulcers).
Neuropathic ulcer
vasculitic ulcers (purpuric, punched out lesions), infected ulcers (purulent discharge, may have systemic signs) and malignancy (e.g. squamous cell
Leg ulcers are classified according to aetiology. In general, there are three main types: venous, arterial and neuropathic ulcers. Other causes include
Chronic leg ulcers
Common Important Problems Chronic leg ulcers
- Large, shallow irregular ulcer

- Exudative and granulating base
Lesion
57
Management
Possible
investigations
- Compression bandaging
(after excluding arterial insufficiency)
- Warm skin
- Normal peripheral pulses
- Leg oedema, haemosiderin and melanin
deposition (brown pigment),
lipodermatosclerosis, and atrophie
blanche (white scarring with dilated
capillaries)
- Normal ankle/brachial pressure index
(i.e. ABPI 0.8-1)
- Malleolar area (more common over

medial than lateral malleolus)
Common sites
Associated
features
- Often painful, worse on standing

- History of venous disease e.g. varicose
veins, deep vein thrombosis
Venous ulcer
History
Chronic leg ulcers
57
- ABPI < 0.8 - presence of arterial

insufficiency
- Doppler studies and angiography
- Vascular reconstruction
- Compression bandaging is contraindicated
- Cold skin
- Weak or absent peripheral pulses
- Shiny pale skin
- Loss of hair
- Painful especially at night, worse when

legs are elevated
- History of arterial disease e.g.
atherosclerosis
- Pressure and trauma sites e.g. pretibial,
supramalleolar (usually lateral), and at
distal points e.g. toes
- Small, sharply defined deep ulcer
- Necrotic base
Arterial ulcer
- Wound debridement
- Regular repositioning, appropriate
footwear and good nutrition
- ABPI < 0.8 implies a neuroischaemic ulcer

- X-ray to exclude osteomyelitis
- Variable size and depth

- Granulating base
- May be surrounded by or underneath a
hyperkeratotic lesion (e.g. callus)
- Warm skin
- Normal peripheral pulses*
*cold, weak or absent pulses if it is a
neuroischaemic ulcer
- Peripheral neuropathy
- Pressure sites e.g. soles, heel, toes,

metatarsal heads
- Often painless
- Abnormal sensation
- History of diabetes or neurological disease
Neuropathic ulcer
Common Important Problems Chronic leg ulcers

58
Scabies
58
Urticaria
Lichen planus
reaction (e.g. some cases of urticaria) or an unknown cause, possibly autoimmune (e.g. lichen planus).
Wickhams striae
An itchy (pruritic) eruption can be caused by an inflammatory condition (e.g. eczema), infection (e.g. varicella), infestation (e.g. scabies), allergic
Chronic fissured hand eczema
Itchy eruption
Common Important Problems Itchy eruption
59
Management
Possible
investigations
Associated
features
Lesion
Common sites
History
Itchy eruption
- Patch testing
- Serum IgE levels
- Skin swab
- Emollients
- Corticosteroids
- Immunomodulators
- Antihistamines
Eczema
- Personal or family history of
atopy
- Exacerbating factors (e.g.
allergens, irritants)
- Variable (e.g. flexor aspects in
children and adults with atopic
eczema)
- Dry, erythematous patches
- Acute eczema is
erythematous, vesicular and
exudative
- Secondary bacterial or viral
infections
59
- Scabicide (e.g. permethrin

or malathion)
- Antihistamines
- Skin scrape, extraction of mite

and view under microscope
- Secondary eczema and

impetigo
- Sides of fingers, finger webs,

wrists, elbows, ankles, feet,
nipples and genitals
- Linear burrows (may be
tortuous) or rubbery nodules
Scabies
- May have history of contact
with symptomatic individuals
- Pruritus worse at night
- Antihistamines
- Corticosteroids
- Bloods and urinalysis to

exclude a systemic cause
- May be associated with

angioedema or anaphylaxis
- Pink wheals (transient)

- May be round, annular, or
polycyclic
- No specific tendency
Urticaria
- Precipitating factors (e.g. food,
contact, drugs)
- Corticosteroids
- Antihistamines
- Nail changes and hair loss

- Lacy white streaks on the oral
mucosa and skin lesions
(Wickhams striae)
- Skin biopsy
- Forearms, wrists, and legs

- Always examine the oral
mucosa
- Violaceous (lilac) flat-topped
papules
- Symmetrical distribution
Lichen planus
- Family history in 10% of cases
- May be drug-induced
Common Important Problems Itchy eruption

60
Congenital naevus
60
Seborrhoeic keratoses
Malignant melanoma
A changing pigmented lesion can be benign (e.g. melanocytic naevi, seborrhoeic wart) or malignant (e.g. malignant melanoma).
Common Important Problems A changing pigmented lesion
Management
Lesion
Common sites
History
61
61
Benign
Malignant
Melanocytic naevi
Seborrhoeic wart
Malignant melanoma
- Not usually present at birth but develop
- Tend to arise in the middle-aged or elderly - Tend to occur in adults or the middle-aged
- Often multiple and asymptomatic
- History of evolution of lesion
during infancy, childhood or adolescence
- May be symptomatic (e.g. itchy, bleeding)
- Asymptomatic
- Presence of risk factors
- Variable
- Face and trunk
- More common on the legs in women and
trunk in men
- Warty greasy papules or nodules
- Features of ABCDE:
- Congenital naevi may be large,
- Stuck on appearance, with well-defined
Asymmetrical shape
pigmented, protuberant and hairy
edges
Border irregularity
- Junctional naevi are small, flat and dark
Colour irregularity
- Intradermal naevi are usually dome-shape
papules or nodules
Diameter > 6mm
- Compound naevi are usually raised, warty,
Evolution of lesion
hyperkeratotic, and/or hairy
- Rarely needed
- Rarely needed
- Excision
Common Important Problems A changing pigmented lesion

62
Henoch-Schnlein purpura
62
Platelet counts and a clotting screen are important to exclude coagulation disorders.
Senile purpura
thrombocytopenic purpura) or non-thrombocytopenic e.g. trauma, drugs (e.g. steroids), aged skin, vasculitis (e.g. Henoch-Schnlein purpura).
A purpuric eruption can be thrombocytopenic (e.g. meningococcal septicaemia, disseminated intravascular coagulation, idiopathic
Purpuric eruption
Common Important Problems Purpuric eruption
- Bloods
- Lumbar puncture
- Antibiotics
Management
- Petechiae, ecchymoses,
haemorrhagic bullae and/or
tissue necrosis
- Systemically unwell
- Acute onset
- Symptoms of meningitis and
septicaemia
- Extremities
Meningococcal septicaemia
Associated
features
Possible
investigations
Lesion
Common sites
History
Purpuric eruption
63
63
- Treat the underlying cause

- Transfuse for coagulation
deficiencies
- Anticoagulants for thrombosis
- Bloods (a clotting screen is

important)
Disseminated intravascular
coagulation
- History of trauma, malignancy,
sepsis, obstetric complications,
transfusions, or liver failure
- Spontaneous bleeding from
ear, nose and throat,
gastrointestinal tract,
respiratory tract or wound site
- Petechiae, ecchymoses,
haemorragic bullae and/or
tissue necrosis
Vasculitis
- Treat the underlying cause

- Steroids and
immunosuppressants if there
is systemic involvement
- No treatment is needed
- No investigation is needed
- Bloods and urinalysis

- Skin biopsy
- Non-palpable purpura
- Surrounding skin is atrophic
and thin
- Systemically well
- Extensor surfaces of hands

and forearms
- Such skin is easily traumatised
- Arise in the elderly population

with sun-damaged skin
Senile purpura
- Palpable purpura (often

painful)
- Dependent areas (e.g. legs,

buttocks, flanks)
- Painful lesions
Common Important Problems Purpuric eruption

- Erysipelas (well-defined edge)

- Cellulitis (diffuse edge)
- Systemically unwell with fever and malaise

- May have lymphangitis
Lesion
Associated
features
Possible
- Anti-streptococcal O titre (ASOT)
investigations - Skin swab
Management - Antibiotics
- Painful spreading rash

- History of abrasion or ulcer
Cellulitis/Erysipelas
64
- D-dimer
- Doppler ultrasound and/or venography
- Anticoagulants
- Usually systemically well

- May present with pulmonary embolism
- Complete venous occlusion may lead to

cyanotic discolouration
- Pain with swelling and redness

- History of prolonged bed rest, long haul
flights or clotting tendency
Venous thrombosis
- Leg elevation and compression

stockings
- Sclerotherapy or surgery for varicose
veins
- Heaviness or aching of leg, which is

worse on standing and relieved by
walking
- History of venous thrombosis
- Discoloured (blue-purple)
- Oedema (improved in the morning)
- Venous congestion and varicose veins
- Lipodermatosclerosis (erythematous
induration, creating champagne
bottle appearance)
- Stasis dermatitis (eczema with
inflammatory papules, scaly and
crusted erosions)
- Venous ulcer
- Doppler ultrasound and/or venography
Chronic venous insufficiency
The main differential diagnoses for a red swollen leg are cellulitis, erysipelas, venous thrombosis and chronic venous insufficiency.
History
A red swollen leg
64
Common Important Problems A red swollen leg
Management
Management
Management and therapeutics
Treatment modalities for skin disease can be broadly categorised into medical
therapy (topical and systemic treatments) and physical therapy (e.g. cryotherapy,
phototherapy, photodynamic therapy, lasers and surgery).
Topical treatments directly deliver treatment to the affected areas and this reduces
systemic side effects. It is suitable for localised and less severe skin conditions. They
consist of active constituents which are transported into the skin by a base (also
known as a vehicle). Examples of active ingredients are steroids, tar,
immunomodulators, retinoids, and antibiotics. The common forms of base are lotion
(liquid), cream (oil in water), gel (organic polymers in liquid, transparent), ointment
(oil with little or no water) and paste (powder in ointment).
Systemic therapy is used for extensive and more serious skin conditions, if the
treatment is ineffective topically or if there is systemic involvement. However, they
have the disadvantage of causing systemic side effects.
Ability to describe the principles of use of the following drugs:

- emollients
- topical/oral corticosteroids
- oral aciclovir
- oral antihistamines
- topical/oral antibiotics
- topical antiseptics
65
Emollients
Examples
Aqueous cream, emulsifying ointment, liquid paraffin and white soft
paraffin in equal parts (50:50)

Quantity
500 grams per tub
Indications
To rehydrate skin and re-establish the surface lipid layer

Useful for dry, scaling conditions and as soap substitutes
Side effects
Reactions may be irritant or allergic (e.g. due to preservatives or perfumes
in creams)
Topical/Oral corticosteroids
Examples
Topical steroids: classified as mildly potent (e.g, hydrocortisone),
moderately potent (e.g. clobetasone butyrate (Eumovate)), potent

(e.g.betamethasone valerate (Betnovate)), and very potent (e.g. clobetasol
propionate (Dermovate))
Oral steroids: prednisolone
Quantity
Usually 30 grams per tube (enough to cover the whole body once)
Indications
Anti-inflammatory and anti-proliferative effects

Useful for allergic and immune reactions, inflammatory skin conditions,
blistering disorders, connective tissue diseases, and vasculitis

Side effects
Local side effects (from topical corticosteroids): skin atrophy (thinning),
telangiectasia, striae, may mask, cause or exacerbate skin infections,

acne, or perioral dermatitis, and allergic contact dermatitis.
Systemic side effects (from oral corticosteroids): Cushings syndrome,
immunosuppression, hypertension, diabetes, osteoporosis, cataract, and

steroid-induced psychosis
Oral aciclovir
Examples
Aciclovir
Indications
Viral infections due to herpes simplex and herpes zoster virus
Side effects
Gastrointestinal upsets, raised liver enzymes, reversible neurological
reactions, and haematological disorders
Oral antihistamines
Examples
Classified into nonsedative (e.g. cetirizine, loratadine) and sedative
66
Management Emollients, Topical/Oral corticosteroids, Oral acyclovir, Oral antihistamines
Management Oral antihistamines, Topical/Oral antibiotics, Topical antiseptics, Oral retinoids
antihistamines (e.g. chlorpheniramine, hydroxyzine)

Indications
Block histamine receptors producing an anti-pruritic effect

Useful for type-1 hypersensitivity reactions and eczema (especially
sedative antihistamines for children)

Side effects
Sedative antihistamines can cause sedation and anticholinergic effects
(e.g. dry mouth, blurred vision, urinary retention, and constipation)
Topical/Oral antibiotics
Examples
Topical antibiotics: fusidic acid, mupirocin (Bactroban), neomycin

Oral antibiotics: penicillins, cephalosporins, gentamicin, macrolides,
nitrofurantoin, quinolones, tetracyclines, vancomycin, metronidazole,

trimethoprim
Indications
Useful for bacterial skin infections, and some are used for acne
Side effects
Local side effects (from topical antibiotics): local skin irritation/allergy
Systemic side effects (from oral antibiotics): gastrointestinal upset, rashes,

anaphylaxis, vaginal candidiasis, antibiotic-associated infection such as
Clostridium difficile, and antibiotic resistance (rapidly appears to fusidic
acid)
Topical antiseptics
Examples
Chlorhexidine, cetrimide, povidone-iodine
Indications
Treatment and prevention of skin infection
Side effects
Local side effects: local skin irritation/allergy
Oral retinoids
Examples
Isotretinoin, Acitretin
Indications
Acne, psoriasis, and disorders of keratinisation
Side effects
Mucocutaneous reactions such as dry skin, dry lips and dry eyes,
disordered liver function, hypercholesterolaemia, hypertriglyceridaemia,

myalgia, arthralgia and depression
Teratogenicity: effective contraception must be practised one month
before, during and at least one month after isotretinoin, but for two years
after Acitretin (consult current BNF for further details)
67
Practical Skills
There are four main aspects to focus on in clinical practice:

i)
Patient education, particularly on the nature of disease, treatment and

ways to achieve full compliance and effectiveness, and prevention strategies
ii) Effective written communication to general practitioner so that patients

care can be continued appropriately
iii) Good prescribing skills
iv) Good clinical examination and appropriate investigations to facilitate
accurate diagnosis
This section highlights several general points on the important clinical skills in
dermatology.
1. Ability to perform the following tasks:

- explain how to use an emollient or a topical corticosteroid
- make a referral
- write a discharge letter
- write a prescription for emollient
- take a skin swab
- take a skin scrape
- measure the ankle-brachial pressure index and interpret the result
2. Describe the principles of prevention in:

- pressure sores
- sun damage and skin cancer
68
Practical Skills
Practical Skills Patient education
Patient education
How to use emollients

Apply liberally and regularly
How to use topical corticosteroids

Apply thinly and only for short-term use (often 1 or 2 weeks only)
Only use 1% hydrocortisone or equivalent strength on the face
Fingertip unit (advised on packaging) strip of cream the length of a
fingertip
Preventing pressure sores

Pressure sores are due to ischaemia resulting from localised damage to
the skin caused by sustained pressure, friction and moisture, particularly
over bony prominences.
Preventative measures involve frequent repositioning, nutritional support,
and use of pressure relieving devices e.g. special beds
Preventing sun damage and skin cancer

Excessive exposure to UV radiation is the most significant
and preventable risk factor for the development of skin cancer (Table 14)
Skin types I and II are at higher risk of developing skin cancer with
excessive sun exposure than other skin types (Table 15)
Table 14. SMART ways to avoid excessive sun exposure

Spend time in the shade between 11am-3pm
Make sure you never burn
Aim to cover up with a t-shirt, wide-brimmed hat and sunglasses
Remember to take extra care with children
Then use Sun Protection Factor (SPF) 30+ sunscreen
69
Table 15. Skin types

Skin types
Description
Always burns, never tans
II
Always burns, sometimes tans
III
Sometimes burns, always tans
IV
Never burns, always tans
Written communication
Writing a referral letter

Important points to include:
Reason(s) for referral, current presentation, and impact of disease
Patients medical and social background
Current and previous treatment, length of treatment, and response to
treatment
Writing a discharge letter

Important points to include:
Reason(s) for admission and current presentation
Hospital course
Investigation results
Diagnostic impression
Management plan (including treatment and follow-up appointment)
Content of patient education given
Prescribing skills
Writing a prescription
General tips:
Include drug name, dose, frequency and an intended duration/review date
30 grams of cream/ointment covers the whole adult body area
1 fingertip unit covers the area of two palms and equals gram
70
Practical Skills Written communication and Prescribing skills
Practical Skills Clinical examination and investigations
Prescribing emollients
General tips
Emollients come in 500 gram tubs
In general, ointment-based emollients are useful for dry, scaling skin
whereas creams and lotions are for red, inflamed and weeping lesions
Prescribing topical corticosteroids

General tips
Prescribe the weakest potency corticosteroid that is effective
Use only for short term
Need to specify the base i.e. cream, lotion or ointment
Clinical examination and investigations
Taking a skin swab
Skin swabs can be taken from vesicles, pustules, erosions, ulcers and mucosal
surfaces for microbial culture.
Surface swabs are generally not encouraged.
Taking a skin scrape
Skin scrapes are taken from scaly lesions by gentle use of a scalpel in suspected
fungal infection (to show evidence of fungal hyphae and/or spores) and from
burrows in scabies (see page 59).
Measuring ankle-brachial pressure index (ABPI)
ABPI is used to identify the presence and severity of peripheral arterial insufficiency,
which is important in the management of leg ulcers.
Measure the cuff pressure of dorsalis pedis or posterior tibial artery using a Doppler
and compare it to the pressure of brachial artery.
The ABPI is measured by calculating the ratio of highest pressure obtained from the
ankle to highest brachial pressure of the two arms, and is normally >0.8.
Inappropriately high reading will be obtained in calcified vessels (often in diabetics).
71
Acknowledgements
We wish to acknowledge the following contributors:
Dr Mark Goodfield, former President (2008-2010) of the British Association of

Dermatologists, for writing the Foreword.
Dr Niels K. Veien for allowing us to use his photographs. All illustrations in this
handbook were obtained from "D@nderm" with his permission.
Dr Susan Burge, retired Consultant Dermatologist, Oxford Radcliffe Hospitals NHS

Trust, Professor Peter Friedmann, Emeritus Professor of Dermatology, Southampton
General Hospital, and Professor Lesley Rhodes, Professor of Experimental
Dermatology, University of Manchester for reviewing and contributing valuable
suggestions.
Mr Kian Tjon Tan, Specialty Registrar in Plastic Surgery, Royal Preston NHS
Foundation Trust for contributing the chapter Background Knowledge.
Dr Yi Ning Chiang, Specialty Doctor in Dermatology, Southport and Ormskirk Hospital

NHS Trust for contributing the chapter Common Important Problems.
72

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Dermatology

A handbook for medical students & junior doctors

British Association of Dermatologists