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Skin disease
• eruptive xanthomata; yellow-orange small papules
appearing all over the body;
• xanthelasmata; yellow plaques commonly found on the
eyelids.
SKIN DISEASE
Psoriasis
Psoriasis is a chronic, relapsing, autoimmune inflammatory
skin disease that occurs in roughly 2% of the UK population. It affects men and women equally, and even though it
may occur at any age, it usually manifests itself before the
age of 35years. It presents with a multifactorial pattern of
inheritance, where 30% of cases thought to have a familial
correlation. The remaining cases may be triggered by multiple environmental factors, including sunlight and infection
(streptococcal and HIV infection), stress, trauma or drugs
(e.g. lithium, chloroquine and β-blockers).
The most common type is chronic plaque psoriasis.
Other types include guttate (widespread raindrop lesions
usually after streptococcal infection) (Fig. 35.1), seborrhoeic (nasolabial and retroauricular), pustular ( palmar–
plantar), flexural (body flexures) and erythrodermic
(widespread body redness) types. It is a T cell-mediated
disease characterized by hyperproliferation of keratinocytes and blood vessels within the skin producing epidermal thickening.
frequently found on the extensor surfaces of the limbs
(e.g. elbows and knees) and over the scalp. They may be
severely itchy. Plaques may differ in size and shape, and can
be discoid, serpiginous or circinate (ring-like). Fissuring
within plaques may occur when they arise at joint sites.
Scale scraping can accentuate the plaque or cause pinpoint
bleeding (Auspitz sign) (Fig.35.2). New lesions often occur at the site of injury to skin typically within 1–2weeks
(Köbner reaction). Fifty percent of patients will have nail
changes, including pitting, onycholysis and subungual
hyperkeratosis. Ten percent will have associated psoriatic
arthropathy – symmetrical polyarthritis, asymmetrical
oligomonoarthritis, psoriatic spondylosis and arthritis
mutilans (distal interphalangeal joints flexion deformity)
(Fig.35.3).
The prognosis of the condition can be difficult to establish, with frequent treatment failure and recurrent relapses. It is worse in early presenters and where a family
history is present. Complications of disease are often associated with significant physiological stress and lowered
quality of life.
Clinical features
The lesions in psoriasis are typically clearly marginated,
salmon-pink plaques topped by a silvery scale, most
Fig.35.1 Guttate psoriasis. (Reprinted with permission
from Dermatology 3rd Edition Bolognia etal.)
348
Fig.35.2 Plaque psoriasis with Auspitz sign. (Reprinted with
permission from Dermatology 3rd Edition Bolognia etal.)
Fig.35.3 Arthritis mutilans with psoriatic nail changes.
(Reprinted with permission from Niels K. Veien.)
Skin disease
3535
Management
Education and avoidance of precipitating factors is very important in management of psoriasis. For mild conditions,
emollient therapy and reassurance are sufficient. In more
troublesome cases, topical therapy can be highly effective.
These include vitamin D and vitamin A analogues, coal tar
preparations, corticosteroids and dithranol. Phototherapy
and photochemotherapy can be used in extensive disease.
Systemic agents are reserved for severe or refractory disease, and include methotrexate, oral retinoids, cyclosporine,
mycophenolate mofetil, fumaric acid esters and biological
agents (Table35.1).
Clinical features
It affects around 20% of children, and in 80% of cases presents before the age of 5years. In most cases, significant improvement or clearing of the condition by adulthood occurs,
although the skin may remain sensitive to irritants throughout life. The characteristics of the condition change with
age. In infants there are exudative, crusted, itchy areas over
extensor surfaces and cheeks. By childhood and adulthood,
the lesions are more localized and are seen on the flexor
areas of antecubital and popliteal fossae, wrists and ankles
and the face and neck. There is pruritus of the inflamed
skin, and long-term scratching often leads to thickened hard
areas (Fig. 35.4). Skin can often become inflamed, and it
Eczema/dermatitis
This is a nonspecific inflammation of the skin characterized by papules and vesicles on an erythematous base. It is a
chronic and relapsing condition, and in most cases presents
in childhood. It has strong environmental and genetic correlates, which are summarized in Table35.2. Different types
can be recognized, but by far the most common is atopic
dermatitis (Table35.3).
Table35.1 Available management options of psoriasis
Agent Description
Topical Emollients Apply three or four times per day
May need as much as 500 g per week
Can include creams, shampoos and bath preparations
Corticosteroids Avoid long-term use (e.g. Dovobet)
Vitamin D analogues As effective as steroids in long-term management
Be aware of hypercalcaemia if overused (e.g. Dovonex)
Coal tar Solution, cream or lotion
Can be uncomfortable to apply/use
Vitamin A analogues Do not use in pregnant women/women planning pregnancy as is
potentially teratogenic (tazarotene gel)
Dithranol For few but relatively large plaques
Needs patient education regarding use and application
Phototherapy Narrowband ultraviolet B Used two or three times per week
Advise not to use sunbeds as self-treatment
Photochemotherapy Photosensitive drug (e.g. PUVA) used two or three times per week with
2–4weekly maintenance therapy
Systemic Methotrexate First-line treatment but with several side effects and so needs close
monitoring
Ciclosporin Not to be used as ‘flare-up’ treatment
Do not offer to males or females trying to conceive
Other agents Retinoids (acitretin)
Fumaric acid esters
Mycophenolate, sulphasalazine, azathioprine
Biological modulators Used only if disease does not respond to other treatments/patient is
intolerant
Stop if no response
Examples include infliximab, etanercept and efalizumab
PUVA, Psoralen and ultraviolet A.
is important to look for signs of underlying infection. For
instance, infection with herpes simplex virus (HSV) is one
of the most worrying infective exacerbations, and manifests
itself as eczema herpeticum. It involves rapidly worsening
areas of erythema with clustered blisters and punched-out
erosions that may lead to systemic compromise.
Investigations to characterize atopic eczema include
prick tests for common allergens and raised serum immunoglobulin E level (condition association with asthma and
349
Skin disease
Table35.2 Most common triggers of eczema
Triggers Description
Environmental
factors
Endogenous
factors
Allergens Dietary and inhaled
allergens, including nuts
or dust mites, are most
commonly associated
with eczema in children
Irritants Both contact irritants
(rough fabric such as
wool) and chemical
irritants (soaps, creams
etc.)
Infections Staphylococcus aureus
Temperature Extremes of temperature
and humidity with most
patients improving in
summer
Diet Food allergens as well
as irritant foods such as
chillies and chocolate
Genetic Genetic mutation
affecting production of
filaggrin (protein required
for maturation of stratum
corneum keratinocytes)
Hormones Mainly in women
(deterioration in
pregnancy, premenstrual
flare-ups)
Stress Exacerbated and
prolonged flare-ups, poor
healing
Fig.35.4 Atopic dermatitis in a child. (Reprinted with
permission from Dermatology 3rd Edition Bolognia etal.)
Table35.3 Different presentations of eczema
Type of dermatitis Characteristics
Contact dermatitis Erythema, vesicles, fissuring due
Seborrhoeic
dermatitis
Discoid eczema Round, itchy, vesicular lesions
Dyshidrotic eczema Itchy, erythematous, vesicular
to contact with irritant/allergen
Erythematous, scaly, itchy, yellow
eruption mostly on oily areas of
skin (scalp, flexures, face) (see
Fig.35.5)
around body
eruptions mostly on palms, soles
and fingers
hay fever). Common complications include infections with
bacteria (Staphylococcus aureus), viruses (HSV) or fungi.
Eczema is often a relapsing condition that gradually abates
with adult life. By the early teenage years, atopic eczema will
have cleared in 60%–70% of individuals, bearing in mind
predictors of worsening prognosis, which include early onset and cooccurrence of asthma.
350
Fig.35.5 Seborrhoeic dermatitis on scalp. (Reprinted with
permission from Dermatology 3rd Edition Bolognia etal.)
Management
Education and reassurance with regard to effective treatments are paramount. Advice regarding environmental
adaptations, recognition of irritants and flare-ups will decrease physical and psychological stress associated with the
condition. Medical treatment is often long-term but successful and concentrates on the use of emollients, steroids
and immunomodulators, which protect skin from breaking
and concurrent infections:
• Emollients: best applied on moist skin, liberally
and frequently (every 4 hours). For optimal results,
complete therapy should be used, including creams,
ointments and bath oils. The general rule of thumb
states 500 g of moisturizer should be used each week
for an adult and 250 g should be used each week for
achild.
• Topical steroids should not be used long-term (2weeks
at a time maximum), and in cases of atopic eczema not
more than twice a day. A mild steroid is used for mild
exacerbation and on more sensitive skin areas such as
the face. More potent steroids are required for severe
flare-ups and lichenified areas.
• Antibiotics such as flucloxacillin or erythromycin
should be used for 14days if there is underlying
infection.
• Bandages containing ichthammol paste and zinc oxide
can reduce pruritus.
• Phototherapy, azathioprine, ciclosporin, alitretinoin or
oral steroids should only be used for severe refractory
eczema and under specialist care.
• Tacrolimus and pimecrolimus are
immunomodulators used when eczema does not
respond to strong corticosteroids or they are
contraindicated.
CLINICAL NOTES
Referral to a specialist is recommended when
diagnosis has become uncertain, management is
not successful, the disease is not controlled and
flare-ups are frequent, or if the patient has marked
psychological stress.
Acne vulgaris
This is a disorder of pilosebaceous follicles stimulated
during puberty by androgens to produce increased
amounts of sebum. This can consequently lead to blockage
of ducts, which can be infected by normally commensal
Skin disease
Fig.35.6 Acne vulgaris. (Reprinted with permission from
Dermatology 3rd Edition Bolognia etal.)
3535
Propionibacterium acnes. Distended by sebum and desquamated keratinocytes, follicles become comedones that can
be described as open (blackheads) or closed (whiteheads)
(Fig.35.6). Acne is most prominent on the face and upper
trunk and usually abates with postadolescent age.
Acne is usually mild and self-limiting, but if it persists
both topical and systemic treatments can be considered
(Table35.4). First-line treatments include a trial of salicylic
or azelaic acids, benzoyl peroxide and topical antibiotics
and retinoids. Systemic treatments often take long to show
improvement and should be continued for 3–4 months.
Options include oral antibiotics, antiandrogens and retinoids. Alternatively, blue light and 140-nm laser therapy
have been found to show results. Severe acne is a serious,
Table35.4 Different types of acne treatment
Treatment Type Action
Topical Salicylic acid
Azelaic acid
Benzoyl peroxide A concentration of 5% to be used initially then increased to 10%. Very
Antibiotics Erythromycin, clindamycin and tetracyclines are most commonly
Retinoids Isotretinoin and tretinoin are antiinflammatory and reduce comedones.
Systemic Antibiotics Antiinflammatory and antiinfective actions. There is no strong evidence to
Antiandrogens The combined oral contraceptive pill is an effective treatment for acne.
Retinoids Isotretinoin is very effective in decreasing sebum production. Its toxicity
Keratolytic preparations, effective initial treatments. May cause irritation
and depigmentation
effective with antiseptic properties, may cause irritation
prescribed. Often combined with, e.g. benzoyl peroxide for better effect
Inform the patient to avoid exposure to strong sunlight and not to use in
pregnancy
prefer one antibiotic to another, but generally doxycycline and lymecycline
are first choices
Dianette is an effective preparation licensed solely for use for acne as it
has an associated much higher risk of development of thrombosis
and side effects, however, allow its use only under specialist care
(teratogenic, dry mouth, myalgia).
351
Skin disease
disfiguring condition, and its management should be coordinated by dermatology specialists.
COMMUNICATION
Even mild acne can be a distressing condition
for young people and requires a sympathetic
systemic approach. It is important to reassure
patients there are effective treatments, and that
the options are vast.
Actinic keratosis
This is a thickened scaly growth induced by ultraviolet light. It often begins as a small rough lesion that then
extends and progresses to erythematous plaque that can
sometimes differentiate to a hyperpigmented area or hyperkeratotic growth (cutaneous horn). It has a malignant potential and can often progress to squamous cell carcinoma
(SCC). It is seen more commonly in light-skinned individuals on areas most exposed to the sun. It is characterized
by ultraviolet-induced gene mutations within keratinocytes
that share common features with SCC histological features.
It can resolve spontaneously, stay chronic and stable or
progress to carcinoma in situ (Bowen disease) or SCC.
Treatment is by limitation of sun exposure, emollients,
5-fluorouracil cream, imiquimod cream, cryotherapy, photodynamic therapy and curettage or excision.
Seborrhoeic keratosis
This a common condition characterized by benign warty
hyperpigmented raised lesions associated with ageing.
The lesions have ‘stuck-on’ appearance with a usually welldefined border. Their surface often shows granules of visible keratin and can be covered by greasy scale. Most lesions
are seen on the trunk and face, and they are usually asymptomatic; often, however, they can become irritated and consequently infected.
The condition is benign but thought to be occasionally
associated with Bowen disease and squamous epithelial
dysplasia. Its management concentrates around reassurance
and cosmetic removal by cryotherapy, curettage and cautery
or shave excision.
in times of stress, causes a burning, stinging neuralgia,
which precedes or accompanies the development of erythematous vesicular lesions. Diagnosis is clinical, but vesicular fluid or scrapings can show HSV. HSV antibodies can
also be detected by serology in asymptomatic individuals.
Transmission is through contact with infected secretions on a mucosal surface or lesion on another anatomical site. Treatment is supportive, with pain relief and skin
soothing. Topical antivirals have been found to have little
effect and therefore are not recommended. Oral therapies
should be started within 5days of the onset of symptoms
and include aciclovir and valaciclovir. Intravenous aciclovir
treatment can be used in severe or immunocompromised
patients at high risk of developing HSV complications such
as encephalitis.
Herpes (varicella) zoster
Primary infection with varicella zoster virus causes chickenpox (varicella), usually in childhood, that presents as
fever and widespread vesiculopapular rash. Following recovery, the virus lies dormant in the dorsal root ganglia
until immunosuppression or illness causes reactivation,
termed ‘shingles’. Typically, dermatomal pain and paresthesia (preeruptive phase) precede the appearance of maculopapular then vesicular lesions restricted to that dermatome
(eruptive phase). The chronic phase is characterized by persistent or recurring eruptions at the site of healed infection.
It is most commonly seen in the thoracic region or in
the ophthalmic division of the trigeminal nerve. Treatment
is with appropriate analgesia and oral antivirals (aciclovir,
valaciclovir, famciclovir), and should be started within 72
hours of the onset of rash. Intravenously administered aciclovir should be considered in immunocompromised patients and those with ophthalmic involvement. Steroids,
even though controversial, can at times be helpful.
Rams syndrome is when varicella zoster virus affects the
geniculate ganglion of the facial cranial nerve and produces
a characteristic rash in the external ear canal, the tongue
and hard palate.
HINTS AND TIPS
Shingles is confined to one dermatome only,
which is why any rash crossing the midline is not
shingles!
Herpes simplex
Two types of HSV have been identified. HSV-1 usually
causes cold sores, but in the United Kingdom is also the
leading cause of genital herpes. HSV-2 is associated with
recurrent anogenital infection. Primary infection is usually
asymptomatic, following which the virus survives latent in
cell bodies of nerve ganglia. Reactivation, which may occur
352
Lichen planus
This mainly affects middle-aged adults. The cause is unknown but may be related to disturbances of immune function. Lichen planus-like reactions occur with certain drugs,
such as sulphonamides, sulphonylureas, methyldopa, thiazides, β-blockers and drugs that alter immune function
(e.g. antimalarials, gold salts, penicillamine).
Neoplastic disease
3535
The lesions are pruritic, purple, polygonal and planar
or flat-topped papules, with a largely peripheral and symmetrical distribution most commonly seen on extensor
surfaces, genitalia or mucosal membranes. Wickham striae
(fine white lacy lines coursing over the papule) are characteristic of the disease, and it can be precipitated by trauma
(Köbner phenomenon). Postinflammatory hyperpigmentation and scarring can occur with chronic disease. Lesions
usually last for 6–12months if untreated. Treatment can be
with steroids, phototherapy and retinoids.
Erythema multiforme
This is a hypersensitivity of the skin to infection or drugs.
It presents as a reaction characterized by an iris or target lesion (circular with central intensity or blistering). Mucosal
membranes, if at all, can be involved (in severe cases described as Stevens–Johnson syndrome and toxic epidermal
necrolysis (TEN); see later). It usually starts on the extremities and symmetrically spreads centrally. It may be itchy but
is nontender. Management concentrates on withdrawal or
treatment of the precipitant and skin conditioning with antiseptics and steroids. The most common infectious agents
causing the condition include viruses (HSV), mycoplasma
pneumonia and fungi. The drugs involved include barbiturates, penicillins, sulphonamides, phenothiazines, NSAIDs
and anticonvulsants.
Stevens–Johnson syndrome and toxic epidermal necrolysis
These conditions are severe dermatological reactions to medication (e.g. allopurinol, antibiotics, antiepileptics) or infection. They range from mild to severe mucosal membrane
involvement and form a spectrum of conditions described as
‘severe cutaneous adverse reactions’. They usually start with
a prodrome period of mild upper respiratory tract infection,
fever and malaise but mucocutaneous lesions quickly develop. Lesions can present as macules or papules that then
become vesicles with extensive erythema. Characteristically,
target lesions are present and Nikolsky sign is positive (blistering of skin within minutes of applied pressure).
Mucosal involvement differentiates between Stevens–
Johnson syndrome and TEN (at least 30% of skin is sloughed
in TEN). The mainstay of management is optimal supportive
treatment with attention to nutrition, fluid balance and prevention of infection. Use of the offending medication should
be stopped, and any causative infection should be treated.
Steroids are usually given, and intravenously administered immunoglobulin may have a role. Mortality in TEN is up to 35%.
Pemphigus vulgaris and bullous pemphigoid
These are autoimmune, bullous conditions affecting mainly
people aged over 60 years. In pemphigus, antibodies are
directed against an epidermal cell adhesion molecule, causing flaccid, fragile blisters to develop within the epidermis.
It affects the mucosa and skin, with denuded areas remaining after the blisters rupture. Treatment is with steroids and
immunosuppressive agents.
In pemphigoid, the antibodies affect the basement membrane, leading to blisters between the dermis and epidermis.
It may occur spontaneously or in response to medication.
The blisters are tense and widespread, occurring particularly in flexures.
Erythema nodosum
This is a hypersensitivity reaction of skin to disease or
infection. The prodrome phase of fevers and arthralgia is
usually followed by painful nodular lesions, usually on the
anterior part of the shins, that go through colour changes
similar to those of a bruise. New crops of lesions emerge
while earlier lesions are fading, and may become necrotic.
They usually last 6–8 weeks but may take longer to heal or
recur. The most common causes are infections or drugs,
but an assortment of associated conditions include sarcoidosis, tuberculosis, leprosy, streptococcal infection, lymphogranuloma venereum, mycoplasma pneumonia and
irritable bowel disease.
Vitiligo
Vitiligo is characteristically well-demarcated, roughly symmetrical areas of depigmentation. There is loss of melanocytes, thought to be due to an autoimmune process. Around
30% of cases are associated with organ-specific autoimmune
disease (e.g. Addison disease, pernicious anaemia, alopecia,
Hashimoto thyroiditis).
Pyoderma gangrenosum
This presents with violaceous nodules, which then undergo
necrosis to produce an ulcer with an overhanging edge.
They heal leaving a scar. There is a clear underlying cause
in around half of cases, such as inflammatory bowel disease,
neoplasia, Wegener granulomatosis and myeloma. Systemic
steroids and ciclosporin are the first-line treatment but biological therapies and other new treatments are also to be
considered.
NEOPLASTIC DISEASE
Basal cell carcinoma
This is the most common, locally invasive, slow-growing,
malignant lesion arising from skin follicles. The lesions
mainly occur in areas of long-term sun exposure such
as the face, especially at the side of the nose or in the
periorbital skin, head and neck. Risk factors include sun
353
Skin disease
exposure, increasing age, male sex and fair skin. Early
lesions are often small and pearly with a raised area of
telangiectasia that then progresses to classic rodent ulcer
with an indurated border (Fig.35.7).
There are several subtypes of basal cell carcinoma,
presenting with different characteristics (Table 35.5).
Treatment is by surgical excision (Mohs microscopic surgery), cryotherapy or radiotherapy, but in noncomplicated
cases a trial of a topical creams such as imiquimod or photodynamic therapy can be used.
Squamous cell carcinoma
This tumour arises from keratinizing cells of the epidermis
or its appendages and is most commonly seen on damaged
or chronically irritated skin, especially areas of sun exposure. It is invasive and can metastasize to other organs. Risk
factors include long-term sun exposure, chemical carcinogens (arsenic, chromium), HPV infection, immunodeficiency and chronic inflammatory conditions.
It presents as hyperkeratotic, crusted and indurated
tumour that may ulcerate, although the clinical appearance is very variable (Fig. 35.8). Bowen disease and keratoacanthoma can often resemble the disease and may
progress to SCC. Investigations include skin biopsy, and
treatment concentrates on surgical excision and radiotherapy but also imiquimod cream and photodynamic therapy.
Electrochemotherapy has also been found to be useful.
Malignant melanoma
HINTS AND TIPS
The sites of malignant melanoma with a poor
prognosis are the back of the arm, neck and scalp
(BANS).
Fig.35.7 Classic appearance of basal cell carcinoma.
(Reprinted with permission from Dermatology 3rd Edition
Bolognia etal.)
Table35.5 Types of basal cell carcinoma
Type Characteristics
Nodular Large, pearly, solitary, erythematous
Superficial Usually multiple on upper trunk and
Morphoeic
(sclerosing or
infiltrative)
Pigmented Blue, brown or grey nodular or
Basosquamous Mixed with SCC. Potentially more
BCC, Basal cell carcinoma; SCC, squamous cell carcinoma.
nodule with telangiectatic vessels.
Often on the face. May ulcerate
limbs but also on face (more often in
women). Presents as erythematous
scaly plaques with central healing
and well-demarcated, thread-like
border. Rarely invasive. Responds to
medical treatment.
Most common on mid-facial sites
with aggressive poorly defined
borders. Characterized by yellow
plaques. Often presents late. Can
recur after treatment
superficial lesion, seen more often
with darker skin
aggressive than other BCC types
This tumour is increasing in incidence, and occurs particularly in fair-skinned people who are exposed to sunlight.
It results from the cancerous growth of melanocytes most
commonly on the skin, but melanomas affecting almost all
organs in the body have been described. If melanoma is confined to the epidermis it is known as ‘melanoma in situ’ and
does not spread to surrounding tissues. If it has infiltrated
through the dermis it can metastasize and becomes invasive
melanoma. There are four types of skin melanoma: superficial spreading (most common), nodular, lentigo maligna and
acral lentiginous (Fig. 35.9). Risk factors include previous
Fig.35.8 Squamous cell carcinoma. (Reprinted with
permission from Dermatology 3rd Edition Bolognia etal.)
354
Infections
3535
A
C
Fig.35.9 Types of malignant melanoma: (A) superficial spreading, (B) nodular, (C) lentigo maligna and (D) acral lentiginous.
(Reprinted with permission from Dermatology 3rd Edition Bolognia etal.)
invasive melanoma, naevi, family history and sun exposure.
The properties that help identify malignant disease are:
• rapid enlargement
• diameter greater than 7 mm
• bleeding or crusting
• increasing variegated pigmentation, particularly blueblack or grey
• an indistinct border or irregular border
• sensory change
• small ‘satellite’ lesions around the principal lesion
Prognosis is related to the depth of a tumour assessed histologically (Breslow thickness), and worsens with increased
depth. Metastasis is common, and in patients with in-transit
metastasis, the 5-year survival rate is only 25%.
Prevention when you are considering melanoma management is important, with avoidance of exposure to
direct sunlight and use of effective sunscreen lotions. Selfexamination should be practised, and people should be
aware of the warning signs and symptoms. Treatment is by
excision (definite), radiotherapy and chemotherapy.
B
D
INFECTIONS
Impetigo
This is a superficial skin infection with S. aureus or β-
haemolytic streptococcus, usually seen in children. Lesions begin as papules before progressing to vesicles (Fig.35.10). These
may form bullae or may break down to form a thick golden
crust. Treatment is with antibiotics, most often flucloxacillin or
clarithromycin if the patient is allergic to flucloxacillin.
HINTS AND TIPS
Breslow thickness (thickness of a tumour) assesses
risk: less than 0.76 m, low; 0.76—1.5 mm, medium;
more than 1.5 mm, high.
Fig.35.10 Impetigo in a child. (Reprinted with permission
from Dermatology 3rd Edition Bolognia etal.)
355
Skin disease
Cellulitis
This is an acute painful and potentially dangerous infection affecting skin and subcutaneous tissue. When
only the dermis and superficial subcutaneous tissue are
involved, cellulitis takes the form of erysipelas (superficial cellulitis). Cellulitis manifests itself as erythematous,
warm, oedematous areas (Fig.35.11). Staphylococcus and
Fig.35.11 Cellulitis of lower limb. (Reprinted with
permission from Dermatology 3rd Edition Bolognia etal.)
Streptococcus are the most common causative organisms,
but a range of aerobic and anaerobic bacteria can also be
involved. Risk factors include breaks in the skin (e.g. due
to trauma, ulcers or drug use), previous skin infection,
elderly age, fungal infection, oedema, obesity and immunosuppression. Treatment is with antibiotics (flucloxacillin and clarithromycin), and in severe cases is given
intravenously.
CLINICAL NOTES
Be aware that cellulitis can very quickly spread
and cause sepsis. It is useful to mark the area
of infection and look for signs of spreading and
tracking, which may be suggestive of ineffective
treatment.
Necrotizing fasciitis
This is a potentially limb/life-threatening infection that is
characterized by infection affecting one or more of the deep
soft tissue compartments (dermis, subcutaneous tissue, fascia, muscle). It is often caused by group A streptococci, and
risk factors include skin injury, an underlying condition
such as alcohol abuse, obesity, renal disease, diabetes and
immunosuppression.
The skin is often affected but may be spared. It presents
as local pain that is disproportionate to the clinical picture,
swelling, skin discolouration and neurovascular compromise. Progression is rapid and unremitting; mortality is
between 20% and 40%. Treatment is with intravenous antibiotics and surgical debridement.
Chapter Summary
• Skin disease and skin manifestations of systemic disease are vast and commonly
diverse. As a clinician, it is important to familiarize yourself with common presentations
and know how to assess skin for a sinister cause. Skin is our biggest organ and very often
manifests pathological changes, and treatment of the underlying cause is vital for the
best outcome. It is also important to consider the impact skin condition has on an
individual in both physical and psychological manners as these are often intertwined.
356
Haematological disorders
36
ANAEMIA
Anaemia is a common clinical problem which may result
from many different pathological processes. It can be classified by the size of the red blood cells (RBCs) seen on microscopy or by the underlying cause (e.g. iron deficiency,
haemolysis). The most common causes include iron deficiency, acute or chronic blood loss, vitamin B12 and folate
deficiency, chronic disease and haemolysis (see later).
Diagnosis
Anaemia is not a diagnosis but a consequence of an underlying problem. Detailed history taking and examination are
essential when you are considering the cause. The World
Health Organization (WHO) defines anaemia as:
• haemoglobin (Hb) level less than 130 g/L in men over
the age of 15years
• Hb level less than 120 g/L in nonpregnant women over
the age of 15 years
• Hb level less than 120 g/L in children aged 12–14years
Iron deficiency is the most common cause worldwide.
Following initial Hb estimation, further investigations are
needed to establish the most likely cause (described later).
Remember that there may be more than one cause of anaemia. For example, folate deficiency and iron deficiency may
be present together (e.g. in coeliac disease). In other diseases, such as rheumatoid arthritis, there are several potential causes of anaemia.
CLINICAL NOTES
Remember that the rate of drop in haemoglobin
level is as important as the level itself; if blood loss
is slow and chronic, very low levels can be tolerated
with only mild symptoms. If the blood loss is acute,
a fall of just 20 g/L can cause significant symptoms.
Management
The anaemia will recur if the underlying problem persists; therefore the cause should be sought and appropriately managed. Anaemia should be corrected, the method
will depend on the type of anaemia and the presence of
complications.
Iron replacement
Addressing the underlying cause in the first instance is important. If a dietary deficiency is considered, commence a
balanced diet with iron-rich foods (dark, green-leaf vegetables, prunes, red meat). Oral iron replacement therapy
(e.g. ferrous sulphate) is the mainstay treatment. Hb levels
should be rechecked 2–4weeks after initiation of treatment
with the aim of an Hb rise of 20 g/L every 3–4weeks. Once
Hb concentration returns to normal, treatment should be
continued for 3months to allow total body iron stores to
be restored.
Side effects of iron supplements include nausea, diarrhoea or constipation and abdominal pain. The stools usually become very dark or black. If side effects occur, the dose
can be reduced or the preparation changed. Intramuscular
or intravenous iron therapy should be given only if oral
therapy is not tolerated.
COMMUNICATION
Ensure patients are clear that over-the-counter
preparations do not contain sufficient iron for
replacement, and that replacement must continue
for at least 3months to adequately replace iron
stores.
Vitamin B12 and folate replacement
Most causes of vitamin B12 deficiency are due to malabsorption (e.g. pernicious anaemia). Replacement is with intramuscularly administered hydroxocobalamin. Depending
on whether there are any neurological symptoms, initial treatment doses differ. Maintenance is with lifelong
3-monthly injections.
Folate deficiency is treated with daily oral replacement.
In most people, 4months of treatment is sufficient to correct anaemia and replace stores.
A balanced diet with foods rich in vitamin B12 and folate (e.g. broccoli, brown rice) is recommended to support
treatment.
Blood transfusion
Transfusion may be necessary in cases of both acute and
chronic blood loss and in patients with cardiovascular
instability (e.g. due to haemorrhage). Blood is given as
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