27 fe Rash: acute generalized

re
sf
skin eruption
ks

ok
oo

The accurate diagnosis of skin disease is usually

Psoriasis
based on visual pattern recognition developed
m

m
through experience rather than analytical Psoriasis, a very common papulosquamous
eruption, is characterized by well-demarcated

co
rule-based approaches. This is a step-by-step
erythematous or purple papules and plaques,
c

approach to assist identification of important

e.

acute generalized eruptions that require urgent topped with silvery scale. There are three forms

e
of acute eruption: erythroderma (see above),
re

re
advice and treatment.
pustular psoriasis (Fig. 27.4) – a form that can
sf

sf

f
Erythroderma

ks
deteriorate rapidly and guttate psoriasis (Fig.
Erythroderma (red skin) describes inflamma 27.5) – with characteristic widespread multiple
oo

tory skin disease manifesting predominantly ‘drop-like’ lesions, most commonly seen in
o

o
as erythema and involving >90% of the body young adults in association with streptococcal
eb

eb
surface area (BSA; Fig. 27.1). The term ‘sub- pharyngitis. Pityriasis rosea is often confused
m

m
erythrodermic’ is sometimes used to describe with psoriasis. It may be a reaction to a
extensive erythema covering <90% BSA. Acute viral infection and initially presents with a single
erythroderma can be life-threatening and most ‘herald patch’ followed by the subsequent
cases need hospitalization and urgent dermatol- development of multiple lesions on the torso
m

ogy review. The major causes are eczema (40%), (Fig. 27.6).
co

psoriasis (25%), cutaneous lymphoma (15%) and

Toxic epidermal necrolysis,
c

drug eruptions 10%).

e.

e.

Stevens Johnson syndrome

Eczema and erythema multiforme
re
sf

‘Eczema’ and ‘dermatitis’ are interchangeable Toxic epidermal necrolysis (TEN) is the severe
ks

ks
terms. Dermatitis is used to denote a group end of a spectrum of acute eruptions caused by
oo

oo

of non-infective inflammatory skin diseases a cell-mediated cytotoxic reaction against epider-

o

that represent a reaction pattern to various mal cells (Fig. 27.7). It is characterized by fever
eb

eb

stimuli. Dermatitis may be classified by aetiology (>38° C), widespread tender erythema affect-
(atopic, irritant, allergic/contact, venous/stasis), ing >30% of the skin surface, and mucosal
m

morphology (seborrhoeic, discoid) or site (palmar, involvement (see below). Erythema is followed
plantar, pompholyx). All produce the same key by extensive, full-thickness, cutaneous and
clinical feature: pruritic, erythematous lesions mucosal necrosis and denudation within a couple
m

with typically indistinct margins. The lesions can of days. Similar features involving <10% of the
progress through a number of phases: acute body surface are termed Stevens–Johnson
co

co

(with vesicles and bullae – Fig. 27.2), subacute syndrome (SJS), also known as ‘erythema
(with scaling and crusting) and chronic (with multiforme major’; if 10–30% of body surface
e

acanthosis, lichenification and fissuring). Lesions area is affected, this is often classified as TEN/
fre

re

may become secondarily infected by bacteria SJS overlap. Drugs, e.g. allopurinol, anticonvul-
sf
ks

forming a crusted yellow exudate (‘impetigo’) (Fig. sants, NSAIDs, cause >80% of cases and have
ok

27 3) or by viruses, e.g. herpes simplex, produc- usually been commenced 1–3 weeks prior to
ing a vesicular pattern (‘eczema herpeticum’) presentation.
o

bo
 Rash: acute generalized skin eruption
241

o
Differential diagnosis

Fig. 27.1 Erythroderma. (From Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill Livingstone, 2008.)
k

Fig. 27.2 Acute dermatitis. (From Gawkrodger DJ. Fig. 27.3 Impetigo. (From Kumar P, Clark M. Kumar &
r

Dermatology ICT, 4th edn. Edinburgh: Churchill Clark’s Clinical Medicine, 7th edn. Edinburgh: Churchill
f

sf
ks

Livingstone, 2008.) Livingstone, 2009.)

27
m

Fig. 27.4 Pustular psoriasis. (From Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill Livingstone, 2008.)
 Rash: acute generalized skin eruption
242

co
Differential diagnosis

Erythema multiforme (minor) represents a

re
similar but milder type of cytotoxic reaction

sf

f
Classically, it presents with ‘target’ lesions,

ks
consisting of three zones: a dark or blistered

oo
centre (bull’s-eye) surrounded by a pale zone
and an outer rim of erythema (Fig. 27.8). The

eb
lesions predominantly occur on the hands/feet
and affect <10% of the BSA without mucous

m
membrane involvement. The underlying cause
is more often viral (especially herpes simplex)
than drug-induced.
Pemphigus/pemphigoid/dermatitis

co
herpetiformis
c

Fig. 27.5 Guttate psoriasis. (From Bolognia J, Jorizzo J,

Rapini R. Dermatology 1st edn. London: Mosby, 2003.) Separation of keratinocytes from each other, or
e

e
from the underlying dermis, produces blistering.

re
The three most common blistering disorders are
sf

f
ks
pemphigus (Fig. 27.9), pemphigoid (Fig. 27 10)

Fig. 27.6 Pityriasis rosea. (From Gawkrodger DJ. Fig. 27.8 Erythema multiforme-target lesions. (From
ks

Dermatology ICT, 4th edn. Edinburgh: Churchill Bolognia J, Jorizzo J, Rapini R. Dermatology, 1st edn.
ok
Livingstone, 2008.) London: Mosby, 2003.)
oo

Fig. 27.7 Toxic epidermal necrolysis. (From Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill Livingstone, 2008.)
 Rash: acute generalized skin eruption
243

o
Differential diagnosis

Fig. 27.9 Pemphigus. (From Bolognia J, Jorizzo J, Rapini R. Dermatology, 1st edn. London: Mosby, 2003.)
c

Fig. 27.10 Pemphigoid. (From Bolognia J, Jorizzo J, Rapini R. Dermatology, 1st edn. London: Mosby, 2003.)
o

and dermatitis herpetiformis (Fig. 27.11) which

e

is commonly associated with coeliac disease.

m

Urticaria/angioedema
Urticaria (Fig. 27.12) is oedema within the dermis
27
m

secondary to mast cell degranulation, and is a

co

common skin reaction Angioedema results from

oedema deeper within the dermis and subcuta-
e.

neous tissues, and may occur in up to 40% of

fre

cases. Although commonly thought to be allergic,

most cases of acute urticaria are not mediated by
ks

immunoglobulin E (IgE). Those that are, arise in

response to drugs (especially antibiotics), foods
oo

(peanuts, eggs, shellfish) and skin contact (latex,

o

Fig. 27.11 Dermatitis herpetiformis. (From Gawkrodger

eb

eb

plants, bee/wasp stings), and may progress to DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill
anaphylaxis. Non-IgE causes include concurrent Livingstone, 2008.)
 Rash: acute generalized skin eruption
244

co
Differential diagnosis

Fig. 27.12 Urticaria. (From Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: Churchill Livingstone, 2008.)
b

b
infection (especially upper respiratory tract infec-
m

tions), drugs that promote mast cell degranulation

co

(opiates, aspirin, NSAIDs, ACE inhibitors) and foods

that contain salicylates and additives.
e.

Purpura (including vasculitis)

r
ks

Purpura (Fig. 27.13) is fixed staining of the

skin by leakage of blood from the intravascular
oo

oo

space and needs to be distinguished from simple

bruising. Causes include:
• septic emboli from systemic infectious
m

diseases
• haematological disorders
• thrombosis involving microcirculation
• vasculitis (inflammation in vessel walls).
m

Acute exanthems
‘Exanthem’ simply means ‘breakout’ and,
e
fre

although the term is mostly used for rashes with

an infectious aetiology, it may be regarded as
ks

a pseudonym for any acute eruption or rash.

Drug eruptions are common and do not
oo

oo

necessarily indicate allergy; ~3% of all patients Fig. 27.13 Vasculitis/purpura. (From Gawkrodger DJ.
eb

eb

admitted to hospital have an eruption due to Dermatology ICT, 4th edn. Edinburgh: Churchill
adverse drug reactions. Those most commonly Livingstone, 2008.)
 Rash: acute generalized skin eruption
245

o
Differential diagnosis

implicated are listed in Box 27.1. In hospital,

re
Box 27.1 Drugs that cause rashes in >1% rashes are commonly attributed to and often
r
of the population
sf

sf

f
caused by medications, but similar cutaneous

ks
• Penicillins signs can be due to underlying or intercurrent
o

oo
• Carbamazepine illness, e.g. viral or bacterial exanthems or internal
• Allopurinol disease, non-specific reactions to treatment,
• Gold e.g. sweat rash due to prolonged bed-rest or

e
• Sulphonamides previously unidentified independent skin disease.

m
• NSAIDs
• Phenytoin
Infective exanthems are largely viral. Many of the
• Isoniazid conditions described above could be considered
• Chloramphenicol specific examples of infective exanthems, e.g.

m
• Erythromycin erythema multiforme post-herpes simplex, guttate
• Streptomycin psoriasis post-pharyngitis and pityriasis rosea.

co

27
 Rash: acute generalized skin eruption
246
Overview

fre
Ful clinical assessment

Yes Urgent
1 >90% body surface area erythematous? Erythroderma

k
Dermatology input

o
No

2 Blisters present?

No Yes
Stevens-Johnson
Yes syndrome / toxic Urgent
m

m
Mucous membrane involvement? epidermal necrolysis / Dermatology input

co
acute pemphigus
No

Yes Consider bullous pemphigoid, erythema

e
Blisters ≥5 mm? multiforme, fixed drug eruption, acute
dermatitis, insect bite
No

Consider herpes simplex / zoster, dermatitis herpetiformis, chickenpox,

bo

impetigo, acute dermatitis

3 Purpura present?

No Yes

Yes
Evidence of infection? Consider meningococcal sepsis / endocarditis
c

No
e

Coagulopathy, anticoagulant therapy,

Yes disseminated intravascular coagulation,
↓Platelets or ↑PT / APTT?
idiopathic thrombocytopenic purpura,
thrombotic thrombocytopenic purpura
No

Consider vasculitis or drug reaction (see text)

e

Yes
4 Pustules present? Likely pustular psoriasis or systemic infection

No

Yes
5 Wheals present? Urticaria Seek precipitant
c

No
e

Yes
6 Underlying chronic dermatosis? Consider acute flare

No
e

7 Likely drug reaction or infective exanthem. Refer Dermatology if persistent or severe symptoms
m
 Rash: acute generalized skin eruption
247

co
Step-by-step assessment

1 >90% body surface area erythematous? when erosions and ulceration (with subsequent

re
crusting) occur on oral, genital and ocular
Estimate the proportion of skin that is erythe-

sf

sf
epithelium; examine these sites in any acute
ks
matous using the guide in Box 27.2; >90% of severe skin eruption.
BSA indicates erythroderma. Admit any patient
oo

oo
Suspect TEN if there is extensive blistering with

o
with acute erythroderma to hospital, assess and peeling of the skin to reveal bright red oozing

eb

eb
stabilize as described in Box 27.3 and arrange dermis (see Fig. 27.6), along with mucous mem-
urgent dermatology review. Subsequent treat- brane involvement; seek immediate Dermatology

m
ment is based on the exact diagnosis and guided review and manage in a burns or critical care
by expert dermatological assessment. unit. If bullae and mucosal lesions are present
but blistering is less extensive, consider SJS
2 Blisters present?

m
and pemphigus (see Fig. 27.9) – arrange prompt
dermatological review in all cases.

co
Blisters form when fluid separates the layers of
.c

the skin; blisters <5 mm diameter are termed In the absence of mucous membrane involve-
ment look for target lesions (see Fig. 27.8) on

e
‘vesicles’, those >5 mm are called ‘bullae’.
the hands and feet suggestive of erythema
fre

Mucous membranes are involved (Fig. 27.14)

fre
multiforme; otherwise, consider bullous pem-

sf
ks
phigoid (see Fig. 27.10), fixed drug eruption or,

ok
Box 27.2 Calculating body surface area if lesions are well localized, an insect bite or
o

contact dermatitis.
Originally developed for calculating surface area for burn If the patient has a painful eruption of vesi-
eb

eb
victims, in adults a simple way of calculating the BSA cles, suspect infection with herpes simplex if it
affected by a cutaneous disorder is the ‘Wallace rule
m

m
is confined to the face, lip or finger (herpetic
of nines’. This system allocates to different body parts
9% (or half thereof) of the total BSA. In extensive skin whitlow) and herpes zoster (shingles; Fig. 27.15)
disease it is sometimes easier to identify unaffected if it follows a dermatomal distribution. In febrile
skin, and assessment is aided by remembering that the patients with widespread vesicles consider
om

patient’s hand is approximately 1% of BSA.

Rule of 9s Box 27.3 Assessment and immediate

.

e.

management of skin dysfunction

4 5% 4.5%
e

fe

The mainstay of emergency dermatology treatment is

9% 9% to provide surrogate skin function until the underlying
k
condition has resolved or is suppressed with suitable
oo

medication. Look for evidence of shock (see Box 30.1,

4.5%

4.5%
4.5

4.5

9% 9% p. 267) and dehydration, and monitor U+E regularly.

%

%
b

eb

Replenish fluid lost through defective skin barrier

1%
function with IV fluids and supplementary electrolytes.
m

9% 9% 9% 9% Take swabs of all areas of suspected infection and,

if the patient is pyrexial, take blood cultures before
commencing antibiotic therapy. Use strict aseptic
technique for blood cultures, ideally through non-
27
m

affected skin, to try to avoid contaminants (more likely

in dermatologica patients due to ↑skin flora load).
co

Remember that many acute cutaneous eruptions are

associated with pyrexia, due not to systemic infection
e.

Anterior Posterior
e

but to loss of temperature homeostasis through

re

vasodilatation. Maintain body temperature with a warm

room and regular antipyretics. Assess the extent of skin
sf

Palmar method compromise as detailed above and restore its barrier

ok

(patient’s palm) 1% function with regular application of thick emollients

oo

(liquid paraffin : white soft paraffin, 50 : 50). Remove

any potential exacerbates by discontinuing all
unnecessary medication.
 Rash: acute generalized skin eruption
248

co
Step-by-step assessment

Fig. 27.15 Herpes zoster. (From Gawkrodger DJ.

e
Dermatology ICT, 4th edn. Edinburgh: Churchill
fre
Livingstone, 2008.)

liver disease, discuss with Haematology if there

bo
is coagulopathy or ↓platelets.
B If ↓platelets are present with normal coagula-

m
Fig. 27.14 Mucous membrane involvement in tion, look for associated features of thrombotic
Stevens–Johnson syndrome. A Oral. B Ocular. (From thrombocytopenic purpura:
Gawkrodger DJ. Dermatology ICT, 4th edn. Edinburgh: • ↓Hb without an obvious alternative cause
Churchill Livingstone, 2008.)
m
• red cell fragmentation on blood film
• ↑↑LDH
• neurological abnormalities (↓GCS,
c

chickenpox or, if there is known eczema, eczema headache, seizures).

e

e
re

re

herpeticum Suspect dermatitis herpetiformis if If any of these is present, seek immedia e

the vesicles are intensely itchy and occur on the Haematology input, as urgent plasma exchange
f

sf
ks

extensor surfaces (see Fig. 27.11). may be life-saving.

Suspect a systemic vasculitis, e.g. polyarteritis
oo

3 Purpura present? nodosa, Henoch–Schönlein purpura, microscopic

eb

polyangiitis, cryoglobulinaemia, rheumatoid vas-

Classify the rash as purpuric if there are dark red
e

culitis or other systemic inflammatory disorder – if

or purple macules/patches that do not blanch
m

there is palpable purpura accompanied by fever,

with pressure (see Fig. 27.13).
↑ESR/CRP, constitutional upset, joint disease
Take urgent blood cultures and treat empiri-
and/or renal involvement (↓GFR, proteinuria,
cally for meningococcal sepsis pending further
haematuria). Perform a full vasculitis/autoimmune
m

investigation if the patient has fever, shock,

‘screen’ and consider skin biopsy ± biopsy of
drowsiness or meningism (see Box 18.2, p.
co

co

other affected organs.

169). Consider septic emboli from endocarditis
Also consider cholesterol embolization or drug
e.

e.

if the patient is febrile and has a predisposing

reaction – seek Dermatology input if the cause
fre

fre

cardiac lesion or a new murmur.

remains unclear.
Look for evidence of an underlying bleeding
ks

tendency – ask about/examine for ecchy-

4 Pustules present?
moses, epistaxis, GI bleeding, menorrhagia
oo

haemarthrosis and mucosal haemorrhage, and Pustules are best thought of as small blisters
o

o
eb

eb

check FBC, PT and APTT. Unless the cause is filled with pus (see Fig. 27.3). The key diagnostic
obvious, e.g. excessive anticoagulation chronic conundrum is whether they are infective or sterile.
m

m
 Rash: acute generalized skin eruption
249

co
Step by-step assessment

In both cases, the patient may be unwell, with patients to miss their dermatological medica-
significant constitutional upset. tions due to lack of prescription or interruption
r

r
sf

sf

f
Assume an infective pustulosis, at least initially, of their regular topical application routine; if this

ks
if the patient has a fever and the lesions have a is the case, suspect an acute flare and look for
ok

oo

oo
follicular appearance (individual, palpably raised resolution of the rash after reinstating routine
bo

lesions, following the distribution of hair follicles). treatment.

eb
Suspect sterile pustulosis due to either pustular
psoriasis or drug reaction if the pustules have Likely drug reaction or infective

m
a subcorneal appearance (more superficial, 7 exanthem. Refer to Dermatology if
often confluent lesions). In either case, admit persistent or severe symptoms
the patient and seek an urgent dermatological Occasionally, serious acute drug eruptions lack
m

om
opinion. the specific features detailed above; seek prompt
dermatological advice in any patient with signs

c
5 Wheals present? of significant systemic upset, mucous membrane
e.

e.
Classify the rash as urticaria if there are wheals: involvement or associated lymphadenopathy, or
fre

transient (<24 hours), erythematous, intensely

pruritic raised skin lesions (see Fig. 27.12). fre
if symptoms are persistent and troublesome.
Consider guttate psoriasis and pityriasis rosea
ks

ks
Look for swelling of the lips, face and throat, if there is an acute papulosquamous eruption (see
above) over the trunk. Suspect the former if the
oo

oo
suggesting associated angioedema; patients may
o

describe the skin sensation as burning rather than lesions are ‘drop-like’ (see Fig. 27.5) and there
eb

eb
itchy. Take a careful food and drug history to is a history of upper respiratory tract infection
identify possible precipitants, although in many within the past 2–3 weeks; suspect the latter if
m

m
cases a cause cannot be identified (idiopathic the lesions form a ‘Christmas tree’ pattern on the
urticaria). Other than avoidance of any identified back (see Fig. 27.6) and follow a ‘herald patch’.
precipitant, the mainstay of treatment is regular Precise identification of infective exanthems is
m

antihistamines; most cases subside quickly with seldom required as most do not need specific
treatment and wil settle conservatively, but seek
co

co

avoidance of the precipitant and/or antihistamine

treatment. Refer patients with persistent (>24 specialist advice if the patient is a returning
e.

traveller with fever or an unusual rash.

e

hours) or chronic (>6 weeks) lesions for outpatient

Review all recent medications, both prescribed
fre

re

dermatological assessment.
and over-the-counter drugs. There is significant
sf

f
ks
variation in the morphology and exposure-to-
6 Underlying chronic dermatosis?
k

onset time (minutes to years) of cutaneous drug

oo

Ask about previous skin disease, recent changes eruptions. If a drug reaction is suspected, e.g.
bo

to dermatological or other medications and spe- a drug from Box 27.1 is involved or there is a
eb

eb

cifically whether the present eruption resembles clear temporal association, attempt to confirm
m

previous rashes. It is very common for hospital by trial discontinuation wherever feasible.

27