Dermatological presentations to emergency

Published on 14/03/2015 by admin

Last modified 22/04/2025

Print this page

This article have been viewed 2257 times

Chapter 40 Dermatological presentations to emergency

John R. Sullivan, Veronica A. Preda, Margot J. Whitfield

Dermatology presentations to emergency department are common, accounting for 15–20% of visits,¹ with the majority of presentations due to an infective aetiology or the result of drug reactions. Overall, there are four basic categories of dermatological presentation to emergency department (see Table 40.1).

Table 40.1 Isolated dermatological disorders

Reason for presentation	Common or important clinical examples
New onset or flare	Eczema (atopic dermatitis)Papular urticaria—mainly a paediatric emergency presentation usually representing an exaggerated local hypersensitivity to an insect bite which can be clinically dramatic and/or severe, such as a blistering skin reaction
Subacute or chronic with complication	Impetiginised scabies, eczema
Dermatological presentations with systemic associations
Fifth disease	Pregnant woman—increased risk of hydrops fetalis or aplastic crisis if underlying haematological disorder
Systemic disorders resulting in acute presentations with prominent cutaneous manifestations
SLE/PAN/cholesterol emboli	Vasculitis, trash foot, broken livedoid eruption
Systemic disorders with associated cutaneous changes or disorders
Inflammatory bowel disease and/or inflammatory arthritis	Pyoderma gangrenosum
Systemic disorders with unrelated/incidental cutaneous findings
Common presentations	Seborrhoeic dermatitis (> 50% elderly but also more common in particular clinical settings, e.g. advanced HIV/AIDS, neurological disorders, especially Parkinson’s disease)

HIV/AIDS, human immunodeficiency virus/acquired immune deficiency syndrome; PAN, polyarteritis nodosa; SLE, systemic lupus erythematosus

Table 40.2 Terminology for skin lesions

Lesion	Description
Bulla(e)	Large fluid-filled lesion > 0.5 cm in diameter
Cyst	Closed cavity/sac with epithelial lining containing solids or fluids
Discoid	Disc-shaped (nummular)
Erythema	Redness of the skin from vascular congestion or increased flow such as in inflammation
Macule	Flat alteration in colour and/or texture of the skin, e.g. colour change due to skin inflammation including erythema and/or hyper/hypopigmentation (change in melanin, haemosiderin); if larger than several centimetres, referred to as a patch
Nodule	Solid mass > 0.5 cm in diameter, palpable
Papule	Solid elevation of the skin < 0.5 cm in diameter
Petechiae	Pinpoint, flat, round, purplish red spots caused by intradermal or submucosal haemorrhage
Plaque	Solid, elevated lesion; may be formed by coalescence of papules
Purpura	Bleeding into the dermis; may be macular or papular
Pustule	Circumscribed collection of pus, commonly staphylococcal, but may be sterile in inflammatory and autoimmune dermatoses, e.g. pustular psoriasis
Telangiectasia(e)	Tiny visible blood vessels in the upper dermis ± inflammation
Verrucous	Rough, warty
Vesicle	Visible accumulation of fluid within or beneath the epidermis, < 0.5 cm
Wheal	Transient area of dermal oedema, pale, compressible, papular or plaque-like

Surface characteristics: scale, crust, horn, excoriation, maceration, lichenification

Table 40.3 Diagnosis of dermatological disease

Diagnosis
Accurate characterisation of skin eruption	E.g. exanthematic eruption, skin rash due to or mimicking a viral infection
Isolated skin presentation versus any worrisome systemic involvement; concerning symptoms or associated findings	E.g. high fever (> 40°C) or ‘sick’ patient presentation
Differential diagnosis
	Infection: viral, bacterial, fungalDrug eruption: isolated (simple) exanthematic hypersensitivity reaction (and/or the manifestation of a systemic hypersensitivity reaction)Connective tissue disease, graft versus host disease (due to an acute disease flare and/or active inadequately controlled disease)
Drug and other exposures
Medications history	When medications, including over-the-counter and alternative or natural therapies, were started and/or stopped; any previous reactions to similar or crossreacting medications, vaccinations or injections
Other exposure	IVDU, environmental exposure, history of infective symptoms, travel
Diagnostic testing
Diagnosis	Most diagnoses are suspected in emergency but confirmed at a later date. e.g. drug reactions largely a diagnosis of exclusion
Differential diagnosis	May require baseline (acute) viral and autoimmune serologyALWAYS perform a bacterial culture for M/C/S if itchy/weeping/crusted/purulent, ± viral culture if painful
Associated diseases/toxicities/complications	E.g. hepatitis, nephritis as part of a drug hypersensitivity syndrome and/or connective tissue disease flare. Drug hypersensitivity reactions are more common in those living with HIV/AIDS, lymphoma ± CTD
Determine probabilities
Paediatric	Infectious aetiology more likely
Adult	Consider comorbidities and always consider drug causes, especially in the elderly
Dermatologist consult
Urgent	E.g. suspected SJS/TEN
Organise follow-up/discuss

CTD, connective tissue disease; IVDU, intravenous drug use; M/C/S, microculture and sensitivity; SJS, Stevens-Johnson syndrome; TEN, toxic epidermal necrolysis

Table 40.4 Infective complications of dermatoses in immunocompetent patients

Bacterial	Staphylococcus aureus (approximately 90%) Always consider risk factors for methicillin resistant S. aureus (MRSA) Streptococcus pyogenes Always consider nephritogenic strain, especially in Indigenous populations Mixed
Viral	Herpes simplex virus 1, 2
Fungal	Trichophyton rubrum and T. tonsurans (especially in rural and remote Indigenous populations)

Table 40.5 Assessing patients with dermatological emergency presentations

Dermatological history

Note: Take advantage of being able to readily and concurrently evaluate and examine the skin early in the consultation process to assist in the provision of an expedient and clinically focused and relevant medical assessment.

Where: site(s) of initial lesion, then subsequent lesions

Associated dermatological symptoms: e.g. irritable, pruritic, burning or tender skin

Temporal disease course/exposures:

• onset/duration—acute, exacerbation of a chronic or intermittent condition

• recent medication and medical history (weeks–months)

• travel (rural/farm or overseas)

• change in symptoms over time

Any other family members/colleagues/school friends affected

Personal and family history of skin disease

Cutaneous changes warning of a potentially severe cutaneous reaction/disease and/or systemic reaction/disease, such as a previously itchy skin eruption that becomes tender and/or blisters

Other dermatological symptoms and manifestations suggesting/warning of associated mucosal involvement preceding, coinciding or following onset of skin changes (e.g. sore throat/pharyngitis, gritty eyes/periorbital puffiness or head and neck swelling/enlarged cervical glands)

Presence or absence of associated symptoms suggesting skin involvement by a systemic disease/associated internal organ involvement/toxicity (e.g. high fever/night sweats, anorexia, arthritis)

Occupational history (e.g. a possibly infective presentation and work history exploring animal exposures) and/or work/close contact with an elderly family member living in a nursing home (e.g. if scabies considered in a patient with an acute/subacute ± itchy skin reaction)

Home environment/activities: blistering, extremely itchy, streaky inflammatory eruption mainly and most severely involving upper limbs and other exposed skin areas starting hours after gardening

Treatments tried and any associated temporal changes in disease symptoms

Examination

Dermatological: distribution, morphology, pattern

Where relevant, also examine mucosal surfaces e.g. for oropharyngeal inflammation/erosion/ulceration

General examination (tailor and target to presentation as illustrated by the following examples):

• Arterial examination including abdominal examination specifically checking for an acutely dissecting abdominal aortic aneurysm as the source of cholesterol emboli in a person presenting with lower back pain and a tender, dusky, ischaemic reticulate lower leg eruption

• Examination for presence or absence of tender lymphadenopathy of draining lymph nodes with cutaneous infections and/or an infective complication of skin disease

MORPHOLOGICAL CLASSIFICATION OF DERMATOLOGICAL PRESENTATIONS

1 Urticaria (hives) ± angio-oedema ± anaphylaxis

• Cutaneous versus systemic reaction.

• Common condition: 15–25% of people have an episode of urticaria ± angio-oedema at some stage in their life. Usually it is acute.²

Flow diagram: adapted from Amar and Dreskin²

Table 40.7 Medications in angio-oedema, anaphylaxis and acute and ‘subacute’ urticaria

Medication	Recommended adult dose	Comment
Adrenaline	0.5–1.0 mL of 1:1000 IM	Used if evidence ofanaphylaxis
H₁ antihistamine Chlorpheniramine Diphenhydramine

4 mg q4–6 h, max 24 mg/day

Mainstay of therapy

Sedating in 50% patients

H₁ antihistamine, 2nd generation

Reasonable to continue antihistamines for approximately 72 hours after acute presentation

Although caution required, medications are safe in general long-term and can be used in higher doses for urticaria

Steroids

Hydrocortisone

Prednisone

100 mg IV

1 mg/kg in divided doses and taper

Acute severe episodes, avoid chronic use, especially in patients with chronic urticaria

Table 40.8 Treatment of chronic urticaria (often a distressed patient with chronic symptoms presenting with a flare)

Simple measures	Keep cool, loose clothing
H₁ antihistamine Chlorpheniramine Diphenhydramine	4mg q4–6 h, max 24 mg/day	Mainstay of therapy Sedating in 50% patients
H₂ antihistamine Ranidine Cimetidine Famotidine	150 mg BD 400 mg BD 20 mg BD	Useful in chronic urticaria in addition to H1 antihistamines
Cyproheptadine	4 mg TDS	Sedating antihistamine plays an important role in chronic urticaria, e.g. with nocturnal exacerbations or insomnia due to urticaria, and appetite stimulant
Doxepin	10–50 mg/day	H1- and H2-blocking properties, sedating, appetite stimulant, higher doses have anxiolytic and antidepressive effects
Steroids Hydrocortisone Prednisone	100 mg IV 1 mg/kg in divideddoses and taper	Acute severe episodes, avoid chronic use, especially in patients with chronic urticaria
Other immunosuppressives	For immunologist referral

2 ‘Spotty, blanching’ exanthematic eruptions

Infection-associated skin eruption or other disease with skin changes mimicking those of an infective exanthem.

Exanthematic eruption

Generalised cutaneous eruption usually associated with a primary systemic infection, often accompanied by oral mucosal lesions (an enanthem).

Clinical features

• Lesion morphology: flat, erythematous macules or papular, less frequently vesicles, pustules petechiae and itch.

• Systemic features: consideration of the seriousness of presentation (not aetiology) to differentiate isolated ‘skin changes only’—no fever, no systemic symptoms, no systemic findings, normal lab tests—versus symptomatic—unwell with fever ± hypotension, internal organ involvement; ± lymphadenopathy ± hepatosplenomegaly.

• Associated exanthem: severe mucosal changes are predictors of serious systemic disease, e.g. oropharyngeal ulceration especially haemorrhagic changes and/or eye or genitourinary.

• Characteristic mucosal changes include:

• drug eruptions

• inflammatory disease

• Koplick spots, red strawberry tongue, mouth changes in Kawasaki’s etc.

Note: For exanthematic ‘spotty, blanching’ eruptions, ALWAYS consider the seriousness of the presentation: skin changes ± mucosal features ± systemic features, i.e. eruption plus systemically well versus eruption plus systemically unwell patient.

Investigations

• If there is suspicion of systemic involvement: full blood count (FBC), urea, electrolytes, creatinine (UEC), liver function test (LFT), C-reactive protein (CRP), urinalysis (U/A), urine microscopy

• Cultures if appropriate: blood, urine, ± lumbar puncture (LP)

• Serology: acute and convalescent titres for specific diagnosis

Differential diagnosis

Table 40.9 Differential diagnosis, exanthematic eruption

Paediatric exanthematic eruption	Adult exanthematic eruption
1. Infection-related—most commonly in children and usually well: • viral • bacterial • parasitic • fungal 2. Drugs—common nuisance drug eruptions

• Drugs ³—just about all medications but particularly:

• antibiotics

• antivirals

• anti-inflammatories

• anticonvulsants

• antipsychotics4 ⁴

• Inflammatory includes connective tissue disease; other, as part of a flare or warning of disease activity in the context of systemic illness

3. Infection-related:

• viral—including adult varicella zoster, seroconversion illness in HIV ⁵

• rickettsial infections e.g. Rickettsia australis⁶—‘recurrent mild chicken pox in an adult’

• bacterial e.g. S. pyogenes causing toxic shock syndrome

• parasitic

• fungal

Things not to miss

Meningitis—meningococcal can present atypically

Serious drug eruption

Reye’s syndrome

Kawasaki’s disease

Things not to miss

Serious drug eruption

Autoimmune causes—rheumatoid arthritis, systemic lupus erythematosus

Malignancy e.g. lymphoma

Adult varicella zoster

Kawasaki’s disease

• Mucocutaneous lymph node syndrome.

• Cutaneous features of an exanthematic eruption, with prominent peeling hands and feet. Often differential is that of an infective illness, but usually fever > 5 days unresponsive to antipyretics.

Table 40.10 Features and management of common viral exanthems in paediatric patients

Disease/virus	Signs/symptoms	Management
Enterovirus	Commonly respiratory or gastroenterology presentations ± exanthem or urticaria	Presentation dependent
Varicella—chicken pox/ Varicella zoster virus (VZV) Reactivation → herpes zoster (HZ)

Incubation 10–21 days

Mid-prodrome—pruritic vesicles that break and crust, starts centrally or facially and spreads to the extremities

New lesions appear 3–5 days, typically take 3 days to crust

Contagious 24 h prior to rash onset and until they crust.

Immunocompromised children with VZV are given VZ immunoglobulin (VZIG) within 96 h of exposure

Acyclovir for immunocompromised with disseminated VZ or HZ

Measles (rubeola)/

Paramyxovirus

Prodrome fever, malaise, coryza, conjunctivitis, cough then erythematous maculopapular rash face, trunk, legs, buccal mucosal lesions, Koplick spots

Incubation 8–12 days

Symptomatic management, contact considerations, vaccinations

Rubella (German measles)/

RNA togavirus

No prodrome during incubation 14–21days. Symptomatic, consider contacts including pregnant contacts

Roseola infantum/

HHV6

Infants 6–8 mo—high fever, relatively well; multiple pale pink macules/papules as fever breaks Supportive

Erythema infectiosum (fifth disease)/ Parvovirus B19

‘ Slapped cheeks’

Sore throat, cough, headache, nausea, fever with rash, slapped cheek appearance followed by lace-like erythema on the extremities and buttocks Supportive but consider concurrent haematological disease or pregnant exposure Scarlet fever/toxins from Streptococcus pyogenes

Commonly confused with Kawasaki’s

Child 4–8 years, high fever, sore throat, headache, vomiting

Exanthem 1–2 days post—small papules with diffuse erythema

Skin may feel rough like sand paper

Linea petechiae = pastia’s lines in the axillae and groin.

Desquamation 7–10 days post, hand and feet worse.

Strawberry tongue; lips normal; tonsils/pharynx usual site of infection ± surgical wounds

Ix: include antiDNAase B, antistreptolysin O titre

If suspected treat with penicillin, (clindamycin or erythromycin if allergic)

Management is to avoid complications, e.g. rheumatic heart disease

Mumps Morbilliform rash with lymphadenopathy, an issue in young males with potential infertility Despite vaccination consider occurrence Mycoplasma pneumoniae

Skin changes may be macular papular or present as purpura

Mainly in school children, cough, coryza

Skin eruptions in approximately 10% children with mycoplasma

Swab throat—PCR

Antimicrobial therapy for Mycoplasma, e.g. rifampicin

Hand, foot and mouth disease (HFMD)/

Enterovirus, coxsackie

Generally mild clinical course

Distinct clinical presentation of oral and distal extremity lesions

Highly contagious, faecal oral spread

Usually in children < 10 years, can affect adults

Hands, feet and buttocks involved; 2–10 mm erythematous macules, with central grey oval vesicle

Skin lesions asymptomatic, resolve in 3–7 days

Mucosal oral ulcers are painful

Associated fever, malaise, diarrhoea, systemic involvement can progress to myocarditis, pneumonia, meningoencephalitis

Symptomatic management

Note: Can be serious, especially in the immunosuppressed population

• Large and medium vessel vasculitis in children < 10 years (usually < 5 years), predilection for Japanese children.

• Cardiac sequelae.

Clinical features

History is typically > 5 days (usually has been unresponsive to antibiotics in the community) and four out of five of the following (mnemonic—CRASH):

• Conjunctivitis, cervical lymphadenopathy (> 1.5 cm)

• Rash (mostly truncal polymorphic morbilliform)

• Aneurysms of the coronary arteries,

• Strawberry tongue, crusting of the lips, fissuring of the mouth and oropharyngeal erythema

• Hands and feet have induration, erythema of the palms and soles, desquamation of the digits

Diagnosis

• Confused with scarlet fever but scarlet fever does not have fissured lips and has a positive streptococcal throat test. Important to ask parents about eye changes occurring prior to other symptoms in the 7 days before, as these may be transient.

• Complications: cardiac, 10–40% untreated cases have coronary vasculitis (dilation/aneurysm) within the first weeks of the illness.

Investigations

• FBC, UEC, LFT, CRP, ESR.

• Evaluate patient 1/52 post-discharge and echo 3–6 weeks after fever; if no coronary abnormality is seen then nil further required.

Management

Aspirin and immediate IVIG to prevent coronary vasculitis.

Note: High dose corticosteroids are contraindicated.

Exanthematic drug eruptions

• The common classic ‘maculopapular’ drug rash = morbilliform, rubelliform, scarlatiniform

• Red spotty changes, flat ± raised ± itch

• Onset mostly within first 5–14 days of therapy

• Otherwise systemically well, asymptomatic to very pruritic

• Resolution occurs with a change in colour from bright red to a brownish red, sometimes followed by scaling or desquamation

Simple exanthematic drug eruptions (common nuisance)

Onset:

• typically 5–14 days

• can begin up to several days after drug cause stopped (within hours with rechallenge)

Associated drugs:

• essentially all

• especially antibiotics, antivirals, anti-inflammatories, anticonvulsants

Course/resolution:

• worsen for several days after drug cause stopped

• then progressively resolve over 7–14 days

• treatment—antihistamine (cetirazine), cortisone cream (0.5% betamethasone valerate)

Note: Infection-like skin eruption may be the tip of an iceberg, may warn of serious life-threatening skin reactions, e.g. SJS, TEN or internal toxicities.

Box 40.2 Clinical features of simple exanthematic drug eruptions

Facial involvement minimal

No periorbital/facial oedema

No lymphadenopathy

No lip, mouth or eye involvement

Rash spotty, non-confluent

Peaks in days then settles (10–14 days)

Management of ‘nonserious or simple’ exanthematic eruptions:

• history

• examination

• investigations to confirm diagnosis, exclude important and serious differential diagnosis

• management of cause

Symptomatic management:

• moisturiser

• moderate potency topical steroid cream, e.g. betamethasone valerate cream 0.02% TDS

• antihistamine (non-sedating mane, e.g. loratidine 10 mg ± sedating nocte, e.g. phenergan 10–25 mg)

Box 40.3 Clinical features of serious drug eruptions

Associated with systemic symptoms and/or high fever; precede/coincide/follow eruption onset

Eruption:

• confluent

• associated periorbital puffiness and/or facial swelling

• tender or painful eruption

• mucous membrane symptoms or signs, e.g. crusting and erosion of lips, gritty eyes

Box 40.4 Examples of serious drug eruptions

Drug hypersensitivity eruptions

Serum sickness—versus serum sickness-like eruptions

Blistering disorders; SJS, TEN

Acute generalised exanthematic pustulosis (AGEP)

Drug-induced lupus (may be considerably delayed) ± PAN

Drug hypersensitivity syndrome (DRESS)

• Triad of:

1. high fever

2. skin eruption

3. internal organ involvement.

• Prodrome: fever, malaise, sore throat (i.e. mimics URTI).

• Skin eruption is most commonly exanthematic but can evolve to erythroderma or SJS/TEN (when an originally itchy rash turns tender/painful and blisters); see relevant sections under ‘Blistering’.

• Onset: typically 1–8 weeks, occasionally months (especially anticonvulsants and allopurinol), recurrence in hours to days on rechallenge.

Serum sickness-like reaction (SSLR)

SSLR has multiple causes including drug-induced cefaclor, amoxicillin, minocycline etc.

Differential diagnosis: autoimmune connective tissue disease, infections such as hepatitis B or C and infective endocarditis, and lymphoma due to cryoglobulins and/or circulating immune complexes.

Box 40.5 Drug hypersensitivity syndrome (DRESS): commonly implicated drugs

Aromatic anticonvulsants (phenytoin, phenobarbitone, carbamazepine), lamotrigine

Sulfonamide antibiotics, dapsone, trimethoprim, minocycline, metronidazole

Azathioprine

Allopurinol

Alternative therapies including Chinese herbal remedies

Abacavir, nevirapine

Table 40.11 Comparison of serum sickness versus serum sickness-like reaction (SSLR)

	Serum sickness	SSLR
Skin: eruption	Urticarial and vasculitic	Exanthematic and urticarial
Fever	✓	✓
Arthritis	✓	– (arthralgia only)
Renal involvement	✓ (nephritis)	–
Serositis/carditis	✓	–
Associated drugs	Streptokinase, antivenoms, digoxin, immune Fab	Cefaclor, buspirone, infliximab, rituximab, griseofulvin
Histopathology	Systemic vasculitis	Inflammatory or unknown
Management	Admission and specialist care Symptomatic relief ± immunosuppressive therapy

Symptomatic

Paracetamol

Topical steroids

Management of suspected potentially serious drug eruptions:

1. Stop all suspected or potentially causal medications or drugs

2. Admission

3. Supportive management

4. Specialist care

Note the overlapping potential internal toxicities of SJS/TEN, DRESS, AGEP:

Respiratory compromise

Carditis (± arrythmias)

Hepatitis

Renal involvement

Box 40.6 Causes of erythroderma

Exfoliative erythroderma syndrome

Psoriasis flare

Eczematous dermatitis—atopic dermatitis flare, contact dermatitis Drug hypersensitivity reaction—antiepileptics, penicillins, sulfonamides, NSAIDs

Acute graft versus host disease (AGVHD)

TEN, SJS, erythema multiforme (EM)

Lymphomas, e.g. cutaneous T cell

3 Generally red, inflamed and scaly: erythroderma ¹³

Exfoliative erythroderma

Clinical features

Generalised red, inflamed and scaly skin eruption ± lymphadenopathy. Pruritus is usually the initial symptom, and malaise and fever may subsequently develop owing to excessive vasodilation. Fluid and protein loss through the skin can lead to life-threatening hypotension, electrolyte imbalance, congestive heart failure and enteropathy. Potentially fatal.

Causes

Many cases are idiopathic, but can be associated with a diverse range of underlying dermatoses, including: eczema, psoriasis, drug reaction (e.g. allopurinol, calcium channel blockers, anticonvulsants and lithium), cutaneous T-cell lymphoma or leukaemia, pityriasis rubra pilaris, paraneoplastic syndrome and dermatomyositis.

Management

1. The cause should be determined and, if a drug reaction is suspected, the offending medication stopped.

2. Management includes supportive therapy, hospital admission, proper hydration, nutrition, electrolyte and cardiac monitoring and temperature support by nursing in a warm room.

3. Skin biopsies can be obtained to help establish the diagnosis.

4. Skin care involves the use of emollients and compresses as well as topical corticosteroid therapy and antihistamines for pruritus. Antibiotic therapy should be administered if signs of infection develop.

Atopic dermatitis (AD) flare ⁷

Atopic dermatitis (eczema) is a common inflammatory skin condition especially of childhood. Relapsing course, severe pruritus. Frequently complicated by secondary skin infections, often bacterial colonisation with Staphylococcus aureus.

Clinical features

Dry, erythematous, pruritic skin lesions. Chronic skin change of lichenification, thickened, hyperpigmented epidermis. Mostly involving flexural areas, history of atopy, asthma, hayfever and family history of atopy.

AD flare and erythroderma; relapsing and remitting episodes with severe itching and failure of routine topical therapies ± superinfection. Consider admission in patients with:

• generalised erythema and exfoliation—erythroderma

• severe, generalised itching who have failed outpatient topical therapies

• severe skin infections.

Differential diagnosis

Contact dermatitis allergic or irritant, photodermatitis and contact urticaria.

Management

1. Use soap-free products.

2. Avoid skin irritants; use cotton clothing as much as possible.

3. Apply wet dressings/wraps of topical corticosteroid or topical calcineurin inhibitor to affected areas and hypoallergenic moisturiser, e.g. sorbolene, to the asymptomatic areas. Ointment-based medications are better used in the flare setting.

4. Antihistamines; non-sedating for during the day, e.g. cetrizine, and sedating, e.g. phenergan, at night.

5. Topical calcineurin inhibitors, e.g. pimecrolimus cream, are particularly useful non-steroid topical immunosuppressants for AD in the thinner areas, e.g. face, groin, axillae.

Infections

Staphylococcus aureus is the most common cause of bacterial infections in children with AD. Severity ranges from minor local skin infections to cellulitis, abscesses, bacteriemia and sepsis. Secondary skin infections may present as erythema with oozing, honey-coloured crusts. Topical mupirocin can be considered for local infected lesions. Main presentation of secondary infection is simply worsening with increased exudation of the eczema.

• Clinical features: secondary S. aureus infection is usually a worsening, increased exudation of the eczema. Fever, malaise, disseminated eruptions of dome-shaped vesicles that may or may not be superimposed on areas of eczematous change. Head and neck are frequently affected. Lesions may spread rapidly to involve extensive areas of the skin. Systemically unwell in some cases, ± lymphadenopathy.

• Management: oral antibiotics, wet dressings and topical steroids.

• Eczema herpeticum: widespread herpes simplex virus infection accompanying atopic eczema can occur in children and adults affected by atopic dermatitis. In severe cases, treat with IV acyclovir dose; ophthalmology review if there is suspected eye involvement.

Follow-up with dermatologist and/or immunologist as many of these children have food allergy, allergic rhinitis and asthma.

Sunburn (‘photo-distributed’/‘exposed’)

Clinical features

Skin exposed to too much UVB smarts, becomes red a couple of hours later. Severe sunburn is painful, may blister in 24 hours, settles in 2–3 days.

Cause

UVB rays penetrate the epidermis and superficial dermis, stimulating the production and release of prostaglandin (PG), LXT, histamine, interleukin and tumour necrosis factor (TNF)-alpha. This stimulates the production of inducible NO synthetase enzyme → high concentrations of NO → dermal vasodilatation and erythema.

Differential diagnosis

Phototoxic reactions caused by drugs are like an exaggerated sunburn.

Treatment

• Symptomatic: baths; cooling; oily lotions, oil in water lotions/creams comforting; potent topical steroids briefly and used early; oral aspirin; sprays with benzocaine relieve pain, occasionally sensitise.

• If the skin reacts badly to light through glass, then think drugs or porphyria and sunscreens usually ineffective.

Box 40.7 Drugs commonly causing photosensitivity

Weller R, Hunter J, Savin J, Dahl M. Clinical dermatology. 4th edn. Blackwell Publishing; 2008

Photodermatitis

• Similar appearance to sunburn.

• May appear after contact with plants; phytophotodermatitis—plants containing psoralens; lemons, limes, celery, parsley, parsnips.

• Or sunscreens as a group causing photoallergic contact dermatitis; in foundation, moisturisers, cosmetics.

Other causes of photosensitivity

Drug-induced lupus erythematosus

4 Blistering/shedding of skin

Varicella zoster/herpes zoster

Note: Always suspect herpes in any neonate with a vesiculobullous or eroded weeping eruption.

Clinical features

• Prodrome: with a unilateral ache, soreness, or neuritic shooting pain which may be non-specific.

• Skin changes: early on little or nothing to see, then erythematous or cellulitic presentation or the classic vesiculobullous eruption in a dermatomal distribution.

If shingles/zoster is suspected treat early, especially in a patient at risk. This includes immunocompromised, very young, sick or elderly.

Other important features include dermatomal distribution (head and neck including periorbital and tip of nose (nasociliary branch)) or a severe and prolonged prodrome which heralds a postherpetic neuralgia.

Any signs of disseminated disease, i.e. lesions beyond 3 dermatomes and lesions outside the confines of a dermatome.

Investigations

Diagnosis is clinical; however, confirmation by PCR. Highest yield is from a fresh vesicle by breaking it aseptically with a 19-gauge needle and scraping from the base with a viral culture swab.

Table 40.12 Presentations of blistering/shedding of skin

Management

Valcyclovir or famcyclovir both have excellent oral availability. Low threshold for admission if there is concern about oral intake or absorption. Systemic acyclovir works best if given early in the course of the disease.

Look for an underlying cause if there is dissemination outside the main affected dermatomes.

Staphylococcal scalded skin syndrome (SSSS)

Aetiology

• Staphylococcus toxin-mediated disease

• Adult risk factors: deficits in cell-mediated immunity e.g. HIV, malignancy, malnutrition, renal failure (exfoliative toxins are renally excreted)

Investigations

Biopsy of the lesions is gold standard for the differentiation.

Table 40.13 Clinical features and focus of SSSS

Child	Adult
Clinical features: ‘Miserable’ but not obtunded, skin tender to touch, i.e. child withdraws to touch Cutaneous involvement often begins in the flexural creases, i.e. neck, axillae, inguinal area, knees Most commonly in children < 5 years

Clinical features:

Only seen in a patient who is immunocompromised with significant renal failure and/or overwhelming sepsis.

Focus of infection often difficult to find Focus of infection usually obvious in contradistinction to children

Avoid biopsy in children, but in emergency department a frozen section of the shed skin can differentiate SSSS from SJS/TEN.

Management

Admit both children (important to exclude all the life-threatening differentials) and adults, specialist consultation.

In adults:

• supportive therapy to treat electrolyte imbalance, hypotension and potential multiorgan failure; inciting factor cessation

• cultures—peripheral, central and swabs

• antimicrobial therapy with di-/flucloxacillin 2 g IV q6-hourly, rare reports of MRSA.

Serious cutaneous adverse reaction (SCAR)

SCAR includes Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).

Note: If SJS or TEN is suspected, urgent specialist review is required.

TEN is rare but most severe, and leads to extensive painful full-thickness epidermal skin death with blistering and sheet-like shedding of > 30% of the epidermis.

SJS, which is more common, leads to < 10% full-thickness epidermal death and shedding, and a 5% mortality. SJS-TEN overlap cases shed 10–30% of the epidermis. The more severe the skin changes, the more likely it is drug-induced and the higher the mortality.

Differential between SJS and TEN is difficult to distinguish until the ultimate extent of skin disease is known, usually 7–10 days from onset.

This is potentially life-threatening due to multisystem involvement and skin-barrier breakdown. Epithelial loss predisposes to bacterial and fungal infections, septicaemia and severe fluid loss with electrolyte disturbance. Mortality ranges from 5% in SJS to 30% in TEN. Mucous membranes are usually involved, with erythema and erosions of buccal, genital and ocular mucosa. Severe ophthalmic involvement may lead to permanent scarring and blindness.

Table 40.14 Early clinical features of SCAR

Mucous membrane involvement, especially if
Multiple areas involved Erosive, ulcerative or haemorrhagic Early changes including crusting of the lips

Skin changes that include

Confluent extensive skin involvement

Prominent central facial or head and neck involvement, especially if periorbital puffiness or facial swelling

Dusky purpuric macules ± tenderness

Box 40.8 Causes of SCAR

Infectious: e.g. Mycoplasma pneumoniae, herpes simplex

Common medications responsible for SJS and TEN ⁸:

• sulfonamides

• anticonvulsants (e.g. phenytoin, carbmazepine, phenobarbitone)

• allopurinol

• NSAIDs

Drug-induced commonly, rarely reported post-vaccination, e.g. MMR, exposure to industrial chemicals, post-mycobacterial infections, Chinese herbal remedies, very rarely idiopathic. The pathogenesis is thought to involve an impaired capacity to detoxify intermediate drug metabolites and genetic susceptibility. Drug administration typically precedes the rash by 1–3 weeks.

Investigations

FBC, including differential with eosinophilia, UEC, LFT, CRP, immunofluorescence, skin swabs, blood cultures, UA, chest X-ray.

Management

Note: STOP potentially causal drugs as soon as diagnosis suspected. This saves lives and is especially for longer acting medications, e.g. traditional aromatic anticonvulsants (phenytoin, carbamazepine, phenobarbitone along with lamotrigine).

1. SJS and TEN:

• Admission to a burn unit if necessary.

• Identify and withdraw all possible causative and/or interacting medications (e.g. stop both lamotrigine and sodium valproate when lamotrigine is suspected as causal).

• Also supportive measures which include: intravenous fluid administration, maintenance of electrolyte and temperature homeostasis, enteral feeding, analgesia and ophthalmological assessment in case of ocular involvement.

• In addition emollients, anticipate and treat infection.

• Low threshold to involve clinical pharmacologist and dermatologist early.

2. Skin care consists of proper wound dressings (e.g. hydrocolloid dressings or saline-soaked gauze), oral hygiene (i.e. chlorhexidine rinses), antihistamine and topical corticosteroid therapy for pruritus and antimicrobial therapy in cases of superinfection due to skin-barrier breakdown. Some centres use high doses of IV immunoglobulin and plasmaphoresis.¹⁰

3. Frequent culture of skin, urine, blood and IVC as the major causes of sepsis are Staphylococcus aureus and Pseudomonas aeruginosa. Avoid systemic corticosteroids.

Pemphigus vulgaris

• Clinical features: most have a chronic or subacute presentation. Rare forms present acutely through emergency department with painful blistering of the mucous membrances.

• Differential: other blistering disorders (see Table 40.15).

• Management: acute presentation of any blistering eruption requires admission. Corticosteroids topical and systemic ± other immunosuppressants. Referral to a dermatologist.

Table 40.15 Differential diagnosis⁹

Bullous pemphigoid

• Clinical features: blistering skin disease of the elderly with large tense bullae arising on normal or erythematous skin. Early inflammatory disease presents with urticaria-like lesions. Oral mucosal lesions. Characterised by intense itch.

• Causes: immunobullous disorder of the skin.

• Management: in itself not usually a cause for admission but usually in the elderly with a complication, e.g. ± cellulitis. In isolation it is not an emergency, but rather treat the secondary infection. Specific management is recommended to be individualised and specialist dermatology input is required; stop the antecedent cause if possible, e.g. drug ± corticosteroids.

Grade 4 acute graft versus host disease (AGVHD)

• Clinical features: usually an inpatient. Usually recent bone marrow transplant or recent procedure from overseas. Similar clinical, pathological and immunological features as TEN. See the section ‘Serious cutaneous adverse reaction’; refer to Table 40.15.

• Differential: refer to Table 40.15.

• Management is supportive and requires specialist collaboration.

5 Vasculitis/purpuric vs ischaemic/necrotic skin ± deeper tissues

Table 40.16 Vasculitis/purpuric vs ischaemic/necrotic skin ± deeper tissues

Differential	Clinical scenario
Meningococcaemia	Always consider and if considered always treat
Disseminated intravascular coagulation	Sick, septic patient reflecting underlying illness
Vasculitis (venular or usual leukocytoclastic vasculitis)—unknown, infection, connective tissue disease, malignancy, drug, multifactorial, including Henoch Schönlein purpura	Often multifactorial aetiology; recent illness, sepsis, drug-inducedThe three Ps of small vessel vasculitis: painful palpable purpura
Vasculitis (larger vessel e.g. arterial, e.g. PAN)	Usually systemic disorder, consider infection and drugs
Embolic; septic, cholesterol etc	Background comorbidities e.g. IHD, IVDU, trauma
Heparin and warfarin necrosis	Anticoagulant therapy
Haemorrhagic and bullous cellulitis	Consider deep fungal infections not only in the immunocompromised population but also in the general population
Haemorrhoagic or necrotic infections of deeper ‘soft’ tissue including necrotising fasciitis	General immune and immunosuppressed
Metabolic and intravascular disorders including: calciphylaxis (ischaemic tissue necrosis, ITN)/catastrophic anticardiolipin syndrome (reticulate ‘dusky’ or cyanotic ± painful purpuric changes early on)	Note: Catastrophic anticardiolipin syndrome may have prominent central nervous system symptoms and signs

Meningococcaemia

• Meningococcal.

• Have a very low threshold to treat even if only considered a diagnostic possibility.

• Always promptly treat: a patient with an infective illness, rapid deterioration or representation in a patient with an infective illness.

• Skin changes are classically petechial/purpuric (i.e. do not completely blanch on pressure) but initial very early lesions may fully blanch.

Clinical features

All ages but especially small children and young adults. Approximately 60% of patients present with a characteristic petechial rash on the trunk and lower limbs, but lesions can also occur on head, palms, soles and mucous membranes. Irregular lesions, smudged appearance. Can progress to ecchymoses, bullous haemorrhage. Petechial skin rash is more typical of acute meningococcaemia, can resemble viral exanthema.

The classic presentation of meningococcaemia is the abrupt onset of maculopapular or petechial rash and flu-like symptoms—fever, chills, malaise and disorientation. Over several hours, the disease may rapidly progress to purpura, disseminated intravascular coagulation, shock and death. Potentially fatal outcome.

Spread through respiratory secretions; living in close quarters with infected persons puts people at increased risk. Predisposing factors: preceding upper respiratory tract infection or infection with mycoplasma.

Cause

Neisseria meningitidis, gram-negative diplococcus.

Differential diagnosis

Includes purpuric enterovirus exanthem.

Management

1. Any febrile patient with a petechial rash should be suspected of having meningococcaemia and treated promptly after blood cultures are obtained.

2. Besides supportive management, therapy with a third-generation cephalosporin (e.g., ceftriaxone) or intravenous penicillin G therapy are the treatments of choice.

3. Chloramphenicol may be used for patients allergic to penicillin.

Necrotising fasciitis

Cutaneous findings may not correlate with the extent of the necrosis as it is a spreading infection of the deep fascia, causing necrosis of the subcutaneous tissues.

Treatment is based on clinical suspicion with broad antimicrobial cover.

Clinical features

Rapidly developing infection with erythema, oedema and extreme pain, which may be disproportionate, ± fever. Lesions are typically on the extremities. Often 1–2 day history of disease onset with blue discolouration associated with bullous eruption.

The organisms can be introduced through minor cuts, burns, blunt trauma or surgical procedures.

Type I necrotising fasciitis is caused by mixed anaerobes, gram-negative aerobic bacilli and Enterococci are implicated in type I, and type II is group A Streptococci.

Risk factors include:

• diabetes mellitus

• peripheral vascular disease

• immunosuppression.

Diagnosis

• Clinical predominantly—without prompt treatment, the infection may develop into frank cutaneous gangrene.

• Shock and organ failure may occur—poor prognosis.

• When skin necrosis is not obvious, diagnosis of necrotising fasciitis must be suspected if there are signs of severe sepsis or some of the following local symptoms and signs: severe pain, indurated oedema, skin hyperaesthesia, crepitation, muscle weakness and foul-smelling exudates.¹¹

• Confirmatory imaging may be useful to assist in defining the extent of disease. This includes CT scan to confirm gas in the subcutaneous tissues.

Management

If necrotising fasciitis is suspected, early treatment while working up for surgical debridement is essential. Broad antimicrobial including antistreptococcal cover is required.

COMMON LOWER LEG EMERGENCY PRESENTATIONS—ULCERS/WOUNDS

Cellulitis

Clinical features

Area of skin and subcutaneous tissue which is red, hot, swollen, tender ± blister formation ± skin necrosis. Frequently on the legs but other sites possible. Patient may feel systemically unwell, fevers, rigors ± confusion in the elderly.

Deeper level of infection than erysipelas. Organisms gain entry via minor abrasions, fissures between the toes, leg ulcers portal of entry in many cases. Predisposing factor: oedema of the legs, e.g. cardiac, venous or lymphatic origin. In immunocompetent individuals, usually caused by Streptococcus pyogenes Haemophilus influenzae may be associated in the context of facial cellulitis and otitis media in children.

Management

1. In presumed streptococcal cellulitis, penicillin is treatment of choice, benzylpenicillin IV.

2. Elevation of the affected area and analgesia.

3. Some patients have recurrent episodes of cellulitis, each episode damaging lymphatics and leading to further oedema. Treat with prophylactic penicillin or erythromycin.

Table 40.17 Common lower leg emergency presentations

Presentation	Differential	Comment
Unilateral erythematous legs	Cellulitis; bacterial, fungal, superinfection, e.g. scabies Always consider primary or secondary deep venous thrombosis (DVT)

Bacterial—staphylococcal and streptococcal infections are most common

Others; in immunosuppressed or atypical presentations (e.g. bullous and haemorrhagic), consider deep fungal or atypical mycobacterium (e.g. Cryptococcus neoformans var gattii, Mycobacterium haemophilum)

Bilateral erythematous legs

( Acute venous eczema flare presentations in the elderly are not always classical, e.g. patient may not complain of itch)

Always consider venous ‘stasis’ eczema (most likely underlying condition)

There can be secondary staphyloccocal infection but it is important to treat the eczema

Always consider DVT ? duplex ± prophylaxis and/or treatment

Always consider contact allergy to product ingredients, e.g. in topical dressings, product (OTC and prescribed)

Potent topical steroid ointment (daily—TDS) sparingly, fragrance-free bland moisturiser generously over the top ± wet wraps and elevation and/or compression bandaging if compression stocking not possible (e.g. setapress) if no significant arterial disease

In isolation not a reason for admission, however prompt LMO follow-up ± community nursing ± dermatologist

Other rare causes Prothrombotic, thrombotic or occlusive vascular presentations, e.g. phlegmasia alba and cerulea dolens Major arterial or venous events which require urgent vascular surgical review and appropriate investigation for cause with therapy

Erysipelas

Superficial streptococcal cellulitis with a well demarcated edge. Face is common for erysipelas. Haemophilus influenzae is an important cause of facial cellulitis in children, often associated with ipsilateral otitis media. Immunocompromised patients have a variety of potential bacteria. Often strikes in the same place twice. Recurrent bouts need long-term prophylactic penicillin; consider referral to infectious diseases.

Table 40.18 Common skin infections elsewhere

Disease	Signs/symptoms	Management
Impetigo: superficial skin infection of the epidermis Staphylococcus aureus or Streptococcus pyogenes

Honey-crusted lesions or vesicles, usually in children around nose and mouth, may be bullous or non-bullous

Keflex, mupirocin

Always ensure M/C/S, patient follow-up LMO (if S. pyogenes, requires 10/7 therapy)

Abscess: localised collection of pus, e.g. hidradenitis suppuritiva, venous access; iatrogenic, IVDU Often febrile and neutrophilia, however elderly/diabetic/immunocompromised may not mount a white cell response or fever; low threshold to treat, especially for LL infection With foot infections always consider portal of entry e.g. interdigital tinea, ± peripheral neuropathy

Furuncle: pus collection in 1 hair follicle, often S. aureus

Carbuncle: pus collection involving many hair follicles

Wash bedsheets and clothing in hot water etc

For recurrent episodes of staphylococcal infections with furunculosis, referral to infectious diseases or dermatology is recommended to address predisposing factors

Incision and drainage or first-generation cephalosporin and/or consider at risk for MRSA

Consider risk of NORSA—non-oxacillin resistant S. aureus

Community strain of MRSA—most appropriate antibiotic, clindamycin

Cellulitis: spreading subcutaneous infection usually Staphylococcus or Streptococcus Cardinal signs of inflammation: red, hot, swollen, tender, loss of function Depending on severity and risk, beta-lactam, e.g. di/flucloxicillin or first-generation cephalosporin Erysipelas/lymphangitis Traditionally streptococcal, but always cover Penicillin

Necrotising fasciitis: infection along the fascial planes

Streptococcus pyogenes (group A) or Clostridium perfringens

Pain, fever, ↑ WCC, systemically unwell

Immediate extensive surgical debridement, add penicillin and clindamycin to prevent spread

High mortality without rapid, extensive debridement

Box 40.10 Consider admission in the context of ulcer presentation for patients with the following

Systemic illness e.g. significant fever and constitutional symptoms

Pain including pain disproportionate to clinical presentation; arterial, neutrophilic including Sweet’s syndrome through to pyoderma gangrenosum, serious infective cause (staphylococcal to deep fungal to mycobacterial)

Immunocompromised population (may be multifactorial ulcer; vasculitis, infection ± DVT in an oncology patient)

Rapidly progressing ulcer or involving the distal extremities, especially atypical locations for a chronic arterial, venous or neuropathic ulcer; consider complicating deep tissue infection, tendonitis, fasciitis, compartment syndrome, osteomyelitis

Consider admission and appropriate emergency investigations: FBC, differential, Swab—M/C/S, imaging—plain X-rays and ultrasound

Pyoderma gangrenosum

In any patient presenting with a painful, rapidly progressive inflammatory ulcer always consider pyoderma gangrenosum. (This warrants an urgent dermatological consult as the diagnosis is one of exclusion but it is an inflammatory rather than infective condition requiring relatively heavy immunosuppression.)

Thus, ruling out infection either clinically by a dermatologist and/or concurrently covering major infective possibilities while awaiting dermatology input is essential.

BITES ¹²

• Animal bites are common.

• Mortality from bites is low.

• Morbidity is common, with both dog and cat bites potentially becoming infected with Pasteurella multocida. Consider rabies with bites from bats.

Complications from bites

Dog bite: may be complicated by infections—Staphylococcus, Streptococcus, Eikenella, Pasteurella, Proteus, Klebsiella, Haemophilus, Enterobacter, Bacteroides and Capnocytophaga.

Cat bite: may be complicated by infections—Pasteurella, Actinomyces, Propionibacterium, Bacteroides, Fusobacterium, Clostridium, Wolinella, Peptostreptococcus and Streptococcus species.

Human bite: high risk of infection. Cover the mix of anaerobes and aerobic organisms.

History

Patient tetanus status.

Clinical features

On examination: breech of the skin and foreign bodies. If the bite is deep, examine neurovascular supply, muscle and tendon integrity and injury to any bones.

ITCHING/PRURITUS ¹³

This is a common topic, not really an emergency issue unless in the context of more complicated disease already addressed above.

Pruritus varies in duration, localisation and severity.

Treatment: treat the cause. If no apparent underlying reason can be found, then use soap sparingly, topical steroid, topical emollients, non-sedating antihistamine during the day, sedating antihistamine at night.

Note: Scabies is an important diagnosis not to miss, especially in the context of a patient admitted with another illness (especially infective) and/or patients requiring surgery where staphylococcal infection may complicate.

Box 40.12 Screening for generalised pruritus

Full history and examination—to rule out secondary causes

FBC, LFT, UEC, ESR, iron studies, thyroid function tests (TFTs)

Urine protein

Chest X-ray

Scabies

When to suspect scabies

• Recent onset of an itchy rash (weeks to months)

• Other friends, partners or family members are also itchy

• Itchy pustules on the hands or feet of young children and infants

• Development of an itchy rash after contact with someone diagnosed with scabies

Clinical features

Itching, typically worse at night. Two types of skin lesions in scabies: the burrow and the scabies rash. Burrows are principally on the hands and feet, sides of the fingers and toes, toe-web spaces, wrists and insteps. Burrows on the trunk are more common in the elderly. Male genitalia with burrows and inflammatory papules are pathopneumonic. Rash of scabies is an eruption of tiny inflammatory papules mainly around axillae and umbilicus. It is the allergic reaction to the mites.

Diagnosis

Scabies should be suspected in anyone with an unexplained itch of recent onset (weeks to months). Common in children and young adults, also the elderly. Acquired by close physical contact with another individual.

Definitive by demonstrating mites microscopically via skin scraping. You cannot see the mite without magnification. The mite leaves squiggly burrows in the skin, which are usually less than a centimetre long. These are most commonly found on the hands (particularly between the fingers), wrists and feet. Scrapings from a number of burrows will reveal the mite, eggs or faeces when examined under magnification. Itchy lumps or nodules can occur on the penis and are characteristic of scabies.

Management

All close contacts of a person who has scabies should be treated, to prevent re-infestation and recurrence of the itchy rash. All members of an affected household should be treated, not just those that are itchy, plus anyone else who has been in close physical contact with members of an infested household. In extended families this will include grandparents, uncles, aunts and other relatives who have had significant physical contact with affected people.

Infestations in nursing homes, other institutions and large close-knit communities can be a major logistical challenge to eradicate.

All members of the same house should be treated at the same time.

If the patient is pregnant, or there is a chance of pregnancy, this should be discussed before use of any cream or tablet to treat scabies. Similarly, discuss treatment of babies, young infants and the old and frail, as special precautions may be required.

Permethrin is the treatment of choice in Australia because of its effectiveness and proven safety. Other treatments such as ivermectin (a tablet taken by mouth) may be considered in severe and complicated cases (this can interact with a number of medications which may cause potentially serious adverse effects, especially in older individuals and those with multiple medical conditions such as heart disease, AIDS, breast cancer and stroke).

Important that malathion 0.5% aqueous preparation is favoured because it does not irritate excoriated or eczematised skin; wash off after 24 hours.

Box 40.13 Scabies treatment (print out and give to patient)¹⁴

1. Before going to bed apply 5% permethrin (Quellada or Lyclear) to the whole body from the neck down (infants and adults over the age of 55 years should also treat the head and neck). It takes around 30 mL or grams to cover the average adult. Permethrin is available over the counter at chemists. Make sure the cream is applied to all body parts paying particular attention to the elbows, breasts, groin/genitals, hands and feet (including under the nails). If one burrow is spared then the infestation will persist.

2. The cream should be left on for at least 8 hours before washing. If you wash your hands during this 8-hour period, reapply cream to the hands.

3. Permethrin cream can sting and irritate. This is normal but, if this is severe, wash off the cream and contact your dermatologist to discuss other options.

4. All bed linen and clothes should then be changed and washed (wash with hot water to kill the mite and its eggs). Dry cleaning, ironing, or hot clothes drying are also effective. Any clothing or bedding that cannot be washed should be put aside for 7 days before using (e.g. placed in a plastic bag). The mite and eggs will die during this time.

5. The treatment of all household members (steps 1–4) can be repeated at 7–10 days to maximise chance of eradication of the infestation. This should be discussed with your doctor.

Sullivan J, Commens C. Patient information pages. Australasian College of Dermatologists website. http://www.dermcoll.asn.au/

Common medications

Box 40.14 Appropriate use of topical corticosteroids for emergency department presentations

Potent topical corticosteroid use is appropriate for control of flares, e.g. atopic dermatitis (even in the context of superinfection with Streptococcus/Staphylococcus). Organise follow-up with LMO 5–7 days later for appropriate long-term weaning and maintenance regimen.

BUT avoid corticosteroid use in the setting of viral skin infections such as herpes simplex and herpes zoster. Caution with use in immunosuppressed patients, e.g. diabetes mellitus (DM).

Groin/foot infection, cover both bacterial and fungal. Bacterial therapy is oral therapy; yeast/tinea is topical antifungal such as hydrazole.

Table 40.19 Carrier vehicle: lotion—low potency, cream—mid-potency, ointment—high potency

Potency	Name	Areas of use
Low	1% hydrocortisone TDS (cream combined with moisturiser usually most appropriate)	Face, axillae, genital areas
Moderate	Betamethasone valerate 0.02%	Ointment for dry, chronic and subacute eczematous presentations Cream for where itch is the main issue rather than dry scaly eczematous skin

High, group II/IV

Mometasone furoate (Elocon, Novasone) ointment vs cream

Methylprednisolone aceponate (Advantan) lotion, cream, ointment and fatty ointment

Triamcinolone (Kenalog)

Appropriate for most emergency presentations of acute/severe eczema or contact dermatitis

Use cream, moisturiser and wet compressors for weeping dermatitis and ointment plus emollient for more dry eczematous presentations (daily up to TDS)

WOUND AND ULCER CARE IN EMERGENCY

Ulcers on lower legs are slower to heal than other body sites and in particular benefit from efforts to address underlying factors to optimise conditions for healing. See Table 40.20 for the causes of leg ulcers. In some patients they are multifactorial in their causation.

Table 40.20 Ulcers—causes and clinical findings

Investigations (emergency)

• Swabs—for microscopy, culture and sensitivity

• Biopsy—(on ward) consider if vasculitis, neoplasia and/or atypical infection are suspected

Management of leg ulcers/wounds

This should involve:

1. correcting or addressing underlying causes such as venous hypertension (leg elevation when resting, compression stockings/bandaging etc)

2. the treatment of complications or complicating factors such as clinical infection

3. wound care

4. appropriate follow up.

Table 40.21 Treatment of leg ulcers/wounds

Treat	Example	Comment
Correct or address underlying cause	Venous hypertension	Compression mainstay of treatment
Infection vs colonised ulcers	Treat if clinically infection, e.g. surrounding skin inflammation and/or fever	In pressure ulcers, treat infection vigorously Avoid treating colonising bacteria Streptococcus pyogenes should be treated