BLISTERING RASHES
Herpes
simplex /
zoster
Eczema
herpeticum
Folliculitis
Impetigo
Erythema
multiforme
Which
becomes….
OE: crops of painful vesicles; if haemorrhagic / multiple dermatomes - ?underlying immunosupp
Ix: Tsanck smear of vesicular fluid
Mng: acyclovir 200mg 5x/day for 5/7 (400mg 5x/day for 10/7 if zoster and within 72hrs onset)  improves rate
of healing, virus shedding, resolution of pain; steroids help post-herpetic neuralgia if commenced early; admit
and IV if immunocomp; capsacian cream helps post-herpetic neuralgia; ABx if established 2Y infection
1Y herpes with active dermatitis; usually in young infants or 20-40yrs; disseminated if immunocomp (10%
mortality)
OE: scaly grouped vesicular rash and umbilicated papules of sudden onset  may ulcerate; esp upper body;
tender, less itch; fever and malaise; bacterial superinfection common; risk of MOF
Ix: Tzanck smear of vesicular fluid
Mng: high dose IV acyclovir; ICU if disseminated; ABx if 2Y infection
Caused by staph aureus, pityrosporum
OE: 1-5mm yellow grey papules / pustules with surrounding erythema; maybe itchy or tender
Mng: topical antiseptics; topical fusidic acid if resistant; ABx if severe
Staph  bullous; staph / grp A strep  non-bullous with surrounding erythema and lymphadenopathy
OE: honey coloured crusts on face, elbow, knees
Mng: PO ABx (improve healing, prevent GN); 15mg/kg fluclox QID PO in children; cephalexin alternative; 15%
staph resistant to erythromycin; soak crusts in chlorhexidine; mupirocin top
Epidemiology: M>F; young>old
Cause: 50% infections (due to HS reaction to herpes simplex, mycoplasma)
drugs HS reaction to penicillin, ceph, sulphonamides
phenytoin, carbamazepine, lamotrigine
allopurinol, NSAIDs, immunization
no cause found in 50%
Ca
OE: malaise and fever, arthralgia, pruritis, burning sensation few days  macules, papules, wheals, urticarial,
blisters, vesicles, bullae,
SJS
Which
becomes….
TEN
target lesions (diagnostic); more distal distribution in mild; maybe MM
involvement (EM minor = no MM involved, EM major
Mng: none if mild; pred otherwise; usually resolves over 7-10/7
Cause: drugs most common cause; mortality 10-15%
OE: >1
= 1 MM involved)
MM involved; epidermal detachment involves <10% BSA; Nikolsky +ive
Mng: saline packs / mouth wash for MM; top 0.5% betamethasone cream;
resolves over 3-6/52; steroids not indicated
burns care; admit if severe;
Epidemiology: F>M; old>young; risk of staph and pseudomonas superinfection; 25-35% mortality
Cause: drugs (90%): sulphonamides
phenytoin
allopurinol; dapsone, omeprazole, immunisation
HIV, immunosupp, lymphoma, leukaemia
OE: prodromal illness  full thickness epidermal necrosis  painful tender erythroderma  widespread
erythema and blistering, bullae which rapidly desquamate; MM’s often involved including eyes; epidermal
detachment of >30% BSA, Nikolsky +ive
TSS
Ix: abnormal LFT’s 50%; abnormal GTT; biopsy
Mng: IVIG; cyclosporine; burns unit; ?anti-TNF drugs; pred not indicated
Cause: colonization with toxin-producing Staph aureus and grp A strep pyogenes; tampon use, burns,
cellulitis, sinusitis, wounds
OE:
TOXIC:
fever >38.9
SHOCK:
SBP <90 or >15 orthostatic postural drop DBP
SYNDROME: Rash - fine punctate macular non-pruritic blanching erythroderma with rough texture,
Petechiae; painless; fades within 3/7
Desquamation - after 5-14/7
Involvement of 3+ body systems: shock, MOF, CNS probs, vaginitis,
SSSS
pharyngitis, conjunctivitis, GI, muscular, renal, hepatic, haem
Epidemiology: most common in infants; also in older patients with renal failure
Cause: staph aureus  epidermolytic toxin
OE: tender erythroderma, scarlatiniform rash  exfoliation beginning on D2  desquamation on D3-5 (bullae,
sloughing); no MM involvement; less severe than TEN; Nikolsky +ive
Mng: fluclox 2g (50mg/kg) Q6h; pred not indicated
Cause: drugs, allergen, Ca
OE: non-tender erythema; skin flaking and scaling; exfoliation; pruritis
Cause: type IV HS reaction to plants, rubber, nickel, chrome, colostomy adhesives
OE: 48hr delay between contact and rash; itchy; erythema; may be vesicular / bullous
Mng: wet dressing; steroids
Epidemiology: more common than pemphigus; mostly in elderly / gestational
Cause: anti-desmoglein 3 ab’s
OE: onset days-wks; blisters on erythematous skin (starts as urticaria); tense roof; don’t expand / rupture on p;
itchy; MM rarely involved
Mng: pred 0.5mg/kg OD PO, or potent top steroids; azathioprine if steroid resistant
Cause: ab to ketatinocyte adhesion molecules; penicillamine, ACEi, B cell lymphoma
OE: intraepidermal bullae; initially tense  flaccid, easily ruptured  erosions; MM often involved; Nikolsky
+ive; vulgaris (most common; age 40-50yrs; chronic and progressive), foliaceus (not on MM, superficial)
Ix: biopsy; epidermal adhesion molecule ab’s 90% sens
Mng: steroids; azathioprine / cyclophosphamide if ineffective; maybe gold, plasmapheresis, intragam
Exfoliative
erythroderma
Allergic
contact
dermatitis
Pemphigoid
Pemphigus
. The answer is C (Chapter 246). The patient has a
bullous disease mainly involving the mouth. The
differential diagnosis includes pemphigus
vulgaris, bullous pemphigoid, and toxic
epidermal necrolysis. An HSV-1 infection would
be vesicular and is more common in children than
adults. The patient does not have gingivitis and
does not need chlorhexadine rinses or a dental
referral. Follow up is required with a
dermatologist for a skin biopsy with
immunofluorescence. Pemphigus vulgaris is a rare
but serious autoimmune, mucocutaneous blistering
disease. Men are affected more than women. Age
of onset is 40-60 years. Over 50% of patients
have oral lesions that precede cutaneous
blisters. Nikolsky's sign is positivethe
flaccid blister spreads with light lateral
pressure. Skin biopsy with direct
immunofluorescence is diagnostic. Serum
autoantibodies to a skin glycoprotein may be
detected by indirect immunofluorescence.
Patients are treated with high-dose systemic
corticosteroids
.
.
.
.
.
after dermatologic consultation. The
average age of onset of bullous pemphigoid is
70 years. The blisters are tense. Oral and
cutaneous lesions tend to occur
simultaneously. Skin biopsy with
immunofluorescence is diagnostic. Serum antibasement membrane autoantibodies may be
detected by indirect immunofluorescence.
Treatment involves systemic
corticosteroids. Patients with either condition
can
.
.
.
present with dehydration due to decreased
oral intake and significant fluid and
electrolyte loss due to the bullae
formation. Dermatologic consultation is advised.