Acute and Emergency Dermatology Flashcards

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1
Q

What is Erythroderma?

A
  • A descriptive term rather than a diagnosis

- “Any inflammatory skin disease affecting >90% of total skin surface”

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2
Q

What are the different causes of Erythroderma?

A
  • Psoriasis
  • Eczema
  • Drugs
  • Cutaneous Lymphoma
  • Hereditary disorders
  • Unknown
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3
Q

What are the principles of management of Erythroderma?

A
  • Appropriate setting: ?ITU or Burns unit
  • Remove any offending drugs
  • Careful fluid balance
  • Good nutrition
  • Temperature regulation
  • Emollients (50:50 liquid paraffin:white soft paraffin)
  • Oral and eye care
  • Anticipate and treat infection
  • > low-threshold for treatment of infection
  • Manage itch
  • Disease-specific therapy
  • > treat underlying cause
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4
Q

What are the different clinical presentations of drug reactions?

A

Mild:
- Morbilliform Exanthem

Severe:
- Erythroderma

  • Stevens-Johnson Syndrome (SJS)/Toxic Epidermal Necrolysis (TEN)
  • Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
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5
Q

Which drugs are most likely to cause drug reactions?

A
  • Abx.
  • Anti-convulsants (aka. anti-epileptics)
  • Allopurinol
  • NSAIDs
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6
Q

What are the clinical features of SJS?

A
  • Fever, malaise, arthralgia
  • Rash:
  • > maculopapular, target lesions, blisters
  • > erosions covering <10% of skin surface
  • Mouth ulceration:
  • > greyish-white membrane
  • > haemorrhagic crusting
  • Ulceration of other mucous membranes
  • > (ie. eyes, nose, genitals)
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7
Q

What are the clinical features of TEN?

A
  • Often presents with prodromal febrile illness
  • Ulceration of mucous membranes
  • Rash:
  • > macular, purpuric, blistering
  • > rapidly becomes confluent
  • > sloughing off large areas of epidermis: “desquamation” >30% BSA
  • > Nikolsky’s sign +ve
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8
Q

What is the management of SJS and TEN?

A
  • Identify and stop culprit drug ASAP

- Supportive Therapy
?possible ITU for TEN-end of the spectrum

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9
Q

What is SCORTEN?

A
  • Predictor of mortality for pts presenting with TEN
  • > 0-1 = >3.2%
  • > 5 or more = >90% mortality
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10
Q

What are the long-term complications of SJS and TEN?

A
  • Pigmentary skin changes
  • Scarring
  • Eye disease and blindness
  • Nail and hair loss
  • Joint contractures
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11
Q

What is Erythema Multiforme?

A
  • HS reaction usually triggered by infection

- Most commonly HSV

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12
Q

What are the clinical features of Erythema Multiforme?

A
  • Abrupt onset of up to 100s of lesions over 24hrs
  • Palms and soles
  • Mucosal surfaces

Evolve over 72hrs:

  • > Pink macules, become elevated and may blister in the centre
  • > “Target” lesions
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13
Q

What are the clinical features of DRESS?

A
  • Onset 2-8 weeks after drug exposure
  • Fever and widespread rash
  • Eosinophilia and deranged liver function
  • Lymphadenopathy
  • +/- other organ involvement
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14
Q

What is the management of DRESS?

A
  • Stop causative drug
  • Symptomatic and supportive
  • Systemic steroids
  • +/- immunosuppression or immunoglobulins
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15
Q

What is the pathophysiology of Pemphigoid?

A
  • Abs directed at dermo-epidermal junction (DEEP)
  • Intact epidermis forms the roof of the blister
  • Blisters are usually tense and intact (bullae, vesicles)
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16
Q

What is the pathophysiology of Pemphigus?

A
  • Antibodies targeted at desmosomes (erosions)

SUPERFICIAL

17
Q

What are the clinical features of Pemphigus?

A
  • Uncommon
  • Middle-aged pts
  • V fragile blisters - may not be seen intact
  • usually affects mucous membranes
  • Pts may be v unwell if extensive
18
Q

How is diagnosis of Pemphigus + Pemphigoid made?

A

Immunofluorescence biopsy

19
Q

What is the treatment of Pemphigus?

A
  • Systemic steroids
  • Dress erosions
  • Supportive therapies
20
Q

What are the clinical features of Pemphigoid?

A
  • Common
  • Elderly pts.
  • Blisters often intact, tense
  • Even if extensive, pts are fairly well systemically
21
Q

What is the treatment of Pemphigoid?

A
  • Topical steroids (if localised)

- Systemic steroids (if diffuse)

22
Q

What are the causes of Erythrodermic and Pustular Psoriasis?

A
  • Can occur w/o a prev. history of Psoriasis
  • Infection
  • Sudden withdrawal or oral or potent topical steroids
23
Q

What are the clinical features of Erythrodermic and Pustular Psoriasis?

A
  • Rapid development of generalised Erythema, +/- clusters of pustules
  • Fever, elevated WCC
24
Q

What is the treatment of Erythrodermic and Pustular Psoriasis?

A
  • Exclude underlying infection, bland emollient, avoid steroids
  • Often requires initiation of systemic therapy
  • > (psoriasis therapy ie. immunosuppressant, sometimes biologic therapy)
25
Q

What is Eczema Herpeticum?

A

Disseminated Herpes Virus infection on a background of poorly controlled Eczema

26
Q

What are the clinical features of Eczema Herpeticum?

A
  • Monomorphic blisters and “punched out” erosions (quite a lot if them!)
  • > generally painful, not itchy
  • Fever and Lethargy
27
Q

What is the management of Eczema Herpeticum?

A
  • Aciclovir
  • Mild topical steroid (for eczema)
  • Treat secondary infection
  • Ophthalmology input if peri-ocular disease
  • In adults: consider underlying immunocompromisation
28
Q

What is the pathophysiology of Saphylococcal Scalded Skin syndrome?

A
  • Initial Staph. infection

- Produces a toxin which targets Desmoglein 1 (causes the cells to peel apart)

29
Q

What are the clinical features of Staphylococcal Scalded Skin syndrome?

A
  • Common in children, can also occur in immunocompromised adults
  • Diffuse erythematous rash with skin tenderness
  • More prominent in flexures
  • Blistering and desquamation follows
  • Fever and irritability
30
Q

What is the management of Staphylococcal Scalded Skin syndrome?

A
  • Requires admission for IV abx initially and supportive care
  • Generally resolves over 5-7 days with treatment
31
Q

What are the clinical features of Urticaria?

A
  • Weal, Wheal or Hive:
  • > central swelling of variable size, surrounded by erythema - dermal oedema
  • > itching, sometimes burning (histamine release into dermis)
  • > fleeting nature, duration: 1-24hrs
  • Angioedema:
  • > deeper swelling of the skin or mucous membranes
32
Q

What causes Acute Urticaria?

A
  • <6 week history*
  • Idiopathic (majority)
  • Infection (viral)
  • Drugs (IgE mediated)
  • Food (IgE mediated)
33
Q

What is the treatment of Acute Urticaria?

A
  • <6 week history*
  • oral anti-histamine
  • if severe: oral steroids
  • avoid opiates and NSAIDs if possible (exacerbate urticaria)
34
Q

What causes Chronic Urticaria?

A
  • > 6 week history*
  • Autoimmune/Idiopathic (majority)
  • Physical
  • > (ie. cold (ice cube on skin), friction, heat, drawing on yourself)
  • Vasculitic
  • Rarely Type 1 HS reaction!!*
35
Q

What is first-line treatment for Acute Urticaria?

A
  • > 6 week history*
  • oral anti-histamine
  • no place for oral steroids*