Acute and emergency dermatology Flashcards

Dermatology emergencies, oh no! what do we do?! in this we will find out

1
Q

What are the consequences of skin failure?

A
• Sepsis
• Hypo- and Hyperthermia
• Protein and fluid loss
• Renal impairment
• Peripheral vasodilation
	○ Can occasionally lead to cardiac failure
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2
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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3
Q

What are the causes of erythroderma?

A
  • Psoriasis
  • Eczema
  • Drugs
  • Cutaneous Lymphoma
  • Hereditary disorders
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4
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 (want avoid any low albumin)
  • Temperature regulation
  • Emollients – 50:50 Liquid Paraffin : White Soft Paraffin
  • Oral and eye care
  • Anticipate and treat infection
  • Manage itch
  • Disease specific therapy; treat underlying cause
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5
Q

Explain Steven Johnson syndrome/ toxic epidermal necrolysis

A
  • 2 conditions which are thought to form part of the same spectrum
  • Rare
    • 1-2/million/year (SJS)
    • 0.4-1.2/million/year (TEN)
  • Secondary to drugs
    • Antibiotics
    • Anticonvulsants
    • Allopurinol
    • NSAIDs
  • Can be delayed onset
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6
Q

What are the clinical features of Steven Johnson syndrome?

A
  • Fever, malaise, arthralgia
  • Rash
    • Maculopapular, target lesions, blisters
    • Erosions covering <10% of skin surface
  • Mouth ulceration
    • Greyish white membrane
    • Hemorrhagic crusting
  • Ulceration of other mucous membranes
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7
Q

What are the clinical features of toxic epidermal necrolysis?

A
  • Often presents with prodromal febrile illness
  • Ulceration of mucous membranes
  • Rash
    • May start as macular, purpuric or blistering
    • Rapidly becomes confluent
    • Sloughing off of large areas of epidermis – ‘desquamation’ > 30% BSA
      * Nikolsky’s sign may be positive
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8
Q

What is the management of SJS and TEN?

A
  • Identify and stop culprit drug as soon as possible
  • Supportive therapy
- Don't know how effective but...
?High dose steroids
?IV immunoglobulins
?Anti-TNF therapy
?Ciclosporin
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9
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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10
Q

What is the aetiology of drug reaction with eosinophilia and systemic symptoms (DRESS)?

A
  • Incidence estimated between 1 in 1000-10,000

- Mortality up to 10%

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11
Q

What are the clinical signs 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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12
Q

What is the management of DRESS?

A
  • Stop causative drug
  • Symptomatic and supportive
  • Systemic steroids (usually oral prednisolone)
  • +/- Immunosuppression or immunoglobulins
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13
Q

What are the clinical features of pemphigus?

A
  • Antibodies targeted at desmosomes
  • Skin: flaccid blisters, rupture very easily
  • Intact blisters may not be seen
  • Common sites: face, axillae, groins
  • Nikolsky’s sign may be +ve
  • Commonly affects mucous membranes
  • Ill defined erosions in mouth
  • Can also affect eyes, nose and genital areas
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14
Q

Explain pemphygoid

A
  • Antibodies directed at dermo-epidermal junction
  • Intact epidermis forms roof of blister
  • Blisters are usually tense and intact
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15
Q

What’s the difference between pemphigus and pemphigoid?

A

Pemphigus

  • Uncommon
  • Middle aged patients
  • Blisters very fragile (may not be seen intact)
  • Mucous membranes usually affected
  • Patients may be very unwell if extensive
  • Treatment: systemic steroids, dress erosions, supportive therapies

Pemphigoid

  • Common
  • Elderly patients
  • Blisters often intact and tense
  • Even if extensive, patients are fairly well systemically
  • Topical steroids may be sufficient if localised; systemic usually required if diffuse
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16
Q

Explain Erythrodermic psoriasis and Pustular Psoriasis

A
  • Can occur without previous history of psoriasis
  • Common causes:
    • Infection
    • Sudden withdrawal of oral steroids or potent topical steroid
  • Rapid development of generalised erythema, +/- clusters of pustules
  • Fever, elevated WCC
  • Exclude underlying infection, bland emollient, avoid steroids
  • Often require initiation of systemic therapy
17
Q

Explain eczema herpeticum

A
  • Disseminated herpes virus infection on a background of poorly controlled eczema
  • Monomorphic blisters and “punched out” erosions
    • Generally painful, not itchy
  • Fever and lethargy
  • Treatment dose Aciclovir
  • Mild topical steroid if required to treat eczema
  • Treat secondary infection
  • Ophthalmology input if peri-ocular disease
  • In adults consider underlying immunocompromise
18
Q

Explain staphylococcal scalded skin syndrome

A
  • Common in children, can occur in immunocompromised adults
  • Initial Staph. infection
    • May be subclinical
  • Diffuse erythematous rash with skin tenderness
  • More prominent in flexures
  • Blistering and desquamation follows
    • Staphylococcus produces toxin which targets Desmoglein 1
  • Fever and irritability
  • Require admission for IV antibiotics initially and supportive care
  • Generally resolves over 5-7 days with treatment
19
Q

Explain urticaria

A
  • aka Weal or Hive:
    • Central swelling of variable size, surrounded by erythema. Dermal oedema
    • itching, sometimes burning
      ~ Histamine release into dermis
      * fleeting nature, duration: 1- 24 hours
  • Angioedema
    • Deeper swelling of the skin or mucous membranes
20
Q

What is the etiology of acute urticaria

A
  • Idiopathic
  • Infection, usually viral
  • DRugs, IgE mediated
  • Food, IgE mediated
21
Q

What is the management of acute urticaria?

A
  • Oral antihistamine
    • Taken continuously
    • Up to 4 x dose
  • Short course of oral steroid may be of benefit if clear cause and this is removed
  • Avoid opiates and NSAIDs if possible (exacerbate urticaria)
22
Q

What is the etiology of chronic urticaria?

A
  • Autoimmune/ idiopathic
  • Physical
  • Vasculitic
  • Rarely a type 1 hypersensitivity reaction