Acute & Emergency Dermatology Flashcards

1
Q

Name consequences cause by the failure of skin functions

A

• Mechanical barrier to infection -> sepsis
• Temperature regulation -> hypo and hyperthermia
• Fluid and electrolyte balance ->
1. Protein and fluid loss
2. Renal impairment and vasodilation

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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

Usually effects older people

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3
Q

What are different causes of erythroderma?

A
  • Psoriasis
  • Eczema
  • Drugs
  • Cutaneous Lymphoma
  • Hereditary disorders (presents as neonates with genetic defect in skin formation)
  • Unknown
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4
Q

What is a drug that causes erythroderma “red man syndrome”?

A

Vancomycin

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5
Q

What are the principles of management for erythronderms?

A
  • Remove any offending drugs
  • Careful fluid balance (don’t want to push into cardiac failure)
  • Good nutrition (loss of protein)
  • Temperature regulation (minimise fluid loss)
  • Emollients - 50:50 liquid paraffin:White soft paraffin (acts as an artificial barrier)
  • Anticipate and treat infection
  • Oral and eye care
  • Disease specific therapy; treat underlying cause
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6
Q

Describe drug reactions

A
  • Can occurs to any drug
  • Commonly 1-2 weeks after drug
  • Mild: morbilliform exanthem
  • Severe: erythroderma, Stevens Johnson Syndrome/Toxic epidermal necrolysis, DRESS
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7
Q

What occurs in Stevens Johnson Syndrome (SJS) and Toxic Epidermal necrolysis (TEN)?

A

Loss of epidermis on top of dermis (erosions)

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8
Q

What differentiates Stevens Johnson Syndrome (SJS) and Toxic Epidermal necrolysis (TEN)?

A

Severity of the two conditions

  • If surface of epidermal detachment < 30% –> SJS
  • Overlap 20-30%
  • TEN -> 30%
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9
Q

What drugs can cause Stevens Johnson Syndrome (SJS) and Toxic Epidermal necrolysis (TEN)?

A
  • Antibiotics
  • Anticonvulsants
  • Allopurinol (used for gout)
  • NSAIDs
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10
Q

What are the clinical features of SJS?

A

• Fever, malaise, arthralgia
• Rash
- Maculopapular, target lesions (dusky centre with red outline), blisters
- Erosions covering <10% of skin surface
• Mouth ulceration
- Greyish white membrane
- Haemorrhagic crusting
• Ulceration of other mucous membranes

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11
Q

What are the clinical features of Toxic Epidermal Necrolysis (TEN)?

A

• Profromal febrile illness
• Ulceration of mucous membranes
• Rash
- Macular, purpuric (small vessel bleed) or blistering
- Sloughing off of large areas of epidermis > 30%
- Nikolsky’s sign - removal of epidermis when rubbed

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12
Q

How is the severity of SJS/TEN determined?

A

SCORTEN

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13
Q

Describe SCORTEN

A
One point given for each positive:
• Age >40
• Malignancy
• Heart rate >120
• Initial epidermal detachment >10%
• Serum urea >10
• Serum glucose >14
• Serum bicarbonate <20
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14
Q

Using the SCORTEN score, how is prognosis determined?

A
0-1 - > 3.2%
2 - 12.1%
3 - 35.3%
4 - 58.3%
> 5 - > 90%
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15
Q

What are the long term complications of SJS/TEN?

A
  • Pigmentary skin changes (as melanocytes found in epidermis)
  • Scarring
  • Eye disease and blindness
  • Nail and hair loss
  • Joint contactures
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16
Q

What is the management for SJS/TEN?

A
  • Identify and stop causative drugs asap

* Supportive therapy

17
Q

What is erythema multiforme?

A

Hypersensitivty reaction usually triggered by infection

Usually by a virus (herpes) and this is how it is differentiated from TEN

18
Q

What occurs in erythema multiforme?

A

Abrupt onset of up to 100s of lesions over 24 hours
• Distal -> proximal
• Palms and soles
• Mucosal surfaces (EM major)
• Evolve over 72 hours - pink macule, become elevated and may blister

19
Q

What is the treatment of erythema multiforme?

A
  • Self living and resolves over 2 weeks

* Symptomatic and treat underlying cause

20
Q

What occurs in DRESS?

A
• Onset 2-8 weeks after drug exposure
• Fever and widespread rash
• Eosinophilia and deranged liver function
• Lymphadenopathy
\+/- other organ involvement
21
Q

What is the treatment of DRESS?

A
  • Stop causative drug
  • Symptomatic and supportive
  • Systemic steroid
  • +/- immunosuppression or immunoglobulins
22
Q

What is pemphigus?

A
  • Antibodies targeted at desmosomes (between keratinocytes, causing separation)
  • Skin – flaccid blisters, rupture very easily
  • Intact blisters may not be seen
  • Common sites – face, axillae, groins
  • Nikolsky’s sign may be +ve
23
Q

What are the clinical features of pemphigus?

A
  • Commonly affects mucous membranes
  • Ill defined erosions in mouth
  • Can also affect eyes, nose and genital areas
24
Q

Describe the pathology of pemphigus

A

Take biopsy
• Immunoflourescence - stain with antibodies, which shows attachment of antigen to keratinocytes
• Histopathology - shows detachment between keratinocytes

25
What is pemphigoid?
* Antibodies directed at dermo-epidermal junction * Intact epidermis forms roof of blister * Blisters are usually tense and intact
26
What are the differences between pemphigus and pemphigoid?
Pemphigus: • Middle age • Blisters fragile - may not be seen intact • Treat with systemic steroid, dress erosions and support Pemphigoid: • Elderly • Blisters often intact and tense • Topical steroid if localised; systemic required if diffuse
27
What are the features of erythrodermic psoriasis and pustular psoriasis?
* Can occur without history of psoriasis * Common causes: infection, sudden withdrawal of steroids * Rapid development of generalised erythema +/- clusters of pustules * Fever, elevated WCC
28
What is used to treat erythrodermic psoriasis and pustular psoriasis?
Systemic therapy
29
What are the clinical features of eczema herpeticum?
Monomorphic blisters (all look similar) and “punched out” erosions Generally painful, not itchy Fever and lethargy
30
What is the treatment of eczema herpeticum?
Aciclovir * Mild topical steroid if required * Treat secondary infection * Ophthalmology input if peri-ocular disease * In adults consider underlying immunocompromise
31
When can eczema herpeticum occur?
Disseminated herpes virus infection on a background of poorly controlled eczema
32
How does Staphylococcal Scalded Skin Syndrome occur?
* Common in children, can occur in immunocommpromised adults | * Initial Staph. infection
33
What are the features of Staphylococcal Scalded Skin Syndrome occur?
* Diffuse erythematous rash with skin tenderness * More prominent in flexures * Blistering and desquamation follows - staphylococcus produces toxin which targets Desmoglein 1 * Fever and irritability
34
What is the treatment of Staphylococcal Scalded Skin Syndrome occur?
* IV antibiotics initially and supportive care | * Generally resolves over 5-7 days with treatment
35
What are the features of urticaria?
Weal, wheal or hive: • Central swelling of variable size, surrounded by erythema. • Dermal oedema • Itching, sometimes burning (histamine release into dermis) Angioedema • Deeper swelling of the skin or mucous membranes
36
What are causes of acute urticaria (<6 week)?
* Idiopathic * Infection * Drugs * Food (food allergy) - 1%
37
What is the treatment of acute urticaria (<6 week)?
* Oral antihistamine * Short course of oral steroid * Avoid opiates and NSAIDs (exacerbate urticaria)
38
What are causes of chronic urticaria (> 6 week history)?
* Autoimmune/idiopathic * Physical * Vasculitic
39
What is used to treat chronic urticaria?
1. Non-sedating H1 antihistamine 2. Anti-leukotriene or angioedema 3. Omalizumab