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Flashcards in Acute & Emergency Dermatology Deck (39)
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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

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

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
4
Q

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

A

Vancomycin

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
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
7
Q

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

A

Loss of epidermis on top of dermis (erosions)

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%
9
Q

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

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

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

12
Q

How is the severity of SJS/TEN determined?

A

SCORTEN

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
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%
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
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
Q

What is pemphigoid?

A
  • Antibodies directed at dermo-epidermal junction
  • Intact epidermis forms roof of blister
  • Blisters are usually tense and intact
26
Q

What are the differences between pemphigus and pemphigoid?

A

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
Q

What are the features of erythrodermic psoriasis and pustular psoriasis?

A
  • 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
Q

What is used to treat erythrodermic psoriasis and pustular psoriasis?

A

Systemic therapy

29
Q

What are the clinical features of eczema herpeticum?

A

Monomorphic blisters (all look similar) and “punched out” erosions

Generally painful, not itchy
Fever and lethargy

30
Q

What is the treatment of eczema herpeticum?

A

Aciclovir

  • Mild topical steroid if required
  • Treat secondary infection
  • Ophthalmology input if peri-ocular disease
  • In adults consider underlying immunocompromise
31
Q

When can eczema herpeticum occur?

A

Disseminated herpes virus infection on a background of poorly controlled eczema

32
Q

How does Staphylococcal Scalded Skin Syndrome occur?

A
  • Common in children, can occur in immunocommpromised adults

* Initial Staph. infection

33
Q

What are the features of Staphylococcal Scalded Skin Syndrome occur?

A
  • 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
Q

What is the treatment of Staphylococcal Scalded Skin Syndrome occur?

A
  • IV antibiotics initially and supportive care

* Generally resolves over 5-7 days with treatment

35
Q

What are the 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)

Angioedema
• Deeper swelling of the skin or mucous membranes

36
Q

What are causes of acute urticaria (<6 week)?

A
  • Idiopathic
  • Infection
  • Drugs
  • Food (food allergy) - 1%
37
Q

What is the treatment of acute urticaria (<6 week)?

A
  • Oral antihistamine
  • Short course of oral steroid
  • Avoid opiates and NSAIDs (exacerbate urticaria)
38
Q

What are causes of chronic urticaria (> 6 week history)?

A
  • Autoimmune/idiopathic
  • Physical
  • Vasculitic
39
Q

What is used to treat chronic urticaria?

A
  1. Non-sedating H1 antihistamine
  2. Anti-leukotriene or angioedema
  3. Omalizumab