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N&SS - Dermatology > Dermergencies > Flashcards

Dermergencies Flashcards

1
Q

What are the emergencies that we encounter in dermatology?

A 
Cutaneous drug reactions
Erythroderma
Urticaria
Autoimmune bullous disease
Eczema herpeticum
Herpes zoster
Generalised pustular psoriasis
Toxic epidermal necrolysis
Necrotising fasciitis
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2
Q

How do nearly 50% of cutaneous drug reactions manifest?

A

Maculopapular erythema

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3
Q

How should a drug reaction manifesting in a maculopapular erythematous rash be managed?

A

ABCDE if serious reaction
Stop the drug -> rash should resolve within 2 weeks of stopping.
Symptomatic management (e.g. antihistamines)

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4
Q

How do roughly 25% of all drug reactions manifest?

A

Urticaria and angioedema

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5
Q

Why is a drug reaction causing urticaria and angioedema an emergency?

A

Angioedema may involve mucous membranes and can be associated with anaphylaxis.

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6
Q

What are some of the common drugs that cause urticaria/angioedema in sensitive individuals?

A

Aspirin
Morphine
Codeine
Penicillins

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7
Q

What kinds of drugs can cause photosensitive drug eruptions and what is the pattern of reaction?

A

Rxn limited to sites exposed to sunlight.

Chlorpromazine
Sulphanilamide
Amiodarone
Tetracyclines
Griseofulvin
Naproxen
High dose frusemide
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8
Q

What is toxic epidermal necrolysis?

A

Immunological mucocutaneous reaction provoked by drug hypersensitivity - acute onset, and potentially life threatening

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9
Q

What is erythema multiforme, and when is it known as Steven’s Johnson syndrome?

A

Rash that is associated with 10% of all drug reactions charactrerised by sudden onset erythematous lesions affecting the skin and mucous membranes classically with target appearance affecting peripheral parts of the body.
Known as SJS when there is fever, malaise, and sore throat associated with it.

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10
Q

How is erythema multiforme/Steven’s Johnson syndrome managed?

A

ABCDE
Stop the drug causing the rash.
Get a specialist involved.
Give steroids (prednisolone 30mg/day)

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11
Q

When do cutaneous drug reactions tend to manifest?

A

1-2 weeks following initiation of therapy.

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12
Q

Which route of access of drugs is more likely to cause anaphylaxis?

A

IV

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13
Q

Which particular condition’s management has a strong association with cutaneous drug reactions?

A

HIV

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14
Q

What is erythroderma, and why is it a dermatological emergency?

A

Generalised (over 90% of skin surface involved) erythema associated with exfoliation. Acute erythroderma is more likely to present as an emergency as it signals skin failure (loss of temperature control, dehydration, protein loss and oedema, infection etc.).

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15
Q

What condition is erythroderma most commonly caused by?

A

Psoriasis

Also eczema and drug reactions.

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16
Q

How does erythroderma present?

A

Whole skin is hot and red, with oss of the features of psoriasis (scale is finer and flakier). Pain and itching are common and usually severe.
Patient is also systemically unwell.

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17
Q

How should erythroderma be managed?

A

ABCDE initially!

Then bed rest in warm room, emollients and cool wet dressings, management of underlying cause/complications, and nutritional support.

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18
Q

What are the differentials for erythroderma?

A
  1. Eczema
  2. Lymphoma
  3. Drug eruption
    Other funky derm stuff
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19
Q

What bloods do ou want to order for someone with suspected erythroderma?

A 
Look for complications:
FBCs
U and Es
LFTs
Inflammatory markers
Blood culture
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20
Q

What can precipitate erythroderma in a patient who has psoriasis or eczema?

A
  • Infection
  • Hypocalcaemia
  • Corticosteroid withdrawal
  • Strong coal tar preparations
  • Drugs (lithium, antimalarials, IL-2)
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21
Q

What complications are associated with erythroderma?

A
  • Dehydration
  • Impaired temperature control -> hypothermia
  • Cardiac failure
  • Infection/sepsis
  • Protein loss -> oedema
  • Anaemia
  • Lymphadenopathy
  • Death
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22
Q

What does urticaria look like?

A

Central white itchy papule or plaque surrounded by an erythematous flare. Vary in size and shape.

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23
Q

What is the pathophysiology of urticaria?

A

Activation of mast cells in skin causing release of histamine and other mediators causing capillary leakage (-> swelling) and vasodilation (-> erythema).

Trigger may or may not be identifiable. Usually caused acutely by allergens e.g. foods, bites, stings, and medications.

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24
Q

What is autoimmune bullous disease?

A

An autoimmune blistering skin disorder which can cause cutaneous and/or mucosal erosions.

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25
Q

How does eczema herpeticum present?

A

Sudden deterioration of eczema characterised by widespread vesicopustular lesions which are tender and gradually become necrotic.

26
Q

What is eczema herpeticum?

A

Secondary infection of atopic endogenous eczema with herpes simplex.

27
Q

Why is eczema herpeticum an emergency?

A

Pts can present with or deteriorate with pyrexia and toxicity with tachycardia.

28
Q

How should eczema herpeticum be managed?

A

ABCDE
Specialist involvement for:
Treat localised disease aggressively with emollients and oral anti-histamines with high dose IV aciclovir.
Refer to ophthal if eye is involved.
IV fluids often needed if mucosal disease is extensive.
Swab regularly to monitor for secondary bacterial infection.

29
Q

What is generalised pustular psoriasis?

A

Relatively rare condition characterised by generalised eruptive form of psoriasis accompanied by fever and toxicity.

30
Q

How does generalised pustular psoriasis present?

A

Red tender skin with clusters of pustules appearing within hours. Pustules are small and yellow on an erythematous background.

31
Q

How should generalised pustular psoriasis be managed?

A

ABCDE!

Ix should include FBC, CRP, albumin, LFTs, U and Es, and blood culture.

Intensive supportive therapy. Bland topical compresses to soothe and debride affected areas.
Medications inc. systemic corticosteroids, methotrexate, ciclosporin, colchicine, and biological therapies.

32
Q

Why are the following investigations done in generalised pustular psoriasis Ix:

  1. Albumin
  2. LFTs
  3. U and Es
A
  1. Hypoalbuminaemia common in generalised pustular psoriasis
  2. LFTs areabnormal
  3. Abnormal renal function could be due to AKI or tubular necrosis.
33
Q

How does toxic epidermal necrolysis present?

A

Prodromal 2-3 day fever with symptoms like a URTI.

Confluent blistering of skin associated with epidermal separation usually following commencement of a new drug.

34
Q

How is toxic epidermal necrolysis diagnosed?

A

Skin biopsy to distinguish from staphylococcal scalded skin syndrome

35
Q

How should toxic epidermal necrolysis be managed?

A

ABCDE
Identify the cause and stop the drug.
Supportie Mx inc. nutrition if extensive mucosal involvement.
Prevent complications such as occular damage and sepsis.

36
Q

What is necrotising fasciitis?

A

An uncommon but life-threatening infections involving any layer of the deep soft tissue compartment.

37
Q

What are the layers of the deep soft tissue compartment?

A

Dermis
Subcut tissue
Fascia
Muscle

38
Q

What does nec fasc mimic in it’s early stages?

A

Cellulitis - this makes it difficult to diagnose initially.

39
Q

What signs might there be with an apparent cellulitis to indicate nec fasc?

A

Pain
Tenderness
Systemic illness out of proportion to localised physical signs

40
Q

What skin lesions are often found with nec fasc that are not found with cellulitis?

A

Bullae and ecchymotic skin lesions

41
Q

If nec fasc is suspected, what needs to be done promptly?

A

Referral to a specialist and prompt surgical debridement.

42
Q

Although muscle is usually spared in nec fasc, what can cause muscle involvement or damage?

A
  • Direct organism spread

- Compartment syndrome -> myonecrosis

43
Q

What are the 4 types of nec fasc?

A

1 - polymicrobial (usually in immune compromised or chronicly ill pts)
2 - Group A strep
3 - Gram neg monomicrobial infection
4 - Fungal

44
Q

What are the risk factors of nec fasc?

A
  • Skin injury (insect/animal/fish bite/sting, trauma, surgical wound)
  • Underlying chronic conditions/immunocompromise
  • IV drug use/alcohol abuse
  • VZV infection in children
45
Q

How quickly can nec fasc become fatal?

A

Depends on the organism, but in some cases it can be fatal witin 48 hours

46
Q

How does nec fasc progress in terms of signs and symptoms from day 1 to day 5?

A

1-2 - local pain, swelling, erythema, pain and systemic unwellness out of proportion to local signs. No abx response.

2-4 - local tense oedema, extends beyond erythema border, grey necrosed skin forms then breaks down, wooden-hard feeling to subcut tissues, bullae may be present and may haemorrhage. Pain decreases/changes as nerves are destroyed. Infection may appear to track. Crepitus due to subcut gas.

4-5 - hypotension, shock, confusion, apathy - not good.

47
Q

If there is uncertainty about the diagnosis, how should nec fasc be managed?

A

Refer anyway as need to have a high index of suspicion for cutaneous infection esp. if RFs present. Early surgical exploration is advised if uncertain.

48
Q

What might bloods show in a pt with nec fasc?

A
  • Raised wbc over 15
  • Hyponatraemia
  • Acidosis
  • Rasied CRP
  • Raised CK
  • Raised urea
49
Q

If nec fasc is suspected, what tests are done immediately?

A
  • Blood cultures

- Wound swab for gram stain and fungal cultrue

50
Q

How should nec fasc be managed by a junior?

A

Call for help ASAP from dermatology or plastics.
ABCDE!!! Pt may be shocked.
ICU might also need to know.

51
Q

What is the definitive Rx for nec fasc?

A

Surgical debridement - extensive with adequate margins.

Immediate broad spec IV abx - discuss with consultant microbiologist.

52
Q

What complications are associated with nec fasc?

A
  • High mortality rate
  • Sepsis/toxic shock
  • Vascular occlusion, ischaemia, tissue necrosis, nerve damage.
  • Large grafts needed
  • Limb compromise -> amputation
53
Q

What is the mortality rate associated with nec fasc?

A

20-40%, even with surgery.

54
Q

What is staphylococcal Scalded Skin Syndrome?

A

Potentially life-threatening syndrome caused by staph infection of the skin leading to red, blistered skin resembling a scald.

55
Q

What is the pathogenesis of SSSS?

A

S. aureus infection of skin causing damage by releasing epidermolytic toxins. These spread from the original site of infection to cause generalised epidermal damage.

56
Q

Who does SSSS affect?

A

Usualy neonates/children under 6, but some adults also get it.

57
Q

Why is SSSS thought to affect neonates most?

A

They have immature kidneys which means toxins aren’t cleared as efficiently.

58
Q

How does SSSS present?

A

Fever, generalised erythema, and skin tenderness.

Prodrome of sore throat or conjunctivitis may preceed.

Large bullae form then rupture easily -> scaled appearance.

59
Q

How is SSSS diagnosed?

A

Clinically, but swabs and skin biopsies can confirm.

60
Q

How should SSSS be managed?

A

ABCDE!!!

They will have lost a lot of fluids and electrolyes so supportive care is essential.

Lubrication, analgesia, systemic abx, and topical therapies should be given.

Involve micro, dermatology, and paediatrician if in a child.

61
Q

What are the complications of SSSS?

A
  • Dehydration
  • Cellulitis
  • Sepsis
  • Pneumonia
62
Q

What is the prognosis asociated with SSSS?

A
  • Good - usualy heals without scarring
  • Mortality 4% in infants, but 70% in adults.
  • If part of an outbreak e.g. on neonatal unit, it can be hard to control.

N&SS - Dermatology (9 decks)

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