Dermatological Emergencies Flashcards

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1
Q

What are the normal skin functions?

A

Mechanical barrier to infections

Temperature regulation

Fluid and electrolyte balance

Vitamin D synthesis

Sensation

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2
Q

What is Acute Skin Failure?

A

Loss of normal temperature control

Inability to prevent loss of fluid, electrolytes and protein

Loss of normal “barrier function”

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3
Q

What are the consequences of acute skin failure?

A

Peripheral vasodilation (can occasionally lead to cardiac failure)

Poor temperature regulation

  • Hypothermia
  • Fever (+/- infection)

Increased fluid losses

Protein loss

Infection

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4
Q

What are the principles of acute skin failure management?

A
  • Appropraite setting (?ITU or burns unit)
  • Remove any offending drugs
  • Careful fluid balance
  • Good nutrition
  • Temperature regulation
  • Emollients
  • Oral and eye care
  • Anticipate and treat infection
  • Disease specific therapy; treat underlying cause
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5
Q

What is erythroderma?

A

Descriptive term rather than a diagnosis

Any inflammatory skin disease affecting >90% of body surface area

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6
Q

What are the common causes of erythroderma?

A

Psoriasis

Eczema

Drugs (almost any)

  • Anticonvulsants
  • Antibiotics
  • Lithium

Cutaneous Lymphomas

Other

  • Pityriases rubra pilaris
  • Hereditary Disorders
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7
Q

What types of of cutaneous drug reactions may occur?

A

Mild
-Drug exanthems

Severe

  • Erythroderma
  • Stevens Johnson Syndrome/ Toxic Epidermal Necrosis
  • Dress syndrome
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8
Q

How common are cutaneous drug reactions?

A

Common
-2-3% of inpatients

Can occur after any drug

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9
Q

Whar is Stevens johnson Syndrome

A

Stevens–Johnson syndrome, a form of toxic epidermal necrolysis, is a life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis. The syndrome is thought to be a hypersensitivity complex that affects the skin and the mucous membranes. The most well-known causes are certain medications (such as lamotrigine), but it can also be due to infections, or more rarely, cancers.

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10
Q

What are the signs and symptoms of Stevens-Johnson Syndrome?

A

SJS usually begins with fever, malaise and arthralgia, which is commonly misdiagnosed and therefore treated with antibiotics.

Rash

  • Macropapular, target lesions, blisters
  • Erosions covering
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11
Q

What is the relation between Stevens Johnson Syndrome and Toxic Epidermal Necrolysis?

A

2 conditions which are thought to form part of the same spectrum

Very rare conditions

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12
Q

What are the signs and symptoms of Toxic Epidernal 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”
  • Nikolsky’s sign may be positive
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13
Q

How is prognosis in SJS/TENS determined?

A

SCORTEN

Age >40
Malignancy
Tachycardia >120bpm
Epidermal detachment >10%
Serum urea >10mmol/L
Serum glucose >14mmol/L
Bicarbonate
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14
Q

What does the predicted mortality with SCORTEN vary between?

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

How do you manage SJS/TEN?

A

Identify and remove culprit drug ASAP

Supportive therapy

Specific therapies:

  • ?High dose steroids
  • ?IV immunoglobulins
  • ?Anti-TNF therapy
  • ?Ciclosporin
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16
Q

What are the long term complications of SJS/TEN?

A

Pigmentary skin changes

Skin scarring

Genital scarring

Joint contractures

Nail loss/ hair loss

Eye disease and blindness

17
Q

What does DRESS syndrome mean?

A

Drug Reaction with Eosinophilia and Systemic Symptoms

18
Q

What are the features of DRESS syndrome?

A

Fever

Rash - morbilliform; erythrodermic; blistering; pustular

Blood eosinophilia

Lymphadenopathy

19
Q

What other organ systems may DRESS syndrome effect?

A

Liver dysfunction

Renal dysfunction

Haematological - oesinophilia, thrombocytopenia, anaemia

rarely GI, cardiac or respiratory involvement

20
Q

What is the management of DRESS syndrome?

A

Withdraw offending drug

  • Allopurinol
  • Anticonvulsants
  • NSAIDs
  • Antibiotics

General skin care, emollients, dressings

Supportive care if skin failure

High dose corticosteroids in severe cases

21
Q

What is Pemphigus?

A

Blistering disorder
Autoimmune disorder

Antibody (IgG) to desmosomes in epidermis

Loss of cell adhesion leads to splitting of epidermis -> blisters

Blisters very fragile

22
Q

What are the clinical features of pemphigus?

A

Skin- flaccid blisters, rupture very easily

Intact blisters may not be seen

Common sites = face, axillae, groins

Nikolsky’s sign may be positive

Commonly affects mucous membranes

  • Ill defined erosions in mouth
  • Can also affect eyes, nose and genital areas
23
Q

What is Nikolsky’s sign?

A

Pressure applied to skin and top layer will easily peel off.

Like rubbing glue off your hands

24
Q

What is pemphigoid?

A

Antibodies directed at demo-epidermal junction

Intact epidermis forms roof of blister

Blisters are usually tense and intact

25
Q

Is pemphigus or pemphigoid more common?

A

Pemphigoid

26
Q

What demographic do pemphigus and pemphigoid effect?

A

Pemphigus = middle ages patients

Pemphigoid = elderly patients

27
Q

What is the difference between pemphigus and pemphigoid blisters?

A

Pemphigus = blisters very fragile- may not be seen intact

Pemphigoid = blisters often intact and tense

28
Q

How are mucous membranes effected in pemphigus and pemphigoid?

A

Mucous membranes effected in pemphigus but not pemphigoid

29
Q

How well are patients with pemphigus and pemphigoid?

A

Pemphigus - patients may be very unwell if extensive

Pemphigoid - even if extensive, patients are fairly well systemically

30
Q

How do you treat pemphigus and pemphigoid?

A

Pemphigus = systemic steroids

Phemphigoid = topical steroids may be sufficient if localised; systemic usually required if diffuse

31
Q

What is pustular psoriasis?

A

Develops rapidly; patient can be extremely unwell

Generalised erythema followed by development of clusters of tiny pustules

Patient may or may not have a history of chronic plaque psoriasis

Fever (often without infection), malaise, tachycardia, increased WCC

32
Q

How do you treat pustular psoriasis?

A

Admit, preferably to dermatology ward

Blood cultures- treat any superimposed infection

Emollients

Avoid topical steroids!

Consider systemic treatment e.g. retinoids, methotrexate, biologics

33
Q

What is eczema Herpeticum?

A

Disseminated herpes virus infection on a background of atopic eczema

More common in children

HSV-1 more common

Multiple small vesicles develop, initially overlying eczematous skin, then becoming disseminated

34
Q

What is the treatment for eczema herpeticum?

A

Send swab for viral culture

Treat weith systemic antivirals (e.g. aciclovir 200mg 5x/ day)

Consider superimposed bacterial infection

Try to avoid topical steroids

Opthalmology input if eye involvement

35
Q

What is staphylococcal scalded skin syndrome?

A

Fairly common in children

Starts with a staphylococcal infection (e.g. impetigo, throat, nose, mouth)

Staphylococcus produces a toxin which causes splitting of the epidermis and widespread desquamation.

Can occur in immunocompromised adults

36
Q

What are the clinical features of staphylococcal scalded skin syndrome?

A

Preceding staph infection (may be subclinical)

Diffuse erythematous rash with skin tenderness

More prominent in flexures

Blistering and desquamination follows

May occur at sites of minor trauma

37
Q

What is the treatment for staphylococcus scalded skin syndrome?

A

Antibiotics (good idea to cover staph and strep)

Topical antibiotic preparations (e.g. Bactroban)

Wound care

Fluid rehydration

Most children are not too systemically unwell