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Derm emergencies Flashcards

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1
Q

how would you describe lesions of Steven-johnson syndrome?

A

*abrupt onset of a tender erythematous rash
- macules, diffuse erythema, targetoid lesions, blisters
- blisters merge to form sheets of skin detachment

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2
Q

what is the pathophysiology of Steven Johnson?

A
  • Immune-complex mediated hypersensitivity reaction to foreign antigens and mostly by medications
  • detachment of epidermis from papilary dermis at epidermal-dermal junction → dusky macular erythema → keratinocyte apoptosis → blistering
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3
Q

what are some causes of it?

A
  • anti-gout medication - allopurinol
  • anticonvulsants and antipsychotics - carbamazepine
  • antibacterials - trimethoprim
  • Nevirapine - HIV medication
  • pain relievers - acetaminophen, ibuprofen, naproxen
  • infections - mycoplasma pneumonia, HIV, herpes
  • SLE
  • radiotherapy - immunocompromised
  • genetic predisposition
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4
Q

how does SJ present?

A

arthralgia
mucosal involvement with eyes, mouth, pharynx, genital and GI involvement
URTI
if severe TEN

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5
Q

what is toxic epidermal necrolysis?

A

complication of SJ where patient becomes systematically unwell and epidermis separates with >30% detachment leading to volume loss

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6
Q

define SJS and TENs in terms of skin detachment.

A

SJS - <10% of body surface area
overlap - 10-30%
TEN - >30%

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7
Q

what are some differentials for SJS?

A
  • drug rash with eosinophilia and systemic symptoms (DRESS)
  • staphylococcal scalded skin syndrome or toxic shock syndrome
  • morbilliform or maculopapular drug reaction
  • bullous pemphigoid
  • graft-vs-host
  • pemphigus vulgaris
  • chemical or thermal burns
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8
Q

what are investigations are carried out for SJS?

A
  • review medication, go back 6m
  • skin biopsy
  • culture
  • imaging
  • bloods: Hb, WCC, LFT, eosinophil, U&E, glucose, CXR
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9
Q

what scoring system is used to predict mortality in SJS?

A

SCORTEN - uses age, malignancy, tachy, epidermal detachment, serum urea, glucose and bicarbonate

score over 5 shows 90% mortality

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10
Q

how long is the acute phase of SJS?

A

8-12 days

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11
Q

How would you manage SJS?

A

stop medication which causes
supportive care
- fluid replacement and nutrition
- wound care
- eye care
- analgesia
- topical steroids, ABX, IV immunoglobulin, ciclosporin

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12
Q

What are the complication of SJS?

A

TEN

acute - dehydration, infection, hypothermia, ocular complications, acute liver and renal failure, shock and organ failure

chronic - skin pigmentation and scarring, pulmonary complications, nail plate loss

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13
Q

what is necrotising fascitis?

A

subset of aggressive skin and soft tissue infections (SSTIs) that cause necrosis of the muscle fascia and subcutaneous tissues

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14
Q

what is the pathophysiology of necrotising fascitis?

A
  • type 1 - polymicrobial, primarily a mixture of anaerobes (bacteroides) and aerobes (S.aureus), common in elderly or co-morbid
  • type 2 - monomicrobial, primarily S.pyogenes, more common in healthy with history of trauma
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15
Q

what is the pathophysiology of gangrene in relation to nec fascitis?

A
  • clostridium (C. perfringens) gas produced within tissue
    • alpha and beta toxins lead to extensive tissue damage
    • tissue crepitusis often present onlight palpationof the affected area
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16
Q

how does necrotising fascitis present?

A

local pain, swelling and erythema with poorly defined margins with pain extending beyond them

skin blistering, offensive discharge, bullae

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17
Q

what are some risk factors for nec fasc?

A

immunosuppression
DM
malnutrition
alcoholism
IVDU

triggered by: trauma, surgery, chicken pox, local skin damage or omphalitis in babies

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18
Q

how might nec fasc present?

A

pain disproportionate to clinical findings
skin discolouration and blistering
fever and malaise
crepitus on palpation
hypotension and tachycardia

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19
Q

how would you investigate nec fasc?

A

FBC, U&E, CRP
CK - myonecrosis
lactate
cultures
G&S
wound swabs
gram stain from derided tissue
CT for spread

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20
Q

what is the bed side finger test in nec fasc?

A
  • small incision down to fascia under local anaesthetic
  • tissue probed with sterile gloved finger
  • NF - absence of bleeding, purulent pus, lack of normal tissue resistance to blunt dissection
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21
Q

what scoring system is used to assess risk of nec fasc?

A

✋🏽 Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC) - assist a clinician in the diagnosis of necrotising fasciitis

  • A score ≤5 is low risk
  • score 6-7 is intermediate risk
  • ≥8 is high risk
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22
Q

how would you reach a diagnosis of nec fasc?

A

Dishwater-like fluidfrom the wound, or anynon-bleeding unhealthy subcutaneous tissuewhen digitated, fat peeling easily from the fascia, or anyunhealthy fasciaare all suggestive

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23
Q

how would you manage nec fasc?

Study These Flashcards
A

CALL SURGEONS
- A to E
- broad spec IV abx (beta lactam, carbapenem, clindamycin, vancomycin)
- debridement
- monitor wound within 24-48h to see if requires more
- reconstructive grafts
- treat shock or derangement

24
Q

what is the appearance of eczema herpeticum?

Study These Flashcards
A
  • painful clusters of blisters which are fluid filled elevations of the skin
    • widely over body - common in face, neck, trunk
  • old blisters - punched out erosions which are circular breaks in continuity of the skin that may bleed to produce pus
25
what is the pathophysiology of eczema herpeticum?
- common in infants and children - skin infection caused by HSV commonly affecting those with eczema - HSV type 1 causes 5-12 days post contact - impaired skin barrier poses risk - is contagious and can spread through direct contact - can pose secondary bacterial infections
26
what are some risk factors for eczema herpeticum?
- eczema - burns - irritant contact dermatitis - friction, env changes, chemical
27
how is eczema herpeticum investigated?
- clinical - PCR for virology
28
how is eczema herpeticum managed?
- oral acyclovir or valacyclovir - mild cases treated for 7-21 days - severe - immunocompromised IV antivirals - supportive - fluids, pain relief, wound care - control spread - PPE, hand hygiene
29
what is the pathophysiology of staphylococcal scalded skin syndrome?
- staphylococcus aureus that produces epidermolytic toxins - protease enzymes that break down proteins that hold skin together - causes breakdown of skin
30
what is the appearance of staphylococcal scalded skin syndrome?
- erythema → painful desquamation and superficial skin sloughing → bullae formation - nikolskys positive - with gentle rubbing
31
what are some risk factors of staphylococcal scalded skin syndrome?
- children - preceding respiratory tract infection - preceding conjunctivitis - preceding otitis media - adults - renal dysfunction - immunocompromised - septic arthritis - pneumonia
32
what is the presentation of staphylococcal scalded skin syndrome?
- commonly children under 5 → older children and adults have immunity - starts as generalised patches of erythema - then skin thin and wrinkled - then formation of fluid filled blisters called bullae - burst and leave very sore, erythematous skin burn or scald like - systemic - fever, irritability, lethargy, dehydration - no mucous membrane involvement
33
what are the investigations for staphylococcal scalded skin syndrome?
- blood cultures negative - superficial wound and bullae fluid cultures - sterile - differentiate from bullous impetigo - biopsy - TEN ruled out - histology - intraepidermal cleavage
34
what is the management of staphylococcal scalded skin syndrome?
- IV abx - nafcillin or oxacillin - vancomycin in MRSA - fluid and electrolyte balance - full recovery without scarring
35
what is the erythroderma?
- intense redness of skin covering atleast 90% of skin surface area - hot, erythematous skin with desquamation or peeling of skin *secondary to pre-existing inflammatory skin disease, rapid epidermal cell turnover
36
what are some risk factors of erythroderma?
- inflammatory skin disease - psoriasis - eczema - drug eruption - allopurinol - gold - sulfonamide - sulfonylureas - isoniazid - cutaneous lymphoma
37
what is the classical presentation of erythroderma?
- red, painful and itchy skin over large area - malaise - PMH - inflammatory disease - DH - generalised lymphadenopathy
38
what are some investigations carried out for erythroderma?
- clinical - baseline obs and blood tests - skin biopsy - if unclear
39
how is erythroderma managed?
- review by dermatology - admission to burns unit or ICU - emollients and cool, wet dressings - treat underlying if known - topical corticosteroids - nursed in warm room (30) and have fluid balance, electrolytes and temperature monitored closely
40
what are some complications of erythroderma?
- Dehydration - Electrolyte imbalance - Secondary bacterial infection - Hypothermia secondary to impaired thermoregulation - Cardiac failure - Death
41
what is the immediate management of burns?
- A-E - **burns caused by heat**: remove the person from source, within 20 min irrigate burn with cool (not iced) water between 10 to 30, cover burn using cling film, layered not wrapped - **electrical burns**: switch off power supply, remove person from source - **chemical burns**: brush any powder off then irrigate with water, attempts to neutralise the chemical are not recommended
42
what is the pathophysiology of a burn?
- local response with progressive tissue loss and release of inflammatory cytokines - systemically - CVS effects from fluid loss and sequestration of fluid into third space - marked catabolic response - immunosuppression is common with large burns and bacterial translocation from gut lumen is a recognised event - sepsis common cause of death
43
how is a burn investigated?
- assess extent: Wallaces rule of nines, Lund and Browder, asses depth of burn
44
what would you refer to secondary care?
- all deep dermal and full thickness burns - superficial dermal burns of more than 3% TBSA in adults, or more than 2% TBSA in children - superficial dermal burns involving the face, hands, feet, perineum, genitalia, or any flexure, or circumferential burns of the limbs, torso, or neck - any inhalation injury - any electrical or chemical burn injury - suspicion of non-accidental injury
45
what long term management steps would you take?
- IVF - urinary catheter - escharotomy to divide burn tissue - conservative management for smaller - excision and skin grafting - no evidence for abx prophylaxis
46
how would you manage a bite?
- cleanse wound, puncture wound may not be sutured unless comsesis at risk, Co-amox, if pen allergy doxy+metronidazole - rabies risk - immunised then human rabies immunoglobulin (HRIG) should be given along with a full course of vaccination
47
how would you manage a human bite?
- mx: co-amox - consider HIV and hep C risk
48
what is the definition of erythema multiform?
immune mediated reaction of skin and mucous membrane to medication, malignancy, viral infection or inflammatory bowel disease usually secondary to viral infection
49
what is the presentation of erythema multiforme?
acute eruption of pruritic, painful target lesions, symmetrical, acral distribution, affecting mucosa, malaise, myalgia, lesions can blister and ulcerate *fever
50
how might you manage erythema multiforme?
self limiting, 2-4 weeks stop offending drug if this is the cause *1- oral antihistamine/topical steroid (itching) 2- local anaesthetic (pain) severe: treat underlying cause (acyclovir, antibiotics)
51
what is acute vs chronic urticaria?
can be acute - less than 6 weeks or chronic - more than 6 weeks *autoimmune condition, where autoantibodies target mast cells and trigger them to release histamines and other chemicals
52
what is the pathophysiology of urticaria?
release of histamine and other pro-inflammatory chemicals by mast cells in the upper dermis causing vasodilatation in skin → localised swelling and marked itching allergic reaction in acute urticaria autoimmune reaction in chronic idiopathic urticaria
53
how might urticaria appear?
- pruritic - erythematous appearance - rounded or irregular shape - multiple papules (< 1 cm) or plaques (> 1 cm) - lesions may coalesce - single area of the body or widespread - with or without angioedema (usually localised) *urticarial lesions (wheals or hives) are migratory, elevated, pruritic, reddish plaques caused by local dermal oedema
54
how would you manage urticaria?
if mild, it will be self-limiting if symptoms require treatment, give a non-sedating antihistamine e.g. cetirizine, loratadine for up to 6 weeks **fexofenadine for chronic urticaria**
55
how would urticaria complicate?
angioedma *vasodilation and extravasation of fluid into deep dermis, subcutaneous tissue and/or submucosa can be IgE/non-IgE mediated but can also be bradykinin-mediated (this is not associated with urticaria)
56
when would you suspect angioedema?
- hoarse cove, throat tightness - lip swelling, airway compromise - diffuse, non-pitting and tense swelling - bowel sx
57
how do you manage urticaria?
cetirizine, loratadine, fexofenadine ← high doses may be required severe angioedema may require corticosteroids

Y4 NSS (11 decks)

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