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Y4 NSS > Derm emergencies > Flashcards

Derm emergencies Flashcards

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?

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?

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
Q

what is the pathophysiology of eczema herpeticum?

A
  • 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
Q

what are some risk factors for eczema herpeticum?

A
  • eczema
  • burns
  • irritant contact dermatitis
    • friction, env changes, chemical
27
Q

how is eczema herpeticum investigated?

A
  • clinical
  • PCR for virology
28
Q

how is eczema herpeticum managed?

A
  • 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
Q

what is the pathophysiology of staphylococcal scalded skin syndrome?

A
  • staphylococcus aureus that produces epidermolytic toxins
    • protease enzymes that break down proteins that hold skin together
    • causes breakdown of skin
30
Q

what is the appearance of staphylococcal scalded skin syndrome?

A
  • erythema → painful desquamation and superficial skin sloughing → bullae formation
  • nikolskys positive - with gentle rubbing
31
Q

what are some risk factors of staphylococcal scalded skin syndrome?

A
  • children
    • preceding respiratory tract infection
    • preceding conjunctivitis
    • preceding otitis media
  • adults
    • renal dysfunction
    • immunocompromised
    • septic arthritis
    • pneumonia
32
Q

what is the presentation of staphylococcal scalded skin syndrome?

A
  • 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
Q

what are the investigations for staphylococcal scalded skin syndrome?

A
  • blood cultures negative
  • superficial wound and bullae fluid cultures - sterile
    • differentiate from bullous impetigo
  • biopsy - TEN ruled out
  • histology - intraepidermal cleavage
34
Q

what is the management of staphylococcal scalded skin syndrome?

A
  • IV abx
    • nafcillin or oxacillin
    • vancomycin in MRSA
  • fluid and electrolyte balance
  • full recovery without scarring
35
Q

what is the erythroderma?

A
  • 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
Q

what are some risk factors of erythroderma?

A
  • inflammatory skin disease
    • psoriasis
    • eczema
  • drug eruption
    • allopurinol
    • gold
    • sulfonamide
    • sulfonylureas
    • isoniazid
  • cutaneous lymphoma
37
Q

what is the classical presentation of erythroderma?

A
  • red, painful and itchy skin over large area
  • malaise
  • PMH - inflammatory disease
  • DH
  • generalised lymphadenopathy
38
Q

what are some investigations carried out for erythroderma?

A
  • clinical
  • baseline obs and blood tests
  • skin biopsy - if unclear
39
Q

how is erythroderma managed?

A
  • 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
Q

what are some complications of erythroderma?

A
  • Dehydration
  • Electrolyte imbalance
  • Secondary bacterial infection
  • Hypothermia secondary to impaired thermoregulation
  • Cardiac failure
  • Death
41
Q

what is the immediate management of burns?

A
  • 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
Q

what is the pathophysiology of a burn?

A
  • 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
Q

how is a burn investigated?

A
  • assess extent: Wallaces rule of nines, Lund and Browder, asses depth of burn
44
Q

what would you refer to secondary care?

A
  • 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
Q

what long term management steps would you take?

A
  • IVF
  • urinary catheter
  • escharotomy to divide burn tissue
  • conservative management for smaller
  • excision and skin grafting
  • no evidence for abx prophylaxis
46
Q

how would you manage a bite?

A
  • 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
Q

how would you manage a human bite?

A
  • mx: co-amox
  • consider HIV and hep C risk
48
Q

what is the definition of erythema multiform?

A

immune mediated reaction of skin and mucous membrane to medication, malignancy, viral infection or inflammatory bowel disease usually secondary to viral infection

49
Q

what is the presentation of erythema multiforme?

A

acute eruption of pruritic, painful target lesions, symmetrical, acral distribution, affecting mucosa, malaise, myalgia, lesions can blister and ulcerate

*fever

50
Q

how might you manage erythema multiforme?

A

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
Q

what is acute vs chronic urticaria?

A

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
Q

what is the pathophysiology of urticaria?

A

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
Q

how might urticaria appear?

A
  • 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)

*urticariallesions (wheals or hives) are migratory, elevated, pruritic, reddish plaques caused by local dermal oedema

54
Q

how would you manage urticaria?

A

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
Q

how would urticaria complicate?

A

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
Q

when would you suspect angioedema?

A
  • hoarse cove, throat tightness
  • lip swelling, airway compromise
  • diffuse, non-pitting and tense swelling
  • bowel sx
57
Q

how do you manage urticaria?

A

cetirizine, loratadine, fexofenadine ← high doses may be required

severe angioedema may require corticosteroids

Y4 NSS (11 decks)

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