Dermatology - Emergencies Flashcards

1
Q

What is erythoderma?

A
  • Overview: exfoliative dermatitis involving at least 90% of the skin surface
  • RFs: previous skin disease (eczema, psoriasis), lymphoma, drugs (sulphonamides, penicillin, allopurinol, captopril), idiopathic
  • Presentation: inflamed, oedematous and scaly skin, systemically unwell with lymphadenopathy and malaise. Acute deteriorations require hospital admission.
  • Erythrodermic psoriasis – chronic disease progresses to exfoliative phase with plaques covering most of the body.
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2
Q

How is erythoderma mxd?

A

Tx underlying cause if known, emollients + wet-wraps to maintain skin moisture

Topical steroids to relieve inflammation

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3
Q

What are some complications of erythoderma?

A
  • secondary infection
  • fluid loss and electrolyte imbalance (skins regulatory function diminished)
  • hypothermia,
  • high-output cardiac failure
  • capillary leak syndrome.
  • Death – 20-40% depending on cause.
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4
Q

What is eczema herpeticum?

A
  • Overview: widespread eruption that occurs as a complication of atopic eczema or other skin conditions (thermal burns, pemphigus vulgaris). Manifestation of a disseminated viral infection.
  • Cause: Herpes simplex virus (HSV1/2)
  • Presentation: extensive crusted papules, blisters and erosions. Systemically unwell with fever and malaise.
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5
Q

What is the mx of eczema herpeticum + complications?

A
  • Mx: IV acyclovir + abx + admission for secondary bacterial infection.
  • Complications: herpes hepatitis, encephalitis, DIC, death.
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6
Q

What is necrotizing fascitis?

A

Overview: life-threatening bacterial infection of the soft tissue and fascia.

  • Type I = polymicrobial (Staph +/- haemophilus +/- E.coli)
  • Type II = haemolytic group a strep +/- MRSA
  • Type III = gas gangrene due to Clostridium perfringens.
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7
Q

What are some RFs for necrotizing fascitis?

A
  • Aspirin
  • NSAIDs,
  • increasing age
  • immune suppression,
  • obesity
  • drug abuse,
  • chronic illness
  • malignancy.
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8
Q

How does necrotizing fascitis arise?

A
  • Infection begins in the superficial fascia, bacteria release enzymes and proteins that result in necrosis of fascial layers.
  • Horizontal spread of infection followed by vertical spread.
  • Thrombosis occludes arteries and veins leading to ischaemia and necrosis.
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9
Q

How does necrotizing fasciittisi present?

A
  • Lower leg most common, symptoms present <24h of minor injury, pain is very severe at presentation and worsens over time.
  • Purplish rash, large dark marks that turn into blisters filled with dark fluid. Wound starts to die and area becomes necrotic.
  • Fine crackling sensation ‘crepitus’ due to fas in the tissues
  • Dishwasher coloured fluid seeps out of skin
  • Flu like symptoms, nausea, fever, diarrhoea, general malaise
  • If untreated, infection can spread to bloodstream > dangerously low BP, high temp.
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10
Q

How is nectrozing fascitis ixd + mxd?

A
  • Ix: WBC, CRP, CK, Urea (all raised), U&Es – low sodium
    • Blood cultures, deep tissue biopsy, gram stain to ID organism
  • Mx:
    • Hospitalisation > ICU (A-E)
    • High dose IV abx (penicillin, clindamycin, metronidazole, vancomycin…)
    • Urgent surgical debridement, may require amputation
    • Hyperbaric oxygen and IVIg may be considered.
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11
Q

What is erythema multiforme and how does it present?

A

Overview: hypersensitivity reaction triggered by infections. Typically affects young adults. Major and minor forms.

Presentation:

  • Several -100s of skin lesions erupt within 24h. first seen on backs of hands or tops of feet then spread towards the trunk. Polymorphorous (eruption at various stages of development)
  • Well demarcated, round, red/pink, macules that progress to papules and then enlarge to form plaques.
  • ‘Iris lesion’- sharp margin, regular round shape, and three concentric zones
    • Minor: mucus membrane involvement is absent or mild.
    • Major: one or more mucus membranes are affected, most often the oral mucosa – swelling with blister formation.
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12
Q

What are some of the causes of erythema multiforme?

A
  • viruses: HSV (the most common cause), Orf*
  • idiopathic
  • bacteria: Mycoplasma, Streptococcus
  • Drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
  • Connective tissue disease e.g. SLE
  • sarcoidosis
  • malignancy
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13
Q

How is erythema multiforme mxd?

A
  • Oral acyclovir for HSV, abx (erythromycin) for Mycoplasma.
  • Stop offensive drug.
  • Supportive tx – antihistamine, topical corticosteroids, mouthwashes containing LA
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14
Q

What is Stevens Johnsons syndrome?

A
  • Overview: rare, potentially life-threatening skin reaction involving sheet-like skin and mucosal loss. Very rare complication of medication use.
  • Mucocutaneous necrosis >/=2 sites affecting <10% of body.

Presentation

  • Fever >39C, sore throat, difficulty swallowing, runny nose, cough, conjunctivitis, general aches and pains.
  • Abrupt onset tender, painful red skin rash starting on the trunk and extending rapidly onto the face and limbs.
    1. Macular, background erythema, targetoid (as in EM), and flaccid blisters.
    2. Blisters merge to form sheets of skin detachment. Nikolsky sign +ve (when rubbed gently will burst)
  • Mucosal involve prominent and severe.
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15
Q

What medicaitons cause stevens johnsons

A
  • penicillin
  • sulphonamides
  • lamotrigine, carbamazepine, phenytoin
  • allopurinol
  • NSAIDs
  • oral contraceptive pill
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16
Q

How is stevens johnsons mxd?

A
  • Stop causative drug
  • Hospital admission to ICU
  • Supportive: nutritional and fluid replacement, temperature maintenance, topical antiseptics, sterile dressings, mouthwashes
17
Q

What is toxic epidermal necrolysis

A
  • Overview: similar to SJS but affects >30% of body surface area.
  • Causes: drug induced – phenytoin, allopurinol, NSAIDs
  • Presentation: full thickness, epidermal necrolysis, fever + flu, blistering and peeling of sheets of skin.
  • Mx: same as for SJS
18
Q

What is Staphylococcal Scalded Skin Syndrome?

A
  • Looks like a burn or scald.
  • Pathophysiology: release of exotoxins (A+B) from toxigenic strains of Staph aureus.
    • Toxins bind to a desmoglein 1 within the desmosomes that adhere skin cells together
    • > Break it up and as a result the skin cells become unstuck
      *
19
Q

How is staphylococcus scalded skin mxd?

A
  • Hospitalization, IV flucloxacillin (vancomycin ?MRSA)
  • Supporitve – paracetamol, fluid and electrolyte monitoring, skin care (petroleum jelly), keep newborns in incubators.
20
Q

What is bullous pemphigoid?

A
  • chronic, acquired, autoimmune blistering disease characterized by auto-antibodies against hemidesmosomal antigens, resulting in the formation of a sub-epidermal blister.
  • Pathophysiology: inflammation resulting from antibody (IgG) binding to various proteins (hemidesmosomes, anchoring filaments + fibrils) within the dermal-epidermal region leads to dermal-epidermal separation and tense blister formation.

Presentation

  • itchy, tense blisters typically around flexures
  • the blisters usually heal without scarring
  • there is usually no mucosal involvement (i.e. the mouth is spared)*
21
Q

What are some RFs for bullous pemphigoid?

A

older age (60-90), MHC class II allele (DQB1*0301), male sex

22
Q

How is bullous pemphigoid ixd + mxd?

A

Investigations: Skin biopsy or direct immunofluorescence testing (linear band of IgG)

Management

  • Topical or oral corticosteroids: prednisolone
  • Sedating antihistamines: diphenhydramine
  • Abx – steroid sparing (tetracycline, doxycycline)
  • Immunosuppressants – azathioprine, mycophenolate mofetil
23
Q

What is pemphigus vulgaris?

A

Overview: autoimmune blistering disease involving the epidermal surfaces of the skin and mucosa.

24
Q

What are some RFs for pemphigus vulgaris?

A
  • Younger age group (30-60)
  • More common in Jewish and Indian pts
  • Specific HLA genetc types
  • Drug-induced – penicillamine, ACEis, ARBs, and cephalosporins
25
Q

How does pemphigus vulgaris present/?

A
  • Most patients first present with lesions on mucous membranes such as the mouth and genitals. Blisters usually develop on the skin after weeks-months
  • Thin walled flaccid blisters with clear fluid that rupture easily (+ ve Nicholskys sign)
  • -> Causes itchy, painful erosions which can be painful, and clow to heal.
  • Inside of the mouth commonly involved.
26
Q

How is pemphigus vulgaris ixd + mxd?

A
  • Ix
    • Skin biopsy – H&E stain
    • Skin biopsy – direct immunofluorescence – pathognomic IgG band on surface of epidermal keratinocytes.
  • Mx
    • Steroids – prednisolone (+bone protection – calcium carbonate + alendronic acid)
    • Immunomodulators – mycophenolate, azathioprine
    • Biologics – rituximab + IVIG
    • Plasmapheresis
27
Q

What is dermatitis herpetiformis?

A

Autoimmune blistering skin disorder associated with coeliac disease. It is caused by deposition of IgA in the dermis.
Risk factors: coeliac disease, younger age, M>F, genetic predisposition (HLA types), FH AI disease.

28
Q

How does dermatitis herpetiformis present?

A
  • Symmetrical distribution of extremely itchy papules and vesicles on normal or erythematous skin.
  • Lesions appear of scalp, shoulders, buttocks, elbows and knees.
  • Often appear in groups or clusters.
29
Q

How is dermatitis herpetiformis ixd + mxd?

A
  • Ix: Screen for coeliac – TTG, IgA anti-endomysial antibodies, total IgA level
    • Nutritional deficiencies – FBC, LFTs, TFTs, Ca2+, vitB12, folate
    • Skin biopsy – subepidermal blisters, neutrophil and eosinophil inflammatory cells in dermal papillae, granular IgA deposits in the dermal papillae on direct immunofluorescence.
  • Mx: Gluten free diet
    • Dapsone – reduced the itch
    • Ultra potent topical steroids + PO steroids
    • Rituximab