Dermatology - Emergencies Flashcards
What is erythoderma?
- 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.
How is erythoderma mxd?
Tx underlying cause if known, emollients + wet-wraps to maintain skin moisture
Topical steroids to relieve inflammation
What are some complications of erythoderma?
- 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.
What is eczema herpeticum?
- 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.
What is the mx of eczema herpeticum + complications?
- Mx: IV acyclovir + abx + admission for secondary bacterial infection.
- Complications: herpes hepatitis, encephalitis, DIC, death.
What is necrotizing fascitis?
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.
What are some RFs for necrotizing fascitis?
- Aspirin
- NSAIDs,
- increasing age
- immune suppression,
- obesity
- drug abuse,
- chronic illness
- malignancy.
How does necrotizing fascitis arise?
- 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.
How does necrotizing fasciittisi present?
- 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.
How is nectrozing fascitis ixd + mxd?
- 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.
What is erythema multiforme and how does it present?
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.
What are some of the causes of erythema multiforme?
- 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
How is erythema multiforme mxd?
- Oral acyclovir for HSV, abx (erythromycin) for Mycoplasma.
- Stop offensive drug.
- Supportive tx – antihistamine, topical corticosteroids, mouthwashes containing LA
What is Stevens Johnsons syndrome?
- 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.
- Macular, background erythema, targetoid (as in EM), and flaccid blisters.
- Blisters merge to form sheets of skin detachment. Nikolsky sign +ve (when rubbed gently will burst)
- Mucosal involve prominent and severe.
What medicaitons cause stevens johnsons
- penicillin
- sulphonamides
- lamotrigine, carbamazepine, phenytoin
- allopurinol
- NSAIDs
- oral contraceptive pill
How is stevens johnsons mxd?
- Stop causative drug
- Hospital admission to ICU
- Supportive: nutritional and fluid replacement, temperature maintenance, topical antiseptics, sterile dressings, mouthwashes
What is toxic epidermal necrolysis
- 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
What is Staphylococcal Scalded Skin Syndrome?
- 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
*
How is staphylococcus scalded skin mxd?
- Hospitalization, IV flucloxacillin (vancomycin ?MRSA)
- Supporitve – paracetamol, fluid and electrolyte monitoring, skin care (petroleum jelly), keep newborns in incubators.
What is bullous pemphigoid?
- 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)*
What are some RFs for bullous pemphigoid?
older age (60-90), MHC class II allele (DQB1*0301), male sex
How is bullous pemphigoid ixd + mxd?
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
What is pemphigus vulgaris?
Overview: autoimmune blistering disease involving the epidermal surfaces of the skin and mucosa.
What are some RFs for pemphigus vulgaris?
- Younger age group (30-60)
- More common in Jewish and Indian pts
- Specific HLA genetc types
- Drug-induced – penicillamine, ACEis, ARBs, and cephalosporins
How does pemphigus vulgaris present/?
- 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.
How is pemphigus vulgaris ixd + mxd?
- 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
What is dermatitis herpetiformis?
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.
How does dermatitis herpetiformis present?
- 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.
How is dermatitis herpetiformis ixd + mxd?
- 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
