Dermatology emergencies Flashcards
Acute urticaria clinical features
Pale, pink raised skin
Pruritic
Acute urticaria mx
Non-sedating antihistamines (eg. cetirizine) are first line
- continue these for up to 6 weeks following an episode of acute urticaria
Sedating antihistamine (eg. chlorphenamine) may be considered for night-time use for troublesome sleep symptoms
Prednisolone - severe or resistant episodes
Uncomplicated drug reactions
Drug induced exanthem (morbilliform drug eruption)
Fixed drug eruption
Type 1 hypersensitivity reactions
Lichenoid drug eruptions
Phototoxic reactions
Severe cutaneous adverse reactions (SCAR)
DRESS
AGEP
SJS-TENS
DRESS
Drug reaction with eosinophilia and systemic symptoms (also known as drug induced hypersensitivity syndrome)
Presents with a morbilliform rash, with systemic symptoms eg. fever, potential multi-organ dysfunctionn, haematological abnormalities, neurological, endocrine or GI manifestations and raised eosinophils
Facial oedema is characteristic
Mx - stop offending agent, supportive treatment due to risk of dehydration, oral prednisolone, IVIG/plasma exchange if life threatening
AGEP
Acute generalised exanthematous pustulosis
Onset is sudden, within 24 hours of drug being commenced → patient febrile with an eruption of sterile pustules
Patient is unwell & rash is itchy & painful
Mx - stop offending agent, use of topical/systemic steroids with best supportive care
SJS-TENS
Steven Johnsons Syndrome and Toxic Epidermal Necrolysis are blistering, desquamating delayed T-cell reactions to drugs, with mucous membrane involvement
Takes many weeks for the reaction to develop after initial drug exposure
SJS = < 10% epidermal detachment, 10-30% = SJS-TENS overlap, > 30% = TENS
Typically carbamazepine, phenytoin & abacavir
SJS-TENS clinical features
Prodrome - viral symptoms
Followed by erythroderma, atypical target lesions & flaccid blisters
Multi-organ dysfunction & death can occur
Nikolsky’s sign is positive
SJS-TENS mx
Offending drug should be stopped
Nursing in a high acuity setting with burns centre management → use of special dressings & paying close attention to fluid loss and infection risk is necessary
Analgesia, support with hydration & nutrition, close monitoring
Ophthalmology input may be required due to eye involvement
Prognosis - SCORTEN & ABCD-10 criteria
Eczema herpeticum
Potentially serious widespread HSV infection, with typically affects people with atopic dermatitis or eczema
Eczema herpeticum clinical features
Appear 5-12 days after contact with an infected individual
Areas of rapidly worsening, painful eczema
Vesicular rash
Punched-out erosions
Possible fever, lethargy, lymphadenopathy or distress
Rarely → can spread to the eye (herpes keratitis) → ophthalmological referral
Eczema herpeticum ix
Viral infection can be confirmed by viral swabs → PCR, viral culture, direct fluorescent antibody stain
Herpetic keratitis → staining with fluorescein - stained dendritic ulcer is diagnostic
Eczema herpeticum mx
Prompt treatment with antiviral meds - oral aciclovir 5 times daily for 10-14 days (if vomiting → IV)
Ocular involvement:
- ganciclovir ointment five times daily for 7-10 days
- corneal transplant may be indicated where vision significantly affected by scarring
Eczema herpeticum complications
Secondary infection
Scarring
Herpetic keratitis
Organ failure & dissemination
Necrotising fasciitis
Life-threatening rapidly-progressing infection that spreads along the fascial planes & subcutaneous tissue
Surgical emergency
Fournier’s gangrene = specifically a necrotising infection of the perineum
Necrotising fasciitis types
Type I - polymicrobial infection, primarily caused by a mixture of anaerobes & aerobes; it is the more common of the two subtypes, especially in elderly or co-morbid patients
Type II - monomicrobial infection, primarily caused by strep pyogenes & is more common in healthy individuals with a history of trauma
Gas gangrene
Form of necrotising fasciitis caused by clostridium species, resulting in gas being produced by the bacteria within the tissue
Extensive tissue damage, alongside large volumes of gas within the tissue
Tissue crepitus is often present on light palpation of the affected area, management same as any nec fasc
Necrotising fasciitis risk factors
Diabetes mellitus
CKD
Alcohol excess
Advanced age or frailty
Malnutrition
Metastatic cancer
Immunocompromised
Necrotising fasciitis clinical features
Rapid progression
Severe pain, out of keeping with the overt clinical signs
O/E - skin erythema, oedema, signs of skin ischaemia, skin crepitus, vesicles/bullae, obvious skin necrosis
Necrotising fasciitis ix
Blood tests - FBC, CRP, U&Es, LFTs, clotting, glucose
Blood gas - raised lactate +/- metabolic acidosis
Blood cultures
Necrotising fasciitis mx
Urgent broad spectrum antibiotics
Resuscitation IV fluids
Urgent surgical debridement, with a relook in 24-48 hours
Transfer to ITU
Reconstructive surgery might be needed after initial debridement → plastic surgery services
Staphylococcal scalded skin syndrome
Severe desquamating rash that primarily affects infants
Staphylococcal scalded skin syndrome pathophysiology
Occurs due to the production of an exfoliative exotoxin by staph aureus
The exotoxin splits the epidermis in the granular cell layer, specifically targeting desmoglein 1
Staphylococcal scalded skin syndrome clinical features
Superficial fluid-filled blisters, often leading to erythroderma (erythema affecting over 90% of the body surface)
Desquamation (peeling of the epidermis) occurs, with a positive Nikolsky sign
Perioral crusting or fissuring is frequently observed, with oral mucosa usually remaining unaffected (contrasts with TEN)
Fever and irritability due to underlying infection
