15 - Emergency Dermatology Flashcards
What is the essential general management for all dermatological emergencies?
- Full supportive care
- Withdrawal of precipitating agents e.g drugs
- Management of complications
- Specific treatment
What is the difference between urticaria and angiooedema?
Urticaria: Wheals (hives) due to swelling in dermis that raises the epidermis (superficial). They last a few minutes to 24 hours and are often very itchy and can burn
Angioedema: Swelling deeper in the skin or mucous membranes. Involves dermis and subcutaneous tissues. Resolves within 24 hours. Can be itchy but often asymptomatic
What is the pathophysiology of urticaria?
Local increase in permeability of capillaries and small venules due to inflammatory mediator release, usually histamine from mast cells but also prostaglandin and leukotrienes
Release of histamine due to immunological (chronic urticaria) or non-immunological causes (acute urticaria)
If bradykinin is also released with histamine this causes angioedema with the urticaria
What are the different classifications of urticaria and what causes them?
Acute (External factor activates mast cells)
- Allergies to food, medications or animals
- Contact e.g latex, stinging nettles
- Medications
- Viral infections
- Dermatographism
Chronic (Autoantibodies target mast cells)
- Chronic idiopathic urticaria
- Chronic inducible urticaria e.g sunlight, exercise, emotions
- Autoimmune urticaria e.g SLE
Why is acute urticaria dangerous?
If allergic urticaria can turn to anaphylactic shock, asphyxiation and drath
What is the typical distribution of urticaria and angiooedema?
Urticaria: generalised, anywhere on the body
Angiooedema: usually localised to the face (particularly eyelids), hands, feet and genitalia. It may involve tongue, uvula, soft palate, larynx.
How is acute urticaria diagnosed?
- Anyone with history of wheals that resolve within 24 hours with or without angioedema
- Can do skin prick tests or radioallergosorbent tests (RAST) if suspect the cause is a drug/food allergy
How is acute urticaria managed?
- Identify and avoid triggers e.g foods, NSAIDs
- Give non-sedating antihistamine every day for six weeks e.g Cetirizine or Fexofenadine
- If acute severe and has angiooedema give above plus short course of oral corticosteroids e.g prednisolone
- Use fan, cool flannel or calamine lotion to help itch
- If itch affecting sleep give chlorphenamine at night
How is anaphylaxis managed?
- Adrenaline
- Fluids
- Corticosteroids
- Antihistamine
If a patient with acute urticaria has been upped 4 times to the maximum dose of Cetirizine and is still having issues they can be referred to secondary care. What treatment options can secondary care offer?
- Anti-leukotrienes such as montelukast
- Omalizumab, which targets IgE
- Cyclosporine
- Refer to psychologist if chronic
- Consider rheumatology referral if chronic as could be due to SLE or small-vessel cutaneous vasculitis
What is the pathophysiology and presentation of erythema nodosum?
Presentation: Tender red nodules (lumps) usually on both anterior shins. As they resolve they look like bruises.
Pathophysiology: Inflammation of the subcutaneous fat (panniculitis) due to a hypersensitivity reaction
What are the causes of erythema nodosum?
- Idiopathic (50%)
- Chronic diseases e.g IBD, sarcoidosis, lymphoma, leukaemia
- Streptococcal throat infections
- TB
- Pregnancy
- COCP
- Abx containing penicillin
- Sulfasalazine
What investigations are done if you suspect erythema nodosum?
Diagnosis on clincal presentation but do investigations to find a cause
- ESR/CRP: for infection
- FBC: look for haematological malignancy
- Throat swab and antistreptolysin O titre (ASOT)
- CXR: look for TB, sarcoidosis, lymphoma
- Faecal Calprotectin: IBD
How is erythema nodosum managed?
- Find and manage underlying cause
- Reassure will resolve spontaneously usually within 6/52 with rest and NSAIDs
- Oral steroids can help resolve quicker if severe or chronic
- Refer to secondary care if not resolved after 6/52
How does erythema multiforme present and what is the pathophysiology?
Presentation: Widespread, itchy, erythematous rash with target lesions (red rings within larger red rings with darkest red in centre). Mucosal involvement absent or limited to one mucosal surface (lips)
Other symptoms of mild fever, stomatitis, muscle and joint aches, headaches and general flu-like symptoms.
Pathophysiology: Hypersensitivity reaction usually to herpes simplex virus. Can be due to mycoplasma pneumonia
How is erythema multiforme managed?
- If unknown cause need to do CXR for Mycoplasma Pneumoniae
- Usually self-resolves within 1-4 weeks but can recur with coldsores
- If affecting oral mucosa and severe may need IV fluids, analgesia and steroids
What is this?
Erythema Migrans - think Lyme Disease
Eczema can have secondary infections due to breaks in the skins barrier. What are the two main secondary infections that can occur and how do they appear?
S.Aureus Infection: Crusty, oozing rash with associated erythema. Avoid abx if systemically well, just carry on with emollients and steroids
Eczema Herpeticum: Punchout erosions, vesicles, crusted papules all due to Herpes Simplex Virus. Needs immediate hospitalisation
What is the typical presentation of eczema herpeticum?
- Widespread, painful, grouped vesicular rash with crust and punched out erosions
- Systemically unewell with fever, malaise, lymphadenopathy
- If there is a secondary bacterial infection on top there can be cellulitis and impetigo
What is the investigations and management of eczema herpeticum?
Ix:
- Clinical diagnosis of pt with atopic dermatitis and classic rash
- Viral and bacterial swabs of blisters
Mx:
- Immediate hospital admission
- Prompt oral aciclovir or IV if too unwell.
- Oral antibiotics (Flucloxacillin) if secondary bacterial infection
- Refer to opthalmologist if near eye
What is necrotising fascitis and why is it a dermatological emergency?
Rapidly spreading infection of the deep fascia. Bacteria multiply and release enzymes that cause thrombosis in the blood vessels and cause secondary tissue necrosis
Will continue to spread if left untreated
Mortality of up to 75%
What are the causes of necrotising fascitis?
An opening in the skin that allows bacteria to enter the body e.g cut/graze, or a large wound due to trauma or surgery
Bacteria like Group A Haemolytic Strep (S.Pyogenes), MRSA, Clostridium Perfringens and other aerobic/anaerobic bacteria can get it and multiply
What are some risk factors for necrotising fascitis?
- Abdominal surgery
- Comorbidities e.g diabetes, malignancy
- Immunosuppression
- 50% of cases in healthy individuals
How does necrotising fascitis present?
- Symptoms within 24 hours of injury
- Severe pain that is getting worse
- Fever, tachycardia and flu-like symptoms
- Erythematous, blistering, necrotic skin
- Subcutaneous emphysema (crepitus)
If left to day 4/5 will go into toxic shock and become hypotensive
What investigations should you do if you suspect necrotising fascitis?
Bloods: FBC, U+Es, CRP, CK, clotting, LFTs
Blood culture, deep tissue biopsy and MRSA sensitivity: to guide abx choice
Imaging (may help): X-Ray may show soft tissue gas but absence does not exclude diagnosis
What is the management for necrotising fascitis?
- Urgent referral for immediate extensive surgical debridement
- High dose IV abx depending on organism
What tool is used to aid the recognition of Necrotising Fascitis and what parameters does it involve?
Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC)
Score of 6 or more should prompt you to refer urgently
How would you describe a rash that occurs in acute meningococcaemia?
Non-blanching purpuric rash on trunk or extremities that can progress to ecchymoses, haemorrhaic bullae and tissue necrosis
Can start as blanching maculopapular rash
What is the presentation of staphylococcal scalded skin syndrome?
- Usually occurs in under 5’s starting with fever
- Starts as generalised patches of erythema making skin look thin and wrinkled.
- Then after 24-48 hours turns to bullae which burst and appear like scalded skin
- Nikolsky sign ie gentle strokes result in exfoliation
- Perioral crusting
What are the investigations and management for SSSS?
Ix:
- History and exam
- Blood culture
- Tzanck smear
Mx:
- Admission and IV antibiotics e.g penicillinase-resistant penicillin, fusidic acid or erythromycin
- Fluid and electrolyte balance as prone to dehydration
- Skin care e.g petroleum jelly
- Paracetamol for fever and pain
What is the commonest type of drug reaction and how does it present?
Morbilliform Drug Reaction
Generalized erythematous macules and papules ± mild fever, within 1–3wks of drug exposure. No mucosal involvement.
Drugs: Amoxicillin, Cephalosporins, anti-epileptics, sulphonamides, allopurinol, thiazides
What is the difference between TEN and Steven-Johnson syndrome?
Spectrum of the same acute disorder. Disproportional immune response to a drug causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin with mucosal involvement
TEN: Usually more than 10% of total body surface area and drug induced. Full thickness epidermal necrosis with subepidermal detachment on histology
SJS: Usually less than 10% of total body surface area and drug or infection induced
How can you distinguish SJS/TEN from SSSS?
How can you distinguish SJS from Erythema Multiforme as they both form target lesions?
SJS is mucocutaneous necrosis with at least two mucosal sites involved but EM is one sire
What are some of the drugs and infections that can trigger SJS/TEN?
Certain HLA types are at risk
Drugs: Antiepileptics, Penicillins, Cephalosporings, Allopurinol, NSAIDs
Infections:
Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV
How do SJS and TEN present?
Both have prodromal flu-like symptoms and URT symptoms 2-3 weeks after starting new drug then a few days later develop rash and mucosal involvement of at least 2 surfaces:
SJS: Painful erythematous macules evolving to form target lesions. Severe mucosal ulceration of ≥2 surfaces eg conjunctivae, oral cavity, labia, urethra
TEN: Widespread painful erythema followed by necrosis of large sheets of the epidermis
What are the complications of TEN/SJS?
- Secondary infection and sepsis
- Dehydration
- Shock and kidney failure
- Electrolyte imbalance
- Permanent skin damage and mucosal damage due to scarring
- Visual complications
- DIC and VTE
How are SJS and TEN diagnosed and managed?
Ix:
- Skin biopsy to distinguish from SSSS. Show full thickness epidermal necrosis with miniml inflammatory cells
- FBCs, U+Es, LFTs to monitor for complications
Mx:
- Recognise early, stop drug and transfer to HDU/burns unit for supportive care
- Nutritional care and fluid/electrolyte balance
- Analgesia
- Topical antiseptics e.g silver nitrate
- Daily visits by ophthalmologists
- ?Steroids, immunoglobulins, immunosuppressants
What is the definition of erythroderma and how does the patient present?
Widespread reddening of the skin that can turn into exfoliative dermatitis involving at least 90% of the skin
Presentation: Inflammed, oedematous, scaly skin with patient being systemicallu unwell with lymphadenopathy and malaise. Can start as morbilliform eruption
What are some of the causes of erythroderma?
- Previous skin disease like eczema, psoriasis
- Drugs: sulphonamides, gold, sulphonylureas, penicillin, allopurinol
- Malignancies e.g lymphoma
- Idiopathic
How is erythroderma managed?
- Treat underlying cause
- Stop any precipitating drug
- Emollients and wet skin wraps to maintain skin moisture
- Topical steroids for inflammation
- Fluid and electrolyte balance
What are some of the complications of erythroderma?
- Secondary infection
- Fluid loss and electrolyte imbalance
- Hypothermia
- High-output cardaic failure
- Capillary Leak Syndrome
