Cutaneous reaction patterns Flashcards
Erythema multiforme
Cuteneous hypersensitivity reaction
Causes: viral infections most common (HSV in 50%, mycoplasma, others). Drugs (NSAIDS, Sulfa drugs, Antiepileptics, Antibiotics)
Clinical features of erythema multiforme
Arises after HSV lesions have crusted or resolved
Abrupt onset of target lesions
Hands, feet and other acral sites
Prodrome rare
Non- toxic
Erythema multiforme management
Supportive care for mild disease : topical corticosteroids, pain management
Sever mucosal disease: prednisone can be used , ophthalmology consult for ocular involvement
Exanthematous Drug Eruption
AKA morbilliform drug rash
Most common drug reaction (can occur with any drug, most common antibiotics, anticonvulsants)
Idiosyncratic delayed (type 4) immune reaction
Clinical features: multi pink macules and barely palpable papules
Starts on face and trunk then spreads to extremities
Pruritic
Fever and mucosal involvement are typically absent
Course: onset 2-14 days after starting medication, subsequent occurences have faster onset, can start even after finishing treatment (AB)
Exanthematous Drug Eruption Treatment
Discontinue culprit drug if possible
Supportive care for pruritus (oral antihistamines, topical corticosteroids)
REsolution: spontaneously resolves in 1-2 weeks, can resolve even with continuation of drug
Lab results of Exanthematous Drug Eruption
Complete blood count
WBC normal (eosinophils are high) H/H and platelts normals
Liver panel AST and ALT are high, alk phos and bilirubin are normal
BUN and creatinine normal
DRESS:
Type 4 hypersensitivity, more common in adults, later onset 2-8 weeks after drug initiation
Causes: antiepileptics, sulfonamides, minocycline, allopurinol, antiretrovirals
Exanthematous Drug Eruption Clinical features
Cutaneous involvement: most commonly morbilliform other cutaneous patterns sometimes seen
Facial edema , lymphadenopathy, fever
Clinical features of DRESS
Most common organs involved
Liver: elevated transaminases
Hematologic: eosinophilia, atypical lymphocytes
Kidney: mild nephritis
Less commonly involved: heart, lungs, brain , GIT
Treatment of DRESS
indentify and stop the culprit drug
Mild cases treated with supportive care (topical corticosteroids, oral antihistamines)
Severe cases (systemic corticosteroids, may require hospitilaztions)
Prognosis and course of DRESS
10% mortalitly
slow resolution over weeks or months
Autoimmune disease may develop later (autoimmune thyroditis, diabetes mellitus, autoimmune hemolytic)
Urticaria
20% of people will have urtcaria Patho physiology (release of histamine, bradykinin, LT C4, PG D2, other vasoactive)
Most commonly type 1 IgE- mediated
Causes of urticaria
Idiopathic
Most commonly identified cause is URI
Other causes: other infections, drug allergies, food allergies
Clinical features of urticaria
Classical lesion is wheal
individual lesion last under a day
Can last up to 6 weeks
Angioedema
treatment H1 antihistamines (Loratidine,certizine, fexofenadine), Sedating H1 anti histamines (diphenhydramine)
Prednisone may help sever cases
Angioedema dn anaphylaxis require emergent care
SJS/TEN
hypersensitivity reaction
Causes: infections more common in kids (viral and myco)
Meds: NSAIDs, sulfa drugs, alloprinol, antiepileptics, antibiotics, antiretrovirals
Malignancy and idiopathic
Risks: female, HIV, SLE, malignancy
Prodrome: occurs 1-14 days prior to cutaneous eruption, flulike illness (fever, malaise, pharyngitis, rhinitis, cough, headache, myalgias, arthralgias, anorexia, nausea, vomiting)
Starts as painful red macules and patches, rapidly evovles into blistering and necrosis
Affects skin and mucosa, Ocular nasal oral and or genital
SJS/TEN systemic involvement and management
Acute: dehydration, malnutrition, pneumonitis, GI bleeding, sepsis
Mortality: SJS: 1-3%, TEN: 25-35%
Long term complications: mucocutaneous scarring, blinding, strictures, sicca syndrome
management: requires inpatient hospital care with multidisiplinary approach, maintain fluid and electorlyte balance, discontinue drug, pain management, meds: corticosteroids, IVIG
vasculitis
inflammation and destruction of blood vessels, classified by size of vessel
leukocytoclastic vasculitis: AKA hypersensitivity vasculitis
Small messel vasculitis of skin with predominantly PMNs, affects children and adults
Approximately men=females
causes: 50% are idiopathic, Upper respiratory infection Group A strep infection, hep B and C HIV, drugs (Abs and NSAIDs), autoimmune disease (Rheumatoid arthritis,SLE, IBD), malignaancy
Clinical features: palpable purpura is characteristic, systemic involvement (fever, joint paain and swelling, GI bleed, renal involvement, cardiopulmonary involvement)
Prognosis: Good if skin limited, self resolves, chronic relapsing course in some, can be potentially fatal if systemic involvement
Treatment: supportice care (analgesics, rest and elevatin) treatment for more severe cases (corticosteroids, colchicine, dapsone, immunosuppressives )
henoch schonlein purpura
subtype of leukocytoclastic vasculitis
Most common in children (peak 2-11 years old)
More common in males
Hallmark shin finding=palpable purpura on butt and legs,
Systemic involvement: arthritis, and arthralgias, GI (nausea vomit and pain, GI bleed, intussusception), nephritis, Rare-testes, lung and heart brain
Skin eruption resolves over 2-4 weeks, nephritis can develop up to 6 months later, even after skin eruption has resolved
Systemic involvemnet can cause longer lasting or permanent complications
Treatment and coarse: supportive care for pruritus (oral antihistamines, topicla corticosteroisds )
NSAIDS for pain, prednisone for sever cases
