Dermatology and Allergy in Pediatrics PDF

Dermatology and Allergy in Pediatrics PRIMARY SKIN LESIONS SECONDARY SKIN LESIONS THE ALLERGY CASCADE Understanding Allergy Types of Allergy  Antigen- Presenting Cell T-Cell...

Dermatology and Allergy in Pediatrics PRIMARY SKIN LESIONS SECONDARY SKIN LESIONS THE ALLERGY CASCADE Understanding Allergy Types of Allergy  Antigen- Presenting Cell T-Cell TH2 B-Cell Mast Cell TH1 Recto, 2005  Minutes Hours Histamine Leukotrienes Cytokines Proteases Cytokines Chemokines Immediate Reaction Late Phase Reaction DERMATOLOGI C MANIFESTATIO NS OF ALLERGIC CONDITIONS  Anaphylaxis  Multi-organ reaction, potentially fatal, caused by release of chemical mediators from mast cells and basophils  Anaphylaxis- IgE dependent  Anaphylactoid –non IgE dependent  Anaphylaxis  Acute symptoms (skin, mucosal surface or both) AND 1 of the ff: respiratory, end organ dysfunction or hypotension  2 or more of the ff occurring after exposure to a LIKELY allergen: respiratory, GI, skin/mucosal surface, hypotension Pattern  Acute – explosive onset within seconds to minutes of exposure to triggering event  Biphasic – followed by a reaction 3 to 8 hours after initial reaction (5-20% of cases)  Protracted – lasts 3 to 21 days from onset of acute reaction  Etiology  Drugs  Insect sting  Food (peanut, treenuts, fish, shellfish, egg, soy milk)  Blood products, IVIg  Work Up  Plasma Histamine (10-30 mins)  Skin Testing  Serum IgE  Management  ABCs  Epinephrine 0.01ml/kg IM every 5 to 15 mins (max: 0.3 mg)  Position (Recumbent)  Fluid Replacement (NSS)  H1 & H2 antihistamines (Diphenhydramine, Ranitidine)  B2 agonist neb  Steroids  Vasopressors (Dopamine)  Management  Glucagon for pts taking beta blockers 20kg 1mg IV  Atropine for symptomatic bradycardia  Observe for at least 24 hrs  Antihistamines & steroids for home  Urticaria  Erythematous, evanescent, edematous, pruritic papules and plaques  Individual lesions last < 24 hours  Varying size and shape  +/- angioedema  Urticaria  Blood vessels leak and leads to swelling of skin  May be caused by food or other allergens  May be triggered by non allergic causes such as heat or exercise, medications, insect bites or infections  Acute or Chronic  Classification  Acute Urticaria- < 6 weeks  Chronic Urticaria-> 6 weeks  Angioedema  Swelling in deep layers of skin (dermis, SC)  Often seen together with urticaria  Seen in soft tissues like eyelids, mouth, genitals  Acute – usually caused by medications or foods  Chronic recurrent – no identifiable cause  Hereditary angioedema (HAE) –rare, serious genetic condition including hands, feet, face, intestinal wall and airways  Does not respond to treatment with antihistamine or epinephrine Etiology  Treatment  Antihistamine -Second generation over first generation  H2 antagonist  Leukotriene Antagonist  Steroids in refractory cases GEL & COOMBS Classification of Hypersensitivity GEL & COOMBS Classification of Hypersensitivity Atopic Dermatitis  Most common skin condition in children  Causes dryness and prone to irritation and inflammation by environmental factors  May also be triggered by food sensitivity  Itching is not only histamine mediated hence anti histamine alone cannot control symptoms  Linked with asthma, allergic rhinitis or food allergy (Atopic march) Atopy is the genetic predisposition to make IgE antibodies in response to allergen exposure  Atopic Dermatitis  “Itch that rash”  INFANT PHASE - birth-2 years old - cheeks, abdomen, extensor  CHILDHOOD PHASE  2-12 years old  Flexural ADOLESCENT/ADULT PHASE - diffuse lesions with increased scaling & decreased excoriations The Allergic March  ATOPIC DERMATITIS Hanafin & Rajka (3 major, 3 minor)  MAJOR  MINOR family history of atopy keratosis pilaris (chicken skin) area of distribution elevated IgE relapsing course food intolerance pruritus predisposition to skin infection  MINOR palmar hyperlinearity xerosis (dry skin) cutaneous reactivity nipple eczema dennie morgan fold pityriasis alba dermatographism  Cutaneous minor criteria Xerosis Pityriasis alba Palmar hyperlinearity Keratosis pilaris Cutaneous minor criteria Allergic shiners Dennie Morgan Fold Atopic Dermatitis - Infant  Extensor s  Face  Trunk Atopic Dermatitis- Childhood/Adulthood Flexural Management  Hydration  Eliminate Triggers  Antihistamines  Emollients  Steroids  UV light  Antibiotics Management  Allergic Contact Dermatitis  When skin comes in contact with an allergen  Examples : laundry detergent, nickel in jewelry, poison ivy, poison oak, plastic or rubber footwear  Nummular Eczema  Coin-shaped, severely pruritic, eczematous plaques  Extensor surfaces of the extremities, buttocks, and shoulders with facial sparing  Flares are generally sporadic but may be precipitated by xerosis, irritants, allergens, or occult staphylococcal infection  Treatment: emollients, wet dressings, and potent topical corticosteroids  Adverse Reaction to Food  untoward reaction following the ingestion of a food or food additive 1. food intolerances (e.g., lactose intolerance), which are adverse physiologic responses 2. food allergies: adverse immunologic responses and can be immunoglobulin IgE-mediated or non–IgE- mediated  Most children “outgrow” milk and egg allergies, while approximately 80-90% of children with peanut, nut, or seafood allergy retains their allergy for life. ADVERSE REACTION TO FOOD  Clinical Manifestation IgE-mediated reactions: acute Non IgE mediated Reaction: delayed  Skin: urticaria, angioedema,  food allergen–specific T cells, secrete flushing cytokines that lead to a “delayed,”  GIT: oral pruritus, nausea, more chronic inflammatory process abdominal pain, vomiting,  Skin: pruritus, erythematous rash diarrhea  GIT: abdominal pain, vomiting,  Respiratory tract: rhinorrhea, diarrhea Respiratory tract nasal pruritus, sneezing dyspnea, Mixed IgE and Non IgE reaction: wheezing  chronic disorders such as atopic  Cardiovascular system: dermatitis, asthma, and allergic hypotension, loss of consciousness eosinophilic esophagitis and gastroenteritis  Diagnosis and Treatment TREATMENT DIAGNOSIS  Appropriate identification and  Medical history elimination of foods  Prick skin tests  Many food allergies are outgrown,  Serum food-specific IgE children should be reevaluated periodically  Extensively heated milk or egg in baked  Elimination diet products are tolerated by the majority of milk and egg allergic children  Regular ingestion of baked products with milk and egg appears to accelerate resolution of milk and egg allergy COMMON PEDIATRIC DERMATOLOGIC DISEASES Neonatal Skin Conditions  MILIA: - lesion is a firm cyst, 1-2 mm in diameter, and pearly, opalescent white - frequently scattered over the face and gingivae and on the midline of the palate - Exfoliate spontaneously in most infants and may be ignored  Neonatal Skin Conditions  DERMAL MELANOCYTOSIS (MONGOLIAN SPOTS): - blue or slate-gray macular lesions, has variably defined margins - occurs most commonly in the presacral - usually fade during the 1st few yr of life due to darkening of the overlying skin  Neonatal Skin Conditions  ERYTHEMA TOXICUM - benign, self-limited, evanescent eruption - lesions are firm, yellow-white, 1-2 mm papules or pustules with a surrounding erythematous flare - At times, splotchy erythema is the only manifestation - Peak incidence occurs on the 2nd day of life, but new lesions may erupt during the 1st few days as the rash waxes and wanes  Disorders Of Sweat Glands:  MILIARIA RUBRA - retention of sweat in occluded eccrine sweat ducts. - erythematous, minute papulovesicles with prickling sensation, localized to sites of occlusion or to flexural areas. Involved skin may become macerated and eroded - Treatment: cooling of the patient by regulation of environmental temperatures and by removal of excessive clothing  Seborrheic Dermatitis  most common in infancy and adolescence  Diffuse or focal scaling and crusting of the scalp, sometimes called cradle cap  greasy, scaly, erythematous papular dermatitis, which is usually nonpruritic  Seborrheic Dermatitis  Malassezia furfur is implicated as a causative agent  TREATMENT - Initial management is conservative - Persistent lesions may be treated with low-potency topical corticosteroids if inflamed and a topical antifungal - Antifungal shampoos such as ketoconazole 2% shampoo should be used cautiously as they are not tear  Psoriasis  Complex multifactorial genetic etiology  Factors contributing to disease flares: infections, trauma, physical or emotional stress  Plaque psoriasis: - most common (>80%) subtype, characterized by erythematous papules that coalesce to form plaques with sharply demarcated, irregular  Psoriasis  Plaque psoriasis: - If unaltered by treatment, a thick silvery or yellow-white scale and removal of the scale may result in pinpoint bleeding (Auspitz sign) - Koebner phenomenon: new lesions appear at sites of trauma - Nail involvement, characterized by pitting of the nail plate, detachment of the plate (onycholysis), yellowish-brown subungual discoloration  Psoriasis  Guttate psoriasis: acute eruption of many oval or round papules < 1.5 cm  TREATMENT: emollients, vitamin D analogs (calcipotriene or calcitriol), mid- to high-potency corticosteroids  Impetigo  most common skin infection in children throughout the world  2 classic forms of impetigo: nonbullous and bullous  Staphylococcus aureus is the predominant organism, May also be streptococcus  Impetigo  Nonbullous impetigo: tiny vesicle or pustule forms initially and rapidly develops into a honey-colored crusted plaque that is generally 10 % to