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• Pruritus & Urticaria • Drug Eruptions • Other Common • Recognize & Refer Nishit Patel, M.D. CONFLICTS OF INTEREST

• No Relevant Conflicts

Special Thanks to Leigh Ann Scalf, MD OBJECTIVES

• Learn to diagnose and manage pruritus without a primary eruption • Diagnosis and treatment of urticaria • Identify features of common drug eruptions • Identify drug rashes that constitute dermatologic emergencies OVERVIEW

Pruritus = “Itching”

Urticaria = “” PRURITUS WITHOUT PRIMARY LESIONS

In other words…”just itching and scratching.”

So, now what?? COMMON PRESENTATION

 Butterfly area over scapulae often spared because the patient cannot reach the area to scratch.  Beware: some patients are very flexible and CAN reach this area!! “BY THE BOOK”

The million dollar work-up can be found in any text book

But…. PRACTICAL PRURITUS WORK UP

 CBC (anemia)  LFT (Hepatic dysfunction)  BUN/Cr (Renal dysfunction)  TSH (Hypothyroidism)  ANA ()  CXR (Cancer)  All “age appropriate” cancer screenings  Get a complete “ROS” URTICARIA GROUPING OF URTICARIA

• Acute Urticaria (<6 wks) • Chronic Urticaria (>6 wks) • Cause • Cause • 50% idiopathic/unknown • 60% - idiopathic/unknown, • 40% Upper respiratory tract autoimmune, infection related infections • 35% • 9% drug reaction • 5% urticarial

• 1% food related • Prognosis – 50% of patients with • Prognosis – Excellent, usually resolves chronic urticaria will resolve in 1 year. within days to weeks Can be very difficult to manage. URTICARIA /

Pruritic wheals Individual lesions disappear within 24 hours. DERMATOGRAPHISM

https://upload.wikimedia.org/wikipedia/commons/thumb/4/42/Dermatographic_urticaria.jpg/1200px- Dermatographic_urticaria.jpg URTICARIA / ANGIOEDEMA

May be associated with: Angioedema  with bronchospasm, laryngospasm, or hypotension URTICARIA / ANGIOEDEMA

If the patient gives a history of anaphylaxis (throat swelling, difficulty breathing):

Give Rx for Epi-Pen (Twin Ject) and “Emergency Plan” Refer to Allergist URTICARIA / ANGIOEDEMA

Immunologic Most commonly associated with and beta- lactam antibiotics Nonimmunologic  and NSAIDS are the most common causes. Also caused by radiocontrast. (*Pre-testing does NOT exclude the possibility of an anaphylactoid reaction to radiocontrast.) URTICARIA / ANGIOEDEMA

 ACE inhibitors can cause angioedema African Americans at nearly 5 times greater risk than caucasians Lisinopril and enalapril > captopril Blockade of kininase II by ACE inhibitors may increase the tissue kinin levels, thus enhancing urticarial reactions and angioedema. OTHER “URTICARIAS”

• Physical Urticaria • “EMPHASIS ON TREATMENT…” URTICARIA • Anti- (non/low-sedating), over-the-counter • Loratidine (Claritin), (Zyrtec), (Allegra), (Xyzal) • Anti-Histamines (non/low-sedating), prescription only • Desloratidine (Clarinex)  5mg daily (AM or PM) • Anti-Histamines (sedating, use at night only) • Diaphenhydramine ()  25mg (at bedtime) • * (Atarax)  10mg/25mg/50mg (at bedtime) • * 10mg/25mg (at bedtime) • Additional Tx Considerations: • *Anti-Histamines (H2- Blockers), Prednison, * (Singulair), (Xolair)

* off label usage EMPHASIZE TRIGGER AVOIDANCE

• Avoid NSAIDs (non-steroidal anti-inflammatory medications Aspirin, (Motrin), Aleve (naproxen), Meloxicam, Celebrex, etc. • Avoid triggers of mast-cell degranulation ( release) • Medications = (narcotic pain medications), contrast dyes (radiology imaging), medications, polymyxin B sulfate ( in topical antibiotics) • Heat/friction • OTHER WORKUP TO CONSIDER

• CBC • C3, C4 • CMP • C1-Inh (qualitative/quantitative) • ESR • • ANA C1q • • TSH Anti-C1q • CH50 • IgE PEARLS

1) Pruritus without primary lesions should be worked up to rule out any underlying etiology. 2) Urticaria: Individual lesions disappear within 24 hours. 3) Immunologic urticaria: Most commonly associated with penicillin and beta-lactam antibiotics 4) Non-immunologic urticaria: Aspirin and NSAIDS are the most common causes. 5) are the mainstay of treatment for urticaria. Drug Eruptions DRUG ERUPTIONS, OVERVIEW

Extremely diverse Almost any drug may be capable of producing a reaction. A certain drug may also cause several different reaction patterns in different patients. IN GENERAL… DRUG ERUPTIONS

Most occur within days to weeks after beginning the offending agent

Occasionally a reaction begins after long-term use of a particular drug

**MORBILLIFORM (AKA: -LIKE, MACULAR AND PAPULAR, SCARLETINIFORM) ERUPTIONS ARE THE MOST FREQUENT OF ALL CUTANEOUS REACTIONS TO DRUGS

“MORBILLIFORM” OR “SCARLETINIFORM” REACTIONS Pruritus common Usually occur with in first 2 weeks of treatment Usually start proximally (groin/axillae), then generalize within 1-2 days PATHOGENESIS

NON-IMMUNOLOGIC IMMUNOLOGIC *Drug reactions : -not simply drug -may result from variations in drug metabolism, immune status, coexistent diseases, and other co-administered medications. EXANTHEM-LIKE ERUPTIONS

Most common culprits:  Sulfonamides Carbamazepine Hydantoins Allopurinol Gold “EMPHASIS ON TREATMENT…”

“Simple exanthems” (skin only!) Supportive care stop offending med, topical steroids, antihistamines FIXED FIXED DRUG ERUPTION

 Adverse reaction to an ingested drug  Usually solitary  Plaque, bulla, or erosion  Upon rechallenge, FDE occurs at identical site within hours of ingestion FIXED DRUG ERUPTION

Usually asymptomatic May be pruritic or burning Painful if eroded Post-inflammatory pigmentary alteration (PIPA) remains between flares – usually . MOST COMMONLY IMPLICATED DRUGS:

Phenolphthalein Antimicrobials  Tetracyclines  Sulfonamides Psychoactive agents Anti-inflammatory agents OCPs  Pseudoephedrine (Sudafed) FIXED DRUG ERUPTION

Treatment: identify and stop offending drug Non-eroded: potent topical steroid Eroded: bacitracin or silvadene PIPA (dermal melanin) does NOT respond to hydroquinone therapy GOOD GONE BAD!

Occasionally, exanthem-like eruptions are associated with: Interstitial nephritis Hepatitis Lymphadenopathy

So, don’t forget to do a thorough history and physical! “GOOD RASH” PEARLS

1) Drug reactions are DIVERSE. 2) Certain drugs are more likely to produce certain reactions. 3) The most common drug reaction is a moribilliform eruption. 4) Simple “skin-only” exanthems require supportive care…stop offending medication, topical steroids, antihistamines. 5) There can be systemic involvement. *Do a thorough history and physical!! 6) Fixed drug eruptions recur in the same location upon re- exposure to the offending agent OTHER COMMON RASHES Image from: https://www.merckmanuals.com/-/media/manual/professional/images/4812-pityriasis-rosea-herald-patch-public- -image-library-high.jpg?la=en&thn=0

• A self-limited papulosquamous eruption that is occasionally pruritic • Seen mainly in adolescents and young adults, favoring the trunk and proximal extremities

• Individual lesions are usually oval in shape and their long axis is oriented along the lines of cleavage

• Less common variants include inverse, vesicular, purpuric and pustular PITYRIASIS ROSEA

 Pathogenesis  ? Viral etiology  Focus on human herpesvirus-7 (HHV-7) and, less so, on HHV-6  Some studies have shown no difference in prevalence of DNA from HHV-6 or HHV-7 in pts w PR  Support for viral etiology: prodromal symptoms experienced by some, clustering of cases, and almost complete absence of recurrent episodes, suggesting immunologic defense against infectious agent  Epidemiology  Female > male  Affects otherwise healthy adolescents and young adults  Typical eruption lasts 6-8 weeks, then resolves spontaneously  May occasionally last > 5 months  ? Slight seasonal variation PITYRIASIS ROSEA - CLINICAL

 “Herald Patch”  Large skin- to pink- to salmon-colored patch or plaque with slightly raised advancing margin  Center – fine scaling (like other lesions)  Margin - larger, more obvious trailing collarette of scale with the free edge pointing inwards  Often on trunk, precedes other lesions by hours to days  Seen in ~50% of cases

 ~5% of pts experience a mild prodrome PITYRIASIS ROSEA - CLINICAL

 Other lesions  Similar to herald patch but smaller  Rapidly appear, usually on trunk and proximal extremities  Long axis following Langer's lines of cleavage  “Christmas tree” pattern on back  More papular and hyperpigmented in pts w/ skin of color  May be pustular initially  Face, palms and soles usually spared PITYRIASIS ROSEA - CLINICAL

 Pruritus in ~25% of pts  Atypical forms of pityriasis rosea  Inverse - axillae and inguinal areas; sometimes the face

 More common in younger children and in those with darkly pigmented skin  Other: urticarial, multiforme- like, vesicular, pustular and purpuric variants PITYRIASIS ROSEA - CLINICAL

 Treatment  Patient education and reassurance  Pruritis

 Counterirritant lotions

 Low- to medium-strength topical  Severe cases

 UVB – reduces severity of PR but not duration or pruritus

 Antihistamines

 Short course oral steroids

ERYTHEMA ANNULARE CENTRIFUGUM (EAC)

• Erythema Annulare Centrifugum (EAC) • Applies to a broad spectrum of clinical findings, “default” diagnosis • Peak age: 40s • No known gender difference • Can last days-decades • Possibly represents a reaction pattern or to one of many Ag’s • , candida, other fungi, viruses (pox, EBV, VZV, HIV), drugs, food, pregnancy, AI endocrinopathies, hypereosinophilic syndrome, neoplasms CLINICAL

• Initial lesions: firm, pink that expand centrifugally & develop central clearing • Can grow to >6cm over 1-2 wks • Superficial gyrate erythema: • Minimally elevated • Central trailing scale (sometimes vesicles @ outer edge) • +/- pruritus • Deep gyrate erythema: • Advancing edge elevated & usually no associated scale • Majority are non-pruritic • No scarring, but can get PIH • Lesions last weeks-months • No systemic sx’s • Rare on palms, soles, scalp, mucous membranes EAC DIFFERENTIAL AND TREATMENT

• DDx: , annular , annular urticaria, allergic urticarial eruption, cutaneous lymphoid hyperplasia, lymphoma cutis, linear IgA bullous dz, Sjogren’s, LE

• TREATMENT: • Resolves if underlying d/o is responsible & treated • Topical steroid to advancing edge • Tacrolimus, calcipotriol, oral metronidazole, etanercept

STASIS DERMATITIS

• Disease of adults • Eruption of lower extremities • Can see concomitant , brownish hyperpigmentation • Most common site is medial malleolus • Pathogenesis: • Venous htn →distension of capillaries → incr permeability → fluid, proteins, RBCs in tissue → protein (fibrin) around blood vessels inhibit O2 diffusion; activation of PMNs & Mφ; release of inflamm mediators; plt accum (focal thrombosis) → fibrosis & tissue remodeling • Treatment: leg elevation, support stockings, topical steroids, Aluminum acetate compresses • Higher risk of ACD sensitization with topical antibiotic application STASIS DERMATITIS

• Complicating pathogenic factors: contact (58%-86%) and irritant dermatitis

• Lipodermatosclerosis- progressive induration occurs over years- inverted wine bottle appearance

• Tx: compression stockings/ bandages; exercise calf muscles; venous surgery; wound dressings, topical steroids and emollients LOCALIZED (PRETIBIAL) MYXEDEMA: CLINICAL • Erythematous to skin- colored, sometimes purple– brown or yellowish, waxy indurated nodules or plaques with classic peau d’orange • Painful, pruritic • Location: anterolateral aspect of the lower legs or feet • Non-pitting • Hypertrichosis and hyperhidrosis LOCALIZED (PRETIBIAL) MYXEDEMA

• Induration of the shins due to mucin deposition • Mucin production stimulated by a serum factor unrelated to thyroid-stimulating Ig’s

• Associated w/ hyperthyroidism • Especially Graves disease (1-5% of pts w/ Grave’s) • W/ exopthalmous (25%) • May also appear in hypothyroid state following treatment of Graves LOCALIZED (PRETIBIAL) MYXEDEMA

 DDx  LSC, hypertrophic LP, lymphedema, obesity-associated lymphedematous mucinosis, and elephantiasis

 Tx  Corticosteroids (topically or intralesionally)  Especially if symptomatic  Other: plasmapheresis, gradient pneumatic compression, IVIg, and octreotide  Treating the hyperthyroidism does NOT improve the cutaneous lesions  May clear spontaneously (after an average of 3.5 years) RECOGNIZE & REFER Images from: • https://www.mayoclinic.org/-/media/kcms/gbs/patient-consumer/images/2013/08/26/10/41/ds00722_im02463_r7_bullouspemphigoidthu_jpg.jpg • https://jamanetwork.com/data/Journals/DERM/11776/dob40010f1.png • https://www.dermnetnz.org/topics/bullous-pemphigoid/

• Most common subepidermal blistering disease • Affects elderly, rarely children • 90 yo’s have 300X risk of developing compared to 60 yo’s • Men>women Images from: Dermatology by Jean L., M.D. Bolognia, Joseph Jorizzo, Ronald Rapini C.V. Mosby (June 1, 2003) BULLOUS PEMPHIGOID: CLINICAL FEATURES

• Early non-bullous phase • Nonspecific, pruritus, eczematous, excoriated eruptions, urticarial lesions • Weeks to months • May be the only signs of the disease • Bullous phase • Erythematous urticarial lesions + tense vesicles/bullae on normal/erythematous skin • Symmetrical, predominately on flexural areas and lower trunk • May form vegetating plaques in intertriginous areas • resolve with PIPA, and milia rarely • Oral involvement in 10-30% Images from: • https://www.facingacne.com/wp-content/uploads/2012/01/Pemphigus-vulgaris.jpg • https://i.pinimg.com/originals/3f/54/b4/3f54b4e8e3e78d5c4e03b7e3d7fbaeac.jpg FOLIACEUS

Images from: https://www.dermquest.com/imagelibrary/large/10559-IMG_9023.JPG & FOLIACEUS

• Pemphigus = of IgG against keratinocyte cell surface • Results in loss of cell-cell adhesion of keratinocytes acantholysis  intraepidermal blisters • P. vulgaris and P. foliaceus • Mean age: 50-60 y/o • Men = women • 0.76 to 5 per 1,000,000 new cases per year • Higher in Jewish and Hispanic descendants of the conversos (SW USA) • 16 to 32 per 1,000,000 • P. vulgaris is more common than P. foliaceus • Except in Brazil, Finland, and Tunisia REFERENCES

 Habif: Clinical Dermatology, 4th ed. 2004 Mosby, Inc.  www.dartmouth.edu  Dermatology by Jean L., M.D. Bolognia, Joseph Jorizzo, Ronald Rapini C.V. Mosby (June 1, 2003)  Contact & Occupational Dermatology by James G. Marks, et al (January 15, 2002)  www.aad.org  Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology by Klauss Wolff, Richard. A. Johnson, Richard Suurmond  Fitzpatrick's Dermatology in General Medicine by Irwin M., Md. Freedberg (Editor), Arthur Z. Eisen (Editor), Klaus Wolff (Editor), K. Frank Austen (Editor), Lowell A. Goldsmith (Editor), Stephen I. Katz (Editor), Thomas B. Fitzpatrick (Editor)