Dermatologic Emergencies History



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Dermatologic Emergencies
History

It is important to establish the onset of the first lesion. The location and description of the first lesion may be helpful in determining the cause of the rash. Then the pattern and distribution of subsequent lesions should be established. Are the lesions transient, do they migrate? It is also important to ask about blisters, vesicles, discharge, ulcerated and weeping areas. It is also important to determine whether or not the rash is itchy. This can be followed by a general medical history followed by exposures, travel, sexual history and immunization history. Finally, enquire about meds including otc and alternative meds and allergies

Physical Exam


Assess vitals

Examine the rash: examine in good light, disrobe patient



Distribution: Generalized vs Localized

Generalized rashes: usually secondary to internal/systemic exposure- drugs, viruses

Localized: local exposure (however some systemic illnesses manifest as local rashes i.e. lupus, HSP)

Pattern- location, symmetry, configuration

Anatomical location – scalp, face, mouth, trunk, axilla, perineum, limbs, palms and soles

Symmetry (systemic exposure) vs Asymmetry (local exposure)

Configuration – relationship of lesion to other lesions


Types of Primary lesions

Macule flat circumscribed discolored lesion <1cm

Patch flat, circumscribed discolored lesion >1cm

Purpura flat non-blanching discoloration of skin

Abscess tender erythematous fluctuant nodule

Nodule raised palpable solid nodule <1cm

Tumor raised palpable solid nodule >1cm

Wheal transient edematous papule/plaque w/ erythema

Vesicle thin walled circumscribed blister <5mm

Bulla thin walled circumscribed blister >5mm

Pustule vesicle with pus

Papule raised solid palpable lesion < 1cm

Plaque raised solid palpable lesion > 1cm


Secondary lesions: scar, erosion, excoriation, fissure, ulcer, telangiectasia
Diagnostic Tests- in Tintinalli but not that practical

-KOH test- place lesion on slide with 20% KOH and examine for hyphae

-Scabies and Lice- scrape specimen onto slide, add drop of mineral oil and examine under microscope

-Tzanck smear: unroof blistering lesions (HSV)

-Woods light: UV @ 365 nm : Erythrasma – red Tinea Versicolor – green/yellow



GENERAL TREATMENT MEASURES

  1. If its wet- dry it. If its dry, wet it

  2. Oral steroids- urticaria, angioedema, toxicodendron dermatitis

    1. Use in caution in diabetes, PUD, immunodeficiency and some psychiatric disorders

  3. Topical steroids – 7 groups based on vasoconstriction. Fluorinated are stronger, but avoid in pregnancy. Group 7 is weakest i.e. 1 and 2.5% hydrocortisone cream and group 1 is strongest i.e. betamethasone. clobetasol

4) Oral antihistamines

5)Antimicrobial agents – topical vs oral



    1. Antibacterial

    2. Antifungal- clotrimazole, miconazole, ketoconazole

    3. Antivirals – acyclovir

    4. Anti-infestation – premethrin, lindane (don’t use in small kids, may cause neurotoxicity)



10 Life Threatening and Serious Skin Disorders


1) ERYTHEMA MULTIFORME - Definition: hypersensitivity reaction with immunoglobulins and complement component deposition in the cutaneous microvascular. Spectrum of disease: minor (localized papules) to major (generalized vesiculobullous lesions and mucous membrane erosions)

Who gets it: More common in males, most common age 20-40

What causes it:1) Idiopathic

2) Infections: Viral- many viruses but HSVI and II are most common, also many bacterial causes- mycoplasma pneumonia is most common

3) Drugs: antibiotics and anticonvulsants

Prodrome of fever malaise, myalgia, arthralgias 1-2 weeks prior to onset. Skin burning

Characteristic lesions: Maculopapular lesions, target lesions, vesiculobullous lesions on extensor surfaces and mucosal surfaces. Centripetal spread

Minor- target lesions/ raised edematous papules, acral distribution

Major- same as minor but 1 or more mucous membranes involved. Epidermal detachment usually less than < 10% TBSA.

Mucous membrane involvement usually oral and usually not as severe as SJS/TEN



Complications: fluid and electrolyte imbalances, secondary infections

Treatment

1) Short course of prednisone 60-80mg 2) Analgesics 3) Antihistamines

4) Antibiotics

May require ICU

Close to 0% mortality with resolution at 2-4 weeks without consequence
2) Toxic Epidermal Necrolysis/SJS

Similar etiology and prodrome as EM but more likely drug related, more mucous membrane involvement (eyes, esophagus, airway, ano/genital), more likely to have central lesions, with more hemorrhagic bullae. Histiologically differs from EM


Who gets it: all ages, both genders

What causes it: 1) Idiopathic,


  1. Drugs antibiotics ( pcn, sulfa), anticonvulsants, oxicam/ NSAIDs,

  2. Infections: Viral HSV and HIV, bacterial infections

  3. Malignancies

Characteristic Lesions: Warm tender erythematous skin progresses to vesicles, bullae with mucous membrane involvement and eventual exfoliation

Nikolsky sign: touching skin adjacent to bullous lesion results in dislodgement of skin (epidermis from dermis). Large areas of denuded dermis

SJS < 10%TBSA epidermal detachment,

Between 10=30% BSA is considered overlapping SJS/TEN

TEN > 30% TBSA epidermal detachment.

Complications:

Infection

Hypovolemia

Perilabial and airway sloughing

Ocular involvement: conjunctivitis, conjunctival erosions, eye edema

Management: ICU or Burn Unit

burns protocol,

IV rehydrate,

remove offending agent.

Consider IVIG and optho consult for eye involvement

Mortality: SJS has 5% mortality, TEN 30% mortality
3) Exfoliative Dermatitis ( Erythroderma)

Erythematous rash involving 90% of the skin that progresses to diffuse exfoliation



Who gets it: all ages, more common in males ( 2:1) and age > 40

What causes it: 1) Preexisting skin disease (10-40%): eczema, psoriasis

2) Malignancies (10-40%)- lymphoma, leukemia, MML, carcinomas, paraneoplastic syndrome

3) Drugs (3-10%)

4) HIV


5) Idiopathic
Characteristic Lesion: Warm erythematous skin. Initially burning and itching that progressives to generalized exfoliation.

Complications: fluid loss, hypothermia, infections

Management: withdraw offending agent, treat underlying condition, replace fluids. May need ICU or burn unit

Mortality: 30%
4) Disseminated Gonococcal infection

Disseminated gonococcal infections follow 1-2% of GU/mucosal infections with N gonorrhoeae. Joint pain ( arthritis/tenosynovitis) with a rash

Who gets it: sexually active adults, more common in females

What causes it: disseminated N gonorrhoeae infections

Prodrome: Preceding mucosal infection followed by fever, arthralgia, tenosynovitis but may not be systemically unwell and primary infection likely absent by this time

Characteristic Lesion: 5-40 lesions- multiple papular vesicular and pustular/hemorrhagic skin lesions on extensor surfaces of wrist, palms, ankles, feet. May be petechial w/ necrotic centres.

Complications: septic arthritis ( knee most common), meningitis, endocarditis

Treatment: Ceftriaxone

Mortality: low

5)Meningococcemia

Initially maculopapular or petechial rash that rapidly progresses to prupura, bullae,DIC, shock and death caused by Neisseria Meningitidis



6) Toxic Shock Syndrome

Severe syndrome with high fever, diffuse erythroderma, mucousmembrane hyperemia, pharyngitis, GI upset associated with staph infection. Similar but rarer STSS (Strep Toxic Shock Syndrome assoc with GAS)



Major criteria

Fever: temperature >38.9°C (102°F)

Rash: diffuse macular erythroderma (sun burn) followed by desquamation: 1 to 2 wk after onset of illness, particularly of palms and soles.

Hypotension: systolic blood pressure <90 mm Hg for adults or <5th percentile by age for children <16 yr of age, or orthostatic syncope, orthostatic drop > 15mmHg

Mucous membrane hyperemia

Multisystem organ failure- 3 other systems: MSK, GI, Renal failure, ARDS, CNS

Who gets it: More common in women (90%) but can effect all ages.

What causes it: Staph infections that produce the exotoxin TSST-1 Previously more common in tampon users. Menstrual related TSS remains somewhat common. Other causes include diaphragms, sponges, nasal packing, body piercing, post op

Prodrome: malaise, myalgia, headache, n&v, diarrhea.

Complications: numerous

Treatment

Stabilise and remove potential sources of infection

anti-staph agents suggested but do not alter course of disease (decrease recurrences)
7) Staph Scalded Skin Syndrome

Staph producing exotoxin (exfoliatin) that cleaves skin within epidermis. More superficial then TEN



Who gets it: mostly kids under 5

What causes it: staph exotoxins

Prodrome: clinically occult staph infection of eyes, naso pharynx or umbilicus

Characteristic lesions: Begins around the mouth and leads to erythematous skin (stage 1) followed by exfoliation (stage 2, day 2) and with desquamation and bullae (stage 3 on days 3-5). Nikolksy positive

Treatment: Penicillinase resistant antibiotic (Clox or Vanco), fluid replacement
8) Bullous disease

Pemphigus Vulgaris- generalized mucocutaneous autoimmune blistering eruption. Begins as clear flaccid fragile blisters. Nikolsky positive. Autoimmune reactio to desmolgein- glue that holds epidermal cells together

95% mucous membrane involvement

Who gets it: ages 40-60 but can occur in all ages

Treatment- fluid and steroids

Bullous pemphigoid- More benign and usually self limited, disease of elderly deeper into dermis therefore blisters are more tense and larger. May begin as hives. Autoimmune reaction to collagen

Who gets it: mostly elderly

Treatment- fluid and steroids, minocycline or tetracycline, immunosuppresors if severe

Pemphigoid Gestationalis- associated with pregnancy
9) Rocky Mountain Spotted Fever

Tick born bacteria Rickettsia ricketsii, potentially fatal multisystem disease from necrotizing vasculitis



Who gets it: all ages, more common on East Coast

What causes it: see above. People in close proximity to deer, cattle, pets, rodents

Prodrome: constitutional symptoms up to 1 week after exposure. Classic triad is fever, rash with tick exposure

Characteristic lesion: discrete maculopapular blanchable lesions that first appear on wrist and ankles. Evolves into petechiae

Complications: hepatosplenomegally, meningismus, renal and hepatic failure, myocarditis. 50% mortality if untreated

Treatment: doxy
10)Angioedema

Well-circumscribed areas of edema caused by increased vascular permeability. Usually presents as acute swelling of face, extremities or genitals. Also may have abdo pain and airway compromise

Who gets it: all ages

What Causes it:

1)Meds- AceI, pcn, NSAIDs, contrast material

2)Food allergens

3)Physical agents- trauma, friction, cold

4) C1 Esterase Inhibitor Deficiency- low levels of C1-INH

a) hereditary ( autosomal dominant)

b) acquired ( autoimmune disorders and B cell malignancies)

Complications: airway compromise, unnecessary abdominal surgeries, peripheral edema. To assess for airway compromise in these patients, watch for difficulty swallowing secretions and a change in voice. Peripheral edema is not pitting, non erythematous and no hives. Usually unilateral and may be associated with minor trauma.

Treatment

If you can’t distinguish between this and anaphylaxis- treat for anaphylaxis

Antifibrinolytics (Amicar)- for acquired only

Anabolic androgens ( danasol)- increase C1- INH

Plasma derived C1-INH (Berinert)- self-administered

FFP if Berinert not available


Infestations

  1. Scabies

Definition: itchy polymorphic rash commonly of hands and feet

Who gets it: Common in children, low SES, immunocompromised

What causes it: Sarcoptes Scabiei T

Prodrome: takes 3 weeks from infection to onset of symptoms

Characteristic lesion: burrow- red linear line or S shaped with central scale


    1. Crusted scabies: large mite burden leading to less itchy but thick hyperkeratosis of hands and feet. Highly contagious

Treatment: premethrin 5 % or lindane 1% lotion left on overnight, wash clothes in hot water, treat contacts and repeat treatment in 1 week


  1. Lice

Definition: pediculosis capitis = head lice, pediculosis corporis = body lice, pediculosis pubis = crabs)

Who gets it: same as scabies

What causes it: see above

Prodrome: Itchiness in affected area

Characteristic lesion: white nits in hair, may see lice clinging to hair shafts near scalp

Ova or nits are adherent to hair shaft and if > 1cm from skin, have likely hatched (need to remain close to scalp because they feed off blood)

Treatment: Nix (premethrin 1%) rinse for 10 min, nits can be removed with 50% vinegar solution applied to hair followed by combing with fine toothed comb

Rashes of Groin

Tinea Cruris (Jock itch)

Definition: Fungal rash involving the groin

Who gets it: all ages, more common in males

Characteristic lesion: erythema with slightly raised scaly edge, may extend to thighs but spares the penis and scrotum

Treatment: topical antifungal i.e. clotrimazole, ketoconazole. Consider polysporin to prevent bacteria super infection. Spectazole has antifungal and antibacterial properties. May require oral antifungals
Erythrasma

Infection caused by Corynebacterium minutissimum. Commonly in groin. Treated with erythromycin. Will illuminate with woods lamp



Rashes on Face and Scalp

Erysipelas and cellulitis– hot red rash on face. Erysipelas more superficial then cellulitis. Caused by GAS and staph

Treatment: Keflex

Herpes Simplex I- cold sores (herpes labialis).

Treatment antiviral or antiviral ointment ( penciclovir, Zovirax)



Herpes Zoster

May involve any of the branches of the trigeminal nerve. V1 (ophthalmic branch) with lesions of nose (Hutchinson’s sign) may have associated keratitis. Keratitis responds to ocular steroids. May also cause Ramsay Hunt syndrome (lesions in auditory canal) or Bell’s Palsy.

Treatment: antivirals (acyclovir 800mg po 5/day for 1 week, Valtrex 1 g po tid x 1 week, famvir 500mg po tid x 1 week. Refer to ophthalmology if needed

Lupus- discoid or malar rash


Tinea Capitus

Superficial infection caused by dermatophytes


Annular configuration with erythema and scaling


Treated with antifungals

If not improving think secondary infection



Rashes of Skin Folds

Candida Intertrigo

Bright red rash with satellite papules and pustules moist chronically occluded areas. Predisposing factors include antibiotics (topical or oral), steroids, immunocompromised states, obesity. Non infectious intertrigo may also be a result of irritation from moisture, heat and friction. Urine and Feces may also cause non infectious intertrigo

Diagnosis: KOH slide prep

Treatment

Topical antifungals, drying agents (Zeasorb AG), astringent agents (Burow solution), keep the area dry

Rashes of lower extremities

Lichen Simplex Chronicus

Itchy well demarcated hyperpigmented plaques. Affects ankles, shins and feet. May also affect groin. Need to rule out fungal infections

Treatment; stop the itch and high potency steroids. Warn pt that it will take a long time to go away
Erythema Nodosum

Inflammatory eruption of subcutaneous fat (panniculitis)

Tends to affect the shins

Poorly demarcated warm erythematous nodules

Multiple etiologies –NODOSUM

NO- no obvious cause (idiopathic) most common

D- drugs sulfonamides, ocp, penicillin, vaccines, bromide

O- oral contraceptive pill, pregnancy

S- sarcoidosis

U- ulcerative colitis (IBS), Behcet Disease

M- microbiology

Bacterial – strep, campy, yersinia, TB, leprosy

Fungal- Blastomycosis, coccidiomycosis, histoplasmosis

Viral- HSV, Mono



Parasites- Leishmaniasis, toxoplasmosis

Management: CBC, blood cultures, throat swab if symptomatic, urine HCG, CXR for sarcoid. Should resolve on own.
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