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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3055_Библиотеки_им_академика_М_И_Перельмана.pdf
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5. Vasculopathy. Ranges from petechiae to purpura with ulcer-
ation and atrophy. Etiologies include idiopathic thrombocy-
topenic purpura, thrombotic thrombocytopenic purpura,
hypercoagulable states, renal failure, hereditary platelet dis-
orders, scurvy, DIC, and lymphoproliferative states
(Waldenstrom macroglobulinemia, leukemias, myeloma) [5].
6. Annular erythema. Erythema chronicum migrans (ECM).
Associated with Lyme disease. An erythematous ring
around a central punctate erythematous papule (indicates
tick site) spreading outwardly with annular appearance.
Vesiculobullous
Blistering rashes with either intraepidermal or subepidermal
bullae and a background of inflammatory or noninflamma-
tory skin. Various conditions already mentioned can also
blister, including meningococcemia, contact dermatitis, vascu-
litis, erythema multiforme, and SJS/TEN [6].
Infectious
Herpes simplex virus. Grouped vesicles on an erythematous
base. Vesicles crust over as they heal.
Herpes zoster. Grouped painful/burning herpetic vesicles on
an erythematous base in a dermatomal distribution. Pain
often precedes rash (Fig. 19.7).
Coxsackie. Vesicles on the tongue or buccal mucosa, hands,
and feet, including the palms and soles. Uncommonly, the
buttocks and genitalia are involved. Vesicles are tender and
may ulcerate, but are usually not pruritic.
Autoimmune, Intraepidermal
Pemphigus vulgaris (PV). Flaccid blisters with crust and ero-
sions present. Oral involvement is common. Positive
Nikolsky sign.
A. Miceli and K. Krishnamurthy
321
Autoimmune, Subepidermal
Bullous pemphigoid. Common condition seen in the elderly.
Tense bullae that do not rupture easily. Common locations
include trunk and flexural areas (Fig. 19.8).
Noninflammatory
Porphyria cutanea tarda. Acral blisters that worsen with sun
exposure, alcohol use, and estrogen [7].
Miliaria crystallina. Numerous small superficial vesicles in
intertriginous areas or head/neck in infants caused by obstruc-
tion of the sweat glands. Can also be seen in febrile adults.
Fig. 19.7 Herpes zoster. Vesicles and crusting involving the trigemi-
nal nerve (V1 and V2) distribution
19. Rash
322
History and Physical Examination
History:
• Duration of rash: acute vs. chronic
• Description: location of rash, color, texture, symptoms
(itchy, painful, changes in color or texture, drainage, fever)
• Medical history: recent changes in health problems, recent
illnesses or hospitalizations, new medications
• Social history: recent travel, contact with plants or bodies
of water, sick contacts, pets, arthropod bites, occupation
(chemical exposures), sexual history
• Environmental changes: new products including but not
limited to perfumes, cosmetics, soaps, shampoos, deter-
gents, hair dye, nail polish, clothing components (nickel in
buttons, leather shoes, etc.)
Physical examination
• Vital signs: presence of fever, signs of hemodynamic
instability.
• Gross inspection [8]:
– Shape: Annular, round, ovoid, linear, serpiginous, targe-
toid, polycyclic (overlapping annular), arcuate (incom-
plete annular), polymorphous (many shapes)
Fig. 19.8 Bullous pemphigoid. Tense bullae on the lower extremi-
ties. Previously published in Buka B, Uliasz A, Krishnamurthy
K. Buka’s Emergencies in Dermatology. New York: Springer; 2013
A. Miceli and K. Krishnamurthy
323
– Color: erythematous, hyperpigmented/hypopigmented,
flesh-colored, red-brown, violaceous, purpuric, dusky
(dark purple/gray that suggests necrosis)
– Primary skin lesions: macules, patches, papules, plaques,
nodules, vesicles, bullae, pustules, hives or urticaria,
petechiae, purpura, furuncle, carbuncle
– Secondary skin changes: excoriations, scale, crust, ero-
sions, ulcerations, fissures, lichenification
– Distribution: generalized, central, peripheral, palms/
soles involved, flexural vs. extensor surfaces, unilateral
vs. symmetric, sun-exposed areas, intertriginous, muco-
sal involvement
– Configuration: linear/geometric (suggests outside influ-
ence), dermatomal, grouped
– Texture: soft, firm, fleshy, indurated
– Patterns: follicular, morbilliform (“measles like” a.k.a.
maculopapular), reticular (“net like”), monomorphic,
guttate (drop like)
• Diagnostic procedures:
– KOH prep: Identifies dermatophyte infection.
– Positive test: presence of hyphae (long, slender, refrac-
tile filaments that cross multiple cell walls). Tinea versi-
color is diagnosed by presence of “spaghetti and
meatballs” appearance, which represents hyphae and
spores [3].
– Scabies prep: Identifies scabies.
– Positive test: Observe mite, eggs, or feces (scybala).
Mineral oil used.
– Wood’s lamp (365 nm) [3]:
– Findings in different skin conditions:
Vitiligo: milky white appearance.
Tinea versicolor: yellow or orange glow.
Tinea capitis: Microsporum species fluoresce blue-
green, Trichophyton schoenleinii fluoresces dull
blue.
Erythrasma: coral-pink color due to Corynebacterium.
Pseudomonas: fluoresces green.
Porphyria: red-pink fluorescence of skin.
19. Rash
324
– Nikolsky sign: Positive if lateral pressure on blister
causes easy rupture of blister. This indicates an intraepi-
dermal process.
– Diascopy: Pressing on a lesion with a glass slide to see
whether or not redness blanches out. Purpura is
non-blanching.
– Skin biopsy: Rashes not responding to conventional
treatment require a biopsy. For autoimmune conditions,
two punch biopsy samples should be taken, one for
H&E and one for direct immunofluorescence (DIF).
• Treatment: Please see diagnostic and treatment Figs. 19.9,
19.10, 19.11, 19.12, 19.13, and 19.14.
Clinical Pearls
• A broad differential diagnosis based on a rash’s reaction
pattern is helpful in diagnosing the rash.
• Consider common rashes first and rule out life-threatening
rashes quickly.
• Perform a KOH on most scaly rashes.
• Punch biopsies (3–5 mm) should be used for nonrespond-
ing or undiagnosed rashes, and a DIF should be performed
for vesiculobullous eruptions.
Reaction
Pattern
Red and
Scaly?
Eczematous?
Papulo-
squamous
Refer to Papulo-
squamous
algorithm
Refer to
“eczema”
algorithm
Refer to
“dermal”
algorithm
Refer to
“vascular”
algorithm
Refer to
“vesiculobullous”
algorithm
Eczema Dermal Vascular
Vesiculobullous
No surface
change?
Blanchable
erythema or
purpura?
Blisters?
Fig. 19.9 Approach to rashes based on clinical reaction patterns
A. Miceli and K. Krishnamurthy
325
PAPULOSQUAMOUS
Psoriasiform
Thick,
scaly plaques
Psoriasis
Ketoconazole
cream/shampoo
Topical or oral
antifungals
Reassurance IM Penicillin
Topical
ketoconazole,
selenium sulfide
diflucan
Topical/intralesional
steroids, oral
metronidazole
Topical or oral
steroids
Supportive
care
Seborrheic
Dermatitis
Pityriasis Rubra
Pilaris
Tinea Corporis Pityriasis Rosea
Secondary
Syphilis
Tinea versicolor Lichen planus (LP) Drug-induced LP
Psoriasis/Eczema,
CTCL or Drug
Greasy scale
Follicular red-
orange plaques
Annular, scaly
plaques
Oval, “Christmas
tree” distribution
Red-brown, scaly.
trunk, palms and
soles
Tan to red or
hypopigmented
with scant scale
Purple, polygonal,
planar, pruritic
Diffuse redness
and scale
(>90% BSA)
Pityriasiform Lichenoi
dE
rythroderma
Topical steroids,
calcipotriene,
immunosuppressives,
biologics
Oral retinoids,
immunosuppressives
Fig. 19.10 Algorithm for rashes with papulosquamous reaction patterns
19. Rash
326
ECZEMA
Vesicular, weeping,
irregular or linear
shape
Acute Contact
Dermatitits
Subacute Eczema Chronic Eczema
Scale, crust forms
Lichenified,
hyperpigmented,
scaly
Topical and/or
oral steroids
Topical steroids
Topical steroids,
moisturization,
bleach baths,
immunosuppressives
Fig. 19.11 Algorithm for rashes with eczematous reaction patterns
A. Miceli and K. Krishnamurthy
327
DERMAL
Subcutaneous Inflammator
yI
nfectious
Erythematous
tender nodules
NSAIDs, steroids,
colchicine
Antibiotics
Antimalarials,
steroids
Topical and/or
intralesional
steroids
Topical or
intralesional
steroids
AntibioticsAntifungals
Antifungals or
Antibiotics
Panniculitis Cellulitis
Lupus
Erythematosus
Granuloma
Annulare
Sarcoidosis Erysipelas Deep fungal
Atypical
Mycobacterium,
Sporotrichosis,
Cat-scratch
Erythema, pain,
warmth, edema
Malar erythema +
photosensitivity
Annular groups of
small papules
Red-brown
indurated plaques
Well-demarcated
red indurated
plaque
Necrotic ulcerative
nodule
Linear nodules
with lymphadenitis
Fig. 19.12 Algorithm for rashes with dermal reaction patterns
19. Rash
328
VASCULAR
Hives or wheals
Erythematous macules
and papules
Diffuse bullae and
desquamation
Targetoid papules
with dusky center
Palpable purpura
Purpura to
ulceration
Annular/Gyrate
Erythema
Urticaria
Antihistamines Supportive Care
Remove
offending
drug
Stop drug, burn
unit, supportive
care
Acyclovir
Treat underlying
cause
Treat underlying
cause
Doxycycline or
amoxicillin
Various treatments
(see vascular
section)
Viral Exanthem Drug Eruption
Toxin-mediated
(SSSS, Scarlet
fever, TSS,
Kawasaki)
SJS/TEN
Erythema
Multiforme
Vasculitis
(Hypersensitivity
vs. Septic)
Vasculopath
yE
CM
“toxic erythema”
Fig. 19.13 Algorithm for rashes with vascular reaction patterns
A. Miceli and K. Krishnamurthy
329
VESICULOBULLOUS
Infectious
Grouped vesicles on
an erythematous base
Nondermatomal Dermatomal Coxsackie
HSVHerpes ZosterPemphigus VulgarisBullous Pemphigoid
Flaccid blisters with
oral involvement
Supportive therapy
Sun protection,
Hydroxychloroquine,
phlebotomy
Cooling measures
Acyclovir, Valacyclovir Acyclovir, Valacyclovir
Prednisone,
Azathioprine
Prednisone,
Doxycycyline &
Niacinamide,
Immunosuppressives
Tense bullae on
trunk, flexural areas
Porphyria Cutanea
Tarda
Miliaria Crystallina
Vesicles on buccal
mucosa, palms, and
soles
(+) Nikolsky (-) Nikolsky
Acral blisters worse
with sun exposure,
alcohol, estrogen
Small superficial
vesicles in
intertriginous areas
Inflammatory Noninflammatory
Fig. 19.14 Algorithm for rashes with vesiculobullous reaction patterns
19. Rash