Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2866_Библиотеки_им_академика_М_И_Перельмана.pdf
Скачиваний:
0
Добавлен:
15.09.2026
Размер:
15 Мб
Скачать
☆
Chapter 20. Rash
419
• Diagnostic procedures:
– Potassium hydroxide (KOH) prep: identifies dermato-
phyte infection.
Positive test: presence of hyphae (long, slender, refractile filaments that cross multiple cell walls). Tinea versicolor is diagnosed by presence of “spa­ghetti and meatballs” appearance, which represents hyphae and spores [3].
– Mineral oil prep: identifies scabies or Demodex mites.
Positive test: observe mite, eggs, or feces (scybala) for scabies. Observe mite for Demodex. Mineral oil used.
– Wood’s lamp (365nm) [4]:
Findings in different skin conditions:
• Vitiligo: milky white appearance.
• Tinea versicolor: yellow or orange glow.
• Tinea capitis: Microsporum species fluoresce blue­green, Trichophyton schoenleinii fluoresces dull blue.
• Erythrasma: coral-pink color due to
Corynebacterium.
• Pseudomonas: fluoresces green.
• Porphyria: red-pink fluorescence of skin.
– Nikolsky sign: positive if lateral pressure causes shear-
ing of the epidermis from the dermis. This indicates an intraepidermal process.
– Asboe-Hansen sign: positive if gentle pressure on the
blister causes lateral expansion of the blister. This also indicates an intraepidermal process.
– Diascopy: pressing on a lesion with a glass slide to see
whether or not redness blanches out. Purpura is non­blanching often indicating vasculitis.
– Skin biopsy: rashes not responding to conventional treat-
ment require a biopsy. For autoimmune conditions, two punch biopsy samples should be taken, one for H&E and one for direct immunofluorescence (DIF). The DIF specimen should be obtained from uninvolved peri­lesional skin for suspected immunobullous processes.
• Treatment: Please see diagnostic and treatment (Figs.20.9,
20.10, 20.11, 20.12, 20.13, and 20.14).
420
A. Howell and K. Krishnamurthy
Reaction
Pattern
Red and
Scaly?
Papulo-
squamous
Refer to Papulo-
squamous
algorithm
Eczematous?
Refer to “eczema” algorithm
No surface
change?
Refer to “dermal”
algorithm
Blanchable
erythema or
purpura?
Refer to
“vascular”
algorithm
Blisters?
VesiculaobullousVascularDermalEczema
Refer to
“vesicullaobullous”
algorithm
F . Approach to rashes based on clinical reaction patterns
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.
• Erosion and/or ulceration can represent an initial vesicu­lobullous eruption.
• Punch biopsies (3–5mm) should be used for nonrespond­ing or undiagnosed rashes, and a DIF should be performed for vesiculobullous eruptions.DisclaimerThis research was supported (in whole or part) by HCA Healthcare and/or an HCA Healthcare affiliated entity. The views expressed in this presentation represent those of the author and do not necessarily represent the official views of HCA Healthcare or any of its affiliated entities.
immuneossupprossi
Chapter 20. Rash
421
PAPULOSQUAMOUS
and scale
(>90% BSA)
Diifuse rodness
Lichenoid Erythroderma
Pityriasiform
plunar, pruritic
Purple, polygonal
Tan to red or
hypopigmented
with scant scale
solos
trunk palms and
Red-brown, scaly,
tree” distribution
Oval, “christmas
plaquos
Annular, scaly
CTCL or Drug
Psoriasis/Eczema,
Drug-induced LPLichen planus (LP)Tinea versicolor
syphilis
Secondary
Pytyriasis RoseaTinea corporation
Care
Supportive
steroids
Tropial or oral
storoids, oral
metronidazole
Tropical/Intralesional
difucan
Tropical
ketaconazole,
solenlum sulfide
IM penicillin
Reassurance
antidungals
Tropical or oral
Pilaris
Dermatitis
Psoriasis
Oral rotnoids
immuneosupprossives
Ketoconazole
cream/shampoo
ve
calcipotriene
Tropical storoids,
biologies
F . Algorithm for rashes with papulosquamous reaction patterns
Fallicular red-
orange plaquos
Psoriasiform
Greasy scale
Thick,
scaly plaquos
Pityriasis Rubra
Seborrhetic
422
A. Howell and K. Krishnamurthy
ECZEMA
Vesicular, weeping,
irregular or linear
shape
Acute Contact
Dermatitits
Tropical and/or
oral steroids
Scale, crust forms
Subtract Eczema Chronic Eczema
Tropical steroids
Lichenified
hyperpigmented,
scaly
Tropical steroids,
moisturization,
bleach baths,
immunosupperssives
F . Algorithm for rashes with eczematous reaction pat­terns
Chapter 20. Rash
423
DERMAL
Inflammatory InfectiousSubcutaneous
Linear nodules
with lymphadenitis
nodule
Necrotic ulcerative
plaque
red indurated
Well-demarcated
Red-brown
indurated plaques
small papules
Annular groups of
Atypical
Cat-scratch
Sporotrichosis,
Mycobacterium,
Sarcoidosis Erysipelas Deep fungal
annulare
Granuloma
Antibiotics
Antifungals or
AntibioticsAntifungals
steroids
Tropical or
intralesional
steroids
intralesional
Tropical and/or
photosensitivity
Malar erythema +
Erythema, pain
warmth, edema
Erythematous
tender nedules
Lupus
Erythemaaosus
Panniculitis Cellulitis
steroids
Antimalarials,
Antibiotics
colchicine
NSAIDs, steroids,
F . Algorithm for rashes with dermal reaction patterns
424
A. Howell and K. Krishnamurthy
VASCULAR
Erythema
AnnulateGyrate
ulceration
Purpura to
Palpable purpura
with dusky centre
Targetoid papules
desquarnation
Diffuse bullae and
Toxin-mediated
ECMVasculopathy
Vasculitis
vs. Septic)
(Hypersensitivity
Erythema
Multiforme
SJS/TEN
Kawasaki)
fever, TSS,
(SSSS, Scarlet
amoxicillin
Doxycycline or
cause
Treat underlying
cause
Treat underlying
Acyclovir
care
unit supportive
Stop drug, brun
section)
(see vascular
Various treatments
and paules
“toxic erythem”
Erythematous macules
Hives or wheals
Drug EruptionViral ExanthemUrticaria
drug
Remove
offending
Antihistamines Supportive Care
F . Algorithm for rashes with vascular reaction patterns
Chapter 20. Rash
vesicles in
Small superficial
intertriginous areas
Noninflammatory
Miliaria Crystallina
cooling measures
425
VESICULOBULLOUS
Tarda
alcohol, estrogen
with sun exposure,
Acral blisters worse
(+) Nikolsky (+) Nikolsky
soles
Vesicles on buccal
mucosa, pains, and
Infections Inflammatory
Porphyria Curanea
Tense bulfae on
trunk, fliexual areas
oral invlovemant
Flaccid blister with
Coxsackie
DermatomalNondermatomal
Phlebotomy
Sun protection,
Hydroxychloroquine,
Bullous PemphigoldPemphigus vulgaris
Supportive thearapy
Herpes zosterHSV
Prednisone,
Doxycycyline &
Prednisone,
Acyclovir, Valacyclovir
Niacinamide,
immunosupperessives
Azathioprine
Grouped vesicles on
an erythematous base
Acyclovir, Valacyclovir
F . Algorithm for rashes with vesiculobullous reaction patterns
426
A. Howell and K. Krishnamurthy

References

1. Gropper CA. An approach to clinical dermatologic diagno­sis based on morphologic reaction patterns. Clin Cornerstone. 2001;4(1):1–14.
2. Drage LA. Life-threatening rashes: dermatologic signs of four infectious diseases. Mayo Clin Proc. 1999;74(1):68–72.
3. Santistevan J, Long B, Koyfman A.Rash decisions: an approach to dangerous rashes based on morphology. J Emerg Med. 2017;52(4):457–71.
4. Bolognia J, Schaffer JV, Cerroni L.Dermatology. Philadelphia: Elsevier Saunders; 2018.
5. Stern RS. Exanthematous drug eruption. N Engl J Med. 2012;366:2492–501.
6. Pickert A. An approach to vasculitis and vasculopathy. Cutis. 2012;89(5):E1–3.
7. Norman GR, Rosenthal D, Brooks LR, Allen SW, Muzzin LJ.The development of expertise in dermatology. Arch Dermatol. 1989;125(8):1063–8.
8. Baroni A, et al. Vesicular and bullous disorders: pemphigus. Dermatol Clin. 2007;25:597–603.
9. Ghatan H. Dermatologic differential diagnosis and pearls. NewYork: Parthenon; 2002.
Chapter 21
Alopecia
ClaraBarranco andKarthikKrishnamurthy

Introduction

Alopecia (or hair loss) includes a group of disorders in which there is an absence of hair where it is usually present. More than 35 million men and 21 million women in the USA expe­rience hair loss. The incidence is highest in Caucasians, fol­lowed by Asians, African Americans, and Native Americans. Though a common problem, hair loss can cause a consider­able amount of emotional and social stress to patients. Moreover, it presents a challenge for practitioners, as there are multiple etiologies with similar clinical presentations.
Understanding the normal hair cycle is key in assessing
alopecias. There are three main phases of the hair follicle
“This research was supported (in whole or in part) by HCA Healthcare and/or an HCA Healthcare affiliated entity. The views expressed in this publication represent those of the author(s) and do not necessarily rep­resent the official views of HCA Healthcare or any of its affiliated entities.”
C. Barranco · K. Krishnamurthy (*) Department of Dermatology, Orange Park Hospital, Orange Park, FL, USA
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022 E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_21
427
428
C. Barranco and K. Krishnamurthy
cycle: anagen (active growth), catagen (regression), and telo­gen (rest). Approximately 85–90% of hair follicles are in the anagen phase, while 10–15% are in the telogen phase, and less than 1% in the catagen phase. There are approximately 100,000 hair follicles on the scalp, and, on average, 50–100 hairs are normally lost every day [1]. Hair loss becomes a clinical problem when there are localized patches of hair loss or when the number of hairs lost daily exceeds the normal amount. Progressive thinning and excessive shedding of the scalp hair are the two most common hair complaints reported [2].
The alopecias are divided into two main categories: scar-
ring (or cicatricial) and non-scarring (or non-cicatricial) alo­pecias (Fig.21.1). When assessing a patient with alopecia, it is important to consider the chief complaint as stated by the patient, the chronicity, the age at onset, whether there is a pattern to the areas of hair loss, and if there have been any major stressors, physical or emotional, in the patient’s life. Androgenetic alopecia, also referred to as female or male pattern hair loss, is the most common type of hair loss due to hormonal effects at the level of the follicle and is what most patients refer to as “balding.” Generalized thinning is most commonly seen in alopecia areata, in which the etiology is autoimmune, or telogen effluvium, in which some physiologic stressor initiates abnormal shedding [2]. Other causes of hair loss include autoimmune conditions, underlying systemic problems like thyroid disease and iron deficiency, infections of the scalp, inflammatory processes, and habitual practices. Regardless of the underlying cause, both physical and psy­chological stress can exacerbate any form of hair loss.
Alopecia is characterized into scarring and non-scarring
categories. Scarring can be divided based on the predominant cell type: lymphocytic, neutrophilic, and mixed. This category includes discoid lupus, central centrifugal cicatricial alopecia, dissecting cellulitis of the scalp, and acne keloidalis. Non­scarring alopecia can be divided based on its distribution. Focally distributed alopecias include alopecia areata, traction alopecia, and trichotillomania. Diffuse distribution includes