Transcript scabies - S3 amazonaws com

Dermatologic Manifestations
of Chronic Disease
Shelbi Hayes. M.D.
Saints Dermatology
October, 26 2012
I. Creating a Framework for
Evaluating Skin Lesions
II. Application of the framework
to the most common manifestations
of chronic disease
I have no financial
disclosures.
Creating a Framework
Question #1
Is this a primary or
secondary lesion?
Macule
Papule
Patch
Plaque
Pustule
Nodule
Pustule
Vesicle
Nodule
Bulla
Pustule
Vesicle
Bulla
Wheals
Wheals
Morphologic categories
Macular-Patch
Papular
Papulosquamous
(scaly papules)
Nodular
Pustular
Vesicular-bullous
Urticarial
Petechial
Telangiectasia
Burrow
Poikiloderma
Hyperkeratotic/scale
Atrophic
Secondary Lesions
Crust
Erosions and ulcers
Excoriations
Fissures
Scars
Lichenification
Atrophy
Creating a Framework
Question #2
Is there scale?
Scale or No Scale?
Scale indicates the disease process
involves the epidermis.
Lack of scale indicated the disease
process affects the dermis or
subcutaneous fat.
Exception: Tinea Incognito, Early
Vesiculobullous Lesions
Creating a Framework
Question #3
What is the configuration?
Configuration
Annular
Arcuate
Geographic
Discrete
Confluent
Serpiginous
Linear
Reticulated
Creating a Framework
Question #4
What is the color?
Color
Pink
Violet
Orange
Blue
Green
Yellow
Black
Brown
Color
Color
Pink—Pityriasis rosea
Violet—Lichen planus
Orange—Juvenile xanthogranuloma
Blue—Amiodarone skin pigmentation
Green—Pseudomonas
Yellow—Xanthomas
Black—Eschar
Brown—Café au lait spots
Creating a Framework
Question #5
What is the distribution?
Immunosuppression
Herpes Simplex
Herpes Simplex
Caused by HSV-1 and HSV-2
Infections occurs at the primary site,
transported via neurons to dorsal root
ganglion where latency is established
Pain, tenderness or tingling occur often
before reactivation.
Grouped vesicles on erythematous base,
however you may not see the primary
lesion when the patient presents!!
Herpes Simplex Virus
Eczema Herpeticum
Herpes Simplex Virus
Eczema Herpeticum
Herpes Zoster
EM-SJS-TEN
Spectrum of epidermal damage +/- mucosal
involvement
EM minor = no mucous membrane
EM in kids usually secondary to HSV, drugs in
adults
SJS-TEN constitute one of the few derm
emergencies
Treat in burn unit, frozen section of bx to check
for necrosis, little inflammation
Fluids, infection prophylaxis, consult ophtho and
uro as indicated
Erythema Multiforme
Erythema Multiforme Major
Also thought to be
a hypersensitivity
reaction
As with EM minor,
but with
involvement of ≥2
mucosal surfaces
(precedes rash by
1-2 days)
Pronounced
constitutional
symptoms
common
Stevens-Johnson Syndrome
Is SJS separate entity from EM major?
Some feel SJS is a distinct entity as the
rash is more erythematous and less acral
than EM major
EM major is more commonly triggered by
infections and SJS by drugs.
Stevens-Johnson Syndrome
Stevens-Johnson Syndrome
Stevens-Johnson Syndrome
Toxic Epidermal Necrolysis
Nikolski’s Sign =
separation of the
epidermis from
the dermis by
rubbing skin
between the
lesions
Toxic Epidermal Necrolysis
(TEN)
A life-threatening, exfoliating disease of
the skin and mucous membranes
Hallmark is full-thickness necrosis of the
epidermis with separation at the
dermoepidermal junction.
SJS vs TEN
Some use %BSA to define with:
<10% = SJS
>30% = TEN
Histologically SJS has a much higher density
cell infiltrate (T-lymphocytes) vs TEN (low
density macrophages and dendrocytes)
TEN - Pathogenesis
Majority of cases are likely adverse drug
reactions (foreign antigen response).
Mean time from drug to onset = 13.6 days
Higher risk drugs
– NSAIDS [38%]
– Antibiotics [36%] (sulfonamides)
– Anticonvulsants [24%] (phenobarb, lamotrigene)
– Corticosteroids [14%]
Use TrimethoprimSulfamethoxazole Judiciously.
Up to 17% of patients can have an
adverse cutaneous reaction.
Occurs within the first 3 weeks.
Warn Patients to alert you immediately.
Do not prescribe if the patient has a family
history of sulfa allergy.
TEN - Clinical Features
Initial symptoms (1-3 days)
– Fever (100%)
– Conjuctivitis (32%)
– Pharyngitis (25%)
– Pruritis (28%)
– Headache, myalgias, arthralgias, vomiting,
and diarrhea may occur
TEN - Clinical Features:
Mucosal Involvement
Erosive mucosal lesions (1-3 days before
skin eruption) occur in 97%
– Oral (93%)
– Ocular (78%)
– Genital (63%)
– Anal
TEN - Clinical Features:
Skin Eruption
Burning / painful skin rash
Usually begins on face / upper trunk
Begins as one of:
– Diffuse erythema
– Irregular bullae
– Poorly defined dusky or erythematous
macules
Scalp usually spared
Multisystem Involvement
GI - Mucosal sloughing in esophagus
(dysphagia, GI bleeding)
Resp - Tracheal/bronchial erosions
(Respiratory decompensation)
Renal – Glomerulonephritis
Profound fluid and electrolyte disturbances
Dermatophytes
Named for area involved: tinea capitis, corporis,
manum, facei, pedis, cruris, etc.
If there is scale, do KOH exam.
Words of a famous dermatologist:
“If it is scaly, SCRAPE it!”
Tinea Pedis
Tinea Cruris-Don’t use steroids!
Tinea Incognito
Scabies
Scabies
Caused by Sarcoptes scabiei
Pregnant female mite burrows in the
stratum corneum, lays eggs about 2-3 per
day. Eggs hatch after about a week.
See burrows, papules, vesicles.
In immunocompromised and elderly, can
be crusted and hyperkeratotic (Norwegian
also called Crusted Scabies).
Scabies
Scabies love babies!
Scabies love warm, occluded
places:
– axilla, webspaces, groin, head of
penis
Distribution
Pruritic,
erythematous
papules on the
head of the
penis=scabies
until proven
otherwise.
Scabies burrow
Crusted Scabies
Verruca Vulgaris
Verruca Vulgaris
Liquid Nitrogen
Candida Antigen
IL Bleomycin
Curretage and cautery
Condyloma
Treatment for CA
Avoid liquid nitrogen
Apply Podophyllin in the office and Rx imiquimod
at home.
S, Pniewski T, Malejczyk M, Jablonska S. Imiquimod is highly
effective for extensive, hyperproliferative condyloma in children.
Pediatr Dermatol. 2003 Sep-Oct;20(5):440-2.
Sharquie KE, Al-Waiz MM, Al-Nuaimy AA. Condylomata acuminata
in infants and young children. Topical podophyllin an effective
therapy.
Notify CPS?
CPS should be notified of concerns of possible
sexual abuse when ano-genital warts are
diagnosed in any child older than 3 years.
It also is important for CPS to be educated by
the reporting medical provider of other possible
nonsexual modes of transmission for the anogenital warts.
Hornor G.Ano-genital warts in children: Sexual abuse or not?
J Pediatr Health Care. 2004 Jul-Aug;18(4):165-70.
Notify CPS?
For children younger than 3 years, CPS
should be notified if other risk factors are
noted during assessment, such as an
abnormal genital examination, the
presence of another sexually transmitted
disease, or psychosocial information that
warrants investigation
Hornor G.Ano-genital warts in children: Sexual abuse or
not? J Pediatr Health Care. 2004 Jul-Aug;18(4):165-70.
Recommendations
Child 2 years or younger
– No report to child protective services needed unless one of the following
is present:
Abnormality noted on ano-genital examination that is of concern for sexual
abuse
Another sexually transmitted disease
Psychosocial/behavioral issue that is of concern for sexual abuse
Parental concern of sexual abuse that warrants investigation
Child 3 years or older
– Report concerns of possible sexual abuse to child protective services
– Nonleading interview of child regarding sexual abuse concerns (should
be completed by a trained forensic interviewer)
Hornor G.Ano-genital warts in children: Sexual abuse or not?
J Pediatr Health Care. 2004 Jul-Aug;18(4):165-70. Review.
Molluscum Contagiosum
Molluscum Contagiosum
Caused by pox virus
Characteristic umbillicated papules, molluscum
bodies on biopsy
May be an STD in adults – suprapubic and
genital lesions
Giant molluscum in AIDS pts, ddx in this pop.
includes crypto and other fungal infections
Tx includes cryo, curettage, cantharidin,
imiquimod or nothing – they will spontaneously
resolve
Auto-Immunity
Lupus
ACLE
Lupus
SCLE
Lupus
DLE
Lupus
Must evaluate all forms of cutaneous lupus
for systemic lupus
– ANA, anti-ds DNA, anti-Ro (especially with
SCLE), complement levels, UA
Review current medications
Treatment is a combination of system
steroids and steroid sparing agents
(especially Plaquenil), mild cases may be
treated with only topical steroids
Dermatomyositis
Dermatomyositis
Scalp involvement is relatively common
and manifests as an erythematous to
violaceous, scaly dermatitis.
Clinical distinction from seborrheic
dermatitis or psoriasis is occasionally
difficult.
Nonscarring alopecia may occur and often
follows a flare of systemic disease.
Dermatomyositis
Heliotrope rash
Gottron papules
Malar erythema
Poikiloderma in a photosensitive
distribution
Violaceous erythema on the extensor
surfaces,
Periungual and cuticular changes
Dermatomyositis
In 40% of patients, the skin disease may
be the sole manifestation at the onset.
Muscle disease may occur concurrently,
precede, or follow the skin disease by
weeks to years.
The disease is often intensely pruritic.
Systemic manifestations may occur.
ROS: arthralgias, arthritis, dyspnea,
dysphagia, arrhythmias, and dysphonia.
Dermatomyositis
Malignancy is possible in any patient with
DM, but it is much more common in adults
older than 60 years. All adults must be
screened.
Children with DM may have an insidious
onset that hides the true diagnosis until
the dermatologic disease is clearly
observed
Vasculitis
Vasculitis
Characterized by size of vessel.
Most common cutaneous disease involves
small vessels, i.e. leukocytoclastic vasculitis
(“Palpable Purpura”).
Medium sized vessel disease includes PAN,
Wegeners, and Churg-Strauss.
Vasculitis
Acronym for DDx of LCV:
Mt Sinai Hospital Center
Meds/Malig
Strep/Serum sickness
Henoch Schonlein/HCV
Connective tissue disease/Cryoglobulinemia
HSP usually <10 y.o. but can be adults,
subsequent to URI. IgA around blood vessels
Watch renal function.
Vasculitis Treatment
1. Identify and eliminate underlying cause.
2. If arthralgias present consider starting NSAIDS.
3. Colchicine, dapsone, and immunosuppressive
agents may be used if vasculitis is chronic.
Fluid Overload
Stasis Dermatitis
Stasis Dermatitis
Stasis Dermatitis
Typically affects middle-aged and elderly
patients.
Occurs on the lower extremities in patients with
chronic venous insufficiency and venous
hypertension.
Prevalence is 6-7% in patients older than 50.
This finding makes stasis dermatitis twice as
prevalent as psoriasis and only slightly less
prevalent than seborrheic dermatitis.
Stasis Dermatitis
Insidious onset of pruritus affecting one or both
lower extremities.
Reddish-brown skin discoloration is an early
sign and may precede the onset of symptoms.
The medial ankle is most frequently involved,
with symptoms progressing to involve the foot
and/or the calf.
H.O. dependent leg edema
H.O. factors that worsen peripheral edema
(CHF, HTN with diastolic dysfunction)
Stasis Dermatitis
Treatment is two-fold:
– Relief of symptoms
– Treatment of underlying venous insufficiency
For pruritus and eczematous component:
Class IV or V topical corticosteroids and
emollients (AVOID NEOMYCIN)
Daily use of support stockings
Id Reaction
Autosensitzation dermatitis
Most often pts with stasis and
contact dermatitis
Follows primary lesions by days
to weeks
Treatment includes treatment of
inciting event, topical and IM
steroid
Pruritus
Extremely common in patients with chronic renal
failure
Much more common in patients on renal
dialysis vs peritoneal dialysis
Independent marker for mortality for patients of
hemodialysis
Pruritus
Antihistamines of some help
– Doxepin
Topical capsaicin cream or Sarna lotion
Efficient hemodialysis
UVB
Diabetes
Eruptive Xanthomas
Patients with poorly
controlled glucose and
elevated triglycerides
Resolution with tight
glucose control
Necrobiosis Lipoidica
Diabeticorum
0.03% of patients with diabetes
Resolution or progression is not
related to glucose control
Very difficult to treat
–Topical or IL steroid
–Topical tacrolimus
–Surgical excision (often recur)
Acanthosis Nigricans
Associated with obesity
and insulin resistance
Improved with weight loss
and glucose control
Treatment includes topical
retinoids and salicylic acid
Diabetic Bullae
Appears on background of
normal skin
Resolves spontaneously
Culture fluid for secondary
infection of it appears cloudy
Diabetic Dermopathy
Patients with poorly controlled
diabetes
Correlates with vacsular damage
secondary to diabetes
No treatment needed
– thought to improve with
improved glucose control
“More is missed by not looking
than by not knowing”
M. McKay, M.D.