Transcript Part II: Contact Dermatitis & Drug Eruptions

Part II: Contact Dermatitis &
Drug Eruptions
Andrew’s Chapter 6, pg 123
Bolognia Chapter 23
Michael Hohnadel, D.O.
Drug Reactions
Generally a low rate of adverse reactions 1/1000 exposures.
 Higher rate for commonly used meds –
PCN and TMP: 30-50/1000.
 Presence of HIV disease or EBV infection
increases rate
 One of the most common reasons pts visit
dermatologist

Patient Evaluation
Diagnose cutaneous
eruption by clinical
1.) Stop all unnecessary meds
pattern(ie urticaria,
2.) Ask about nonprescription
exanthem, vasculitis,
meds and meds delivered
erythema multiforme, etc)
by other means:
 Ask two questions:
suppositories, eye drops,
1.) Which med can cause this
implants, patches, etc
pattern of rxn?
3.) No matter how atypical the
2.) How commonly does this
presentation always
med cause this rxn
consider pts meds as a
pattern?
possible cause
Three rules:

Additional testing ?

Skin testing is most useful in evaluating
type I (immediate) hypersensitivity
– Most frequently used in evaluating adverse
rxn’s to penicillin, local anesthetics, insulin,
and vaccines

Radioallergosorbent (RAST) tests have 20%
false-negative rate in penicillin type I
allergy and therefore RAST must be
followed by skin testing
– RAST test cannot replace skin testing
Pathogenesis


In most patterns pathogenesis is UNKOWN!!
Types:
1. Immunologic - Response by the pt to the drug or its
metabolite
2. Nonimmunologic - may result from normal
pharmacologic effects of drug (urticaria worsening from
aspirin ingestion)

Likelihood may be determined by metabolism:
– Anticonvulsant and sulfonamide rxn’s, the P-450 system
of individuals generates toxic metabolites of the med
that binds to proteins and stimulates an immunologic rxn
– This defect can be found in family members (HLA
subtypes)

Immune status and clinical condition may be a
factor.
– AIDS pts may be related to glutathione deficiency.
Pathogenesis
Exanthems


Most common form of adverse cutaneous eruption
Characterized by erythema, often with papules
throughout. Lesions first appear proximally - especially
groin and axilla, generalizing within 1-2 days
– Pruritus is usually prominent and is a distinguishing factor
from a viral exanthem
– Tend to occur within the first two weeks of tx.
» but may occur later, even up to 10 days after tx

Most common cause: Antibiotics, especially semisynthetic penicillin & sulfamethoxazole/trimethoprim
– Ampicillin given during infectious mononucleosis and Bactrim
given to AIDS pts cause exanthems in a large # of pts treated.
Exanthems
Secondary to Phenobarbitol
Treatment

Simple exanthems - supportive tx
– Eruption may resolve even if offending med is continued
– Topical steroidal medications and antihistamines may allow
course of tx to be completed.
– Rechallenge may or may not result in reappearance of eruption
– In HIV infection and rarely, in persons with normal immune
status rechallenge may result in a more severe blistering rxn

Complex exanthems
– These present with fever, rash, and variably , with eosinophilia,
lymphadenopathy, hepatitis, nephritis, and rarely heart, lung &
brain
– Hypersensitivity syndromes are seen mostly with:
anticonvulsants, and long-acting sulfonamides; less commonly
with allopurinol, gold, dapsone, and sorbinil.
Anticonvulsant Hypersensitivity Syndrome



Assoc. with: diphenylhydantoin, phenobarbital,
carbamazepine, and other anticonvulsants.
1 of 5000 pts tx with these meds.
Presentation:
– Initially morbilliform, but may have various morphologies
including eczema, bullae, SJS like sloughing.
– Syndrome begins with fever between 2 and 6 weeks after
agent is started.
» Eruption begins with prominent facial swelling.
» Other: pharyngitis, lymphadenopathy (75%), hepatosplenomegaly.
– Widespread pinpoint pustules may develop esp in dark
skinned individuals.
– Lab: eosinophilia, atypical lymphocytosis, elevated liver
function tests (51%), and occasionally nephritis

Can lead to death from hepatitis
Anticonvulsant Hypersensitivity Syndrome
Pathogenesis
 Inability to detoxify arene oxide metabolites of these
meds
 Metabolites bind to proteins and elicit an immune
response leading to an adverse drug rxn
 Cross rxn with different anticonvulsants are common
(because meds are metabolized by same pathway)
Management
 Ruling other infectious etiologies
 Discontinue offending med
 Supportive tx. If liver or renal involvement or if pt is
ill then hospitalization, systemic steroids may be used
Sulfonamide Hypersensitivity
Syndrome



Clinical syndrome similar
to anticonvulsants.
Pts develop severe bullous
rxn like Stevens-Johnson
syndrome or TEN.
Pts are almost always slow
acetylators who produce
toxic hydroxylamine
metabolites during
metabolism of the
sulfonamide.
Allopurinol Hypersensitivity Syndrome

Presentation: Weeks to months (average 7 wks) after
allopurinol is begun, a morbilliform eruption (50%) that often
evolves to an exfoliative erythroderma(20%)
– Typically occurs in pts with preexisting renal failure, whose
dose is not adjusted for their renal function
– Bullous eruptions including TEN’s may occur(25%).
– Asociated: fever, eosinophilia, sometimes hepatitis, and
typically worsening renal failure

Course and Treatment:
– Syndrome may be steroid responsive, but is slow to resolve
and frequently lasts months after allopurinol has been
stopped
– 25% of pts die as a consequence
– Dialysis does not accelerate resolution of this syndrome
Allopurinol Hypersensitivity Syndrome
Exfoliative dermatitis caused by allopurinol
Drug-Induced Pseudolymphoma


Exposure to a medication results in cutaneous
inflammatory infiltrates that resemble lymphoma such
as MF. Rare reaction.
Diagnosis:
– Consistent with lymphoma with atypical lympocytes.
– Lymphadenopathy and circulating Sezary cells may also be
present
– Gene rearrangement may be positive!!
– Usually, keratinocyte necrosis and dermal edema help make
pseudolymphoma dx.


Resolves with discontinuation of the med.
Primary meds responsible: anticonvulsants, sulfa drugs,
dapsone, and antidepressants
Urticaria



1.
Meds may induce urticaria by immunologic and
nonimmunologic mechanisms.
Presentation: Wheals or angioedema. My be part of a
more severe anaphylactic rxn with bronchospasm,
laryngospasm, or hypotension
Types:
Nonimmunologic
– Aspirin and NSADS are the most common cause.
– They alter prostaglandin metabolism, enhancing
degranulation of mast cells.
– Other agents: radiocontrast, opiates, tubocurarine,
polymyxin-B.
– Pretest with RAST may be helpful but will not exclude
possiblity of rxn (esp with radiocontrast agents.)
Urticaria
1.
Immunologic
– Most commonly associated with penicillin and related
beta-lactam antibiotics
– It is associated with IgE antibodies to penicillin or its
metabolite
– Skin testing is useful in evaluating pts with a history
of urticaria associated with penicillin exposure.
» Pt may be given a desensitization protocol.
– Pts with PCN allergy have an increased rate of rxn to
cephalosporins.
» Third-generation cephalosporins are much less likely to
induce a rxn in a pcn allergic pt than the first- or second
generation ones
» May not be as cross reactive as is commonly believed.
Urticaria
Urticaria 2nd to PCN
Angioedema





Known complication of the use of ACE inhibitors.
Blacks 5x > Whites.
ACE inhibitors are a common cause of accuired
Angioedema. (Lisinopril and enalapril > captopril).
Effect is dose dependent and may resolve with decreased
dose.
ACE users with one episode of angioedema have a 10x
risk of a second episode which may be more severe.
Angioedema may represent a consequence of a normal
pharmacological effect of the ACE inhibitors
– Blocking of kininase II by ACE inhibitors may increase tissue
kinin levels, enhancing urticarial rxn’s and angioedema

Episodes may require hospitalization 45% of the time,
ICU 27% of the time, and intubation 18% of the time.
Angioedema
Deep, poorly defined swelling
Angioedema
Photosensivity Reactions
Meds may cause phototoxic, photoallergic, lichenoid and
pseudoporphyria like reactions.
 Most drug-induced photosensitivity is triggered by radiation in the
UVA range (spectrum and depth)
 Most common drugs: NSAIDs, sulfamethoxazole/trimethoprin,
thiazide diuretics and related sulfonylureas, quinine and quinidine,
and certain tetracyclines.
Phototoxic vs Photoallergic:
 Phototoxic reactions: (sunburn)

–
–
–
–
Related to dose of both med and UV irradiation
Does not require prior exposure or participation by the immune system
Rxn’s can appear from hrs to days after to exposure
Tetracyclines(especially demeclocyline), amiodarone, and the NSAIDs are
common culprits
– TX: May include dose reduction and photoprotection
Photosensivity Reactions

Photoallergic reactions
– Typically eczematous, pruritic, and occur after some period of
drug exposure.
– They involve the immune system, and are confirmed by positive
photopatch testing
– In general, they are not as drug dose dependent as phototoxic
reactions
Examples:
 Amiodarone photosensitivity develops in 75% of tx pts,
and occurs after a cumulative dose of 40g.
 NSAIDs, especially piroxicam
– Characteristic rxn is a vesicular eruption of dorsa of hands,
sometimes associated with dyshidrosiform pattern on the lateral
aspects of hands and fingers
– May be related to thimersol exposure earlier in life.
Photo Reactions
Phototoxic reaction to MTX .
Phototoxic reaction from TCN
Pseudoporphyria

Presentation: Photodistributed bullous rxn which
clinically and histologically resembles PCT.
– Not Seen: Hypertrichosis, skin fragility,
dyspigmentation, and sclerodermoid changes. Porphyrin
studies are normal.


Naproxen is most commonly reported cause
Resolves when the drug is discontinued.
Anticoagulant-Induced Skin Necrosis


Most common Patient: Obese, postmenopausal women are
predisposed secondary to the fact that lesions tend to occur in
areas with abundant subcutaneous fat (breast, abdomen, or
buttocks)
Warfarin necrosis: 3 –5 days after therapy is begun, red,
painful plaques develop that become necrotic.
– The higher the initial dose, the higher the risk.
– Cause: Hereditary or acquired deficiency of antithrombotic agents
protein C and less commonly protein S. Temporary hypercoagulable
state.
– TX: Stop warfarin, admin: vit K and Protein C

Heparin necrosis: Local and widespread reactions
–
–
–
–
6-12 days after injection - tender red plaques that undergo necrosis.
Any type heparin may cause.
Heparin antibody causing platelet coagulability is often found.
May result in widespread thrombosis.
Warfarin Necrosis
Pt underwent knee surgery and
was placed on low dose warfarin
afterwards.
Heparin Necrosis.
Heparin induced necrosis, note ischemia.
Vitamin K Reactions



Presentation: 1-2 weeks after injection of vitamin-K,
pruritic, deep seated, red plaques involving the dermis
and subcutaneous tissue develop at the site of injection.
Commonly located on posterior arm and over hip or
buttocks. Lesions on hip tend to progress around the
waist and down thigh, forming a “cowboy gun belt &
holster” pattern.
Most affected pts have liver disease & are being tx for
elevated PTT’s
Allergic reaction at site of vitamin K injections
Injection Site Reactions

IM injection may produce a syndrome calledEmbolia Cutis Medicamentosa (Nicolau syndrome)
– Immediately after injection there is a local intense pain, and
ischemic palor
– Within mins-hrs site develops an erythematous macule that
evolves into a livedoid violaceous patch with dendrites.
– This becomes hemorrhagic, then ulcerates, and eventually
heals with an atrophic scar




Etiology: Peri-arterial injection with thrombosis
Muscle and liver enzymes may be elevated and
neurologic symptoms and sequela occur 1/3 of pts.
Uncommonly, amputation may be needed
Treatment: Conservative-dressing changes,
debridement, bed rest, and pain control. Rarely
surgical intervention is needed
Injection Site Reactions
Cutaneous reaction to IV infusion and
extravasation of chemotherapeutic
agent
Acute Generalized Exanthematous Pustulosis



Frequency: Not uncommon. 90% of time is related to
medication
Eruption occurs around 5 days after med is started (50% occur
within 24 hrs)
Presentation: A scarlatiniform erythema rapidly develops into >
100 non-follicular pustules less than 5 mm in diameter.
Widespread desquamation occurs after a few days
–
–
–
–

Edema of face, purpura, and target lesions may appear in the background
Mucous membranes are involved in 22%
Fever is universal
Neutrophilia in 90%, and eosinophilia in 30%. Normal Liver funct.
Causes: Mercury is sole cause in 13% of cases in France, betalactams in 44%, and macrolides in 17%. Sulfonamides have NOT
been reported to cause this rxn. 17% of pts have a history of
psoriasis
Acute Generalized Exanthematous Pustulosis



Treatment: Once inciting agent is discontinued,
eruption usually resolves within 15 days without
sequelae
Patch testing with the suspected agent may reproduce a
pustular eruption on an erythematous base at 48 hrs
Histology:
– Early lesions show marked papillary edema, neutrophil
clusters in dermal papillae, and perivascular eosinophils
– Well developed lesions show intraepidermal or subcorneal
spongiform pustules
– May be an associated leukocytoclastic vasculitis
– Presence of eosinophils, and marked papillary edema help to
distinguish this eruption from pustular psoriasis
Acute Generalized
Exanthematous
Pustulosis
Putules on Skin
Histology:
Pustules with
neuts and edema.
Drug-Induced Pigmentation


Etiology: Post inflammatory hyperpigmentation or actual
deposition of drug in skin.
Minocycline causes three types of pigmentation:
1. Blue-black discoloration in areas of prior inflammation(not related to
total or daily dose exposure)
2. Appearance of a similar colored pigmentation on normal skin of
anterior shims (is dose dependent)
3. Least common - Generalized, muddy brown hyperpigmentation.

Chloroquine, hydroxychloroquine, and quinacrine all may
cause a blue-black pigmentation of face, extremities,ear
cartilage, oral mucosa, and nails
– Pretibial hyperpigmentation is most common

Amiodarone after 3-6 months causes photosensitivity in 3057% of pts.
– 1-10% of pts a slate-gray hyperpigmentation develops in areas of
photosensitivity
– Pigmentation fades after med is discontinued
Minocycline
Amiodarone pigmmentation
Drug-Induced Pigmentation

Clofazimine may cause a pink discoloration that gradually
becomes reddish blue or brown. (esp in Hansen’s disease)
– Major cause of noncompliance.

Zidovudine causes a blue or brown hyperpigmentation most
frequently in nails
– Lunula may be blue, or whole nail plate may be dark brown
– Diffuse hyperpigmentation of skin, pigmentation lateral tongue, and
increased tanning are less common
– Occurs in darkly pigmented pts, is dose dependent, clears after med
discontinued

Chlorpromazine, thioridazine, imipramine, and clomipramine may
cause a slate-gray hyperpigmentation in sun-exposed areas after
long periods of ingestion
– Frequently, corneal and lens opacities are present
– Therefore all pts with hyperpigmentation from these meds should have
ophthalmologic exam
Drug-Induced Pigmentation


Purple pigmentation in
patient who had been
on high doses of
chlorpromazine
There is sparing of
deep creases of the
face
Drug-Induced Pigmentation
Heavy metals gold, silver, and bismuth produce blue to
slate-gray hyperpigmentation.
 Pigmentation occurs after yrs of exposure, mainly in
sun-exposed areas. It is permanent.
 Bismuth also pigments gingival margin.
 Arsenical melanosis is characterized by black,
generalized pigmentation or by pronounced truncal
hyperpigmentation that spares the face.
Fixed Drug Reactions


Common
Present anywhere on body (50% occur on oral and
genital mucosa)
– Represent 2% of all genital ulcers evaluated at clinics for
STD’s

Presentation:
– Six or less lesions occur, typically one.
– Clinically begin as a red patch that soon evolves to an iris or
target lesion identical to EM.
– Eventually may blister and erode.
» Lesions of oral mucosa and genitalia usually present as erosions.
– Postinflammatory hyperpigmentation results.
Fixed Drug Eruption

Causes: NSAIDs, especially pyrazolone derivatives,
naproxen, mefenamic acid; sulfonamides, trimethoprim,
or combinations are common.
– Barbiturates, tetracyclines, phenolphthalein(in laxatives), and
erythromycin


Unknown pathogenesis
Variant: Nonpigmented fixed drug eruption
– It is characterized by large, tender, often symmetrical
erythematous plaques that resolve completely within weeks,
only to recur on re-ingestion of offending drug
– Pseudoephedrine by far most common.
– Baboon syndrome !!
Fixed
Drug
Eruptions
Phenophthalein - A
naproxen - B ,
Ciprofloxin - C ,
TMP/sulfamethoxa
zole - D
Bullous Drug Reactions

Uncommon:
– 0.4 - 1.2 per million person years for TEN
– 1.2 to 6.0 per million person years for StevensJohnson syndrome.

Definition:
– SJS < 10% of body surface area involved
– 10-30% are overlap cases
– >30 % TEN

Likely a disease spectrum.
SJS v. TEN
Systemic symptoms, amount of epidermal involvement and
confluence are key factors.
SJS &TEN

Causes:
– Greater then 100 meds have been reported as a cause.
– Most common: TMP/sulfamethoxazole(1-3/100,000)
Fansidar-R, sulfadoxine with pyrimethamine
(10/100,000), carbamazepine(14/100,000).
– Antibiotics (especially long-acting sulfa drugs and
penicillins).
– Other: anticonvulsants, anti-inflammatory and
allopurinol are also causes.

Mechanism: FAS – FAS ligand up-regulation and
activation ?
Proposed
TEN
Mechanism
and Rational
for IVIG
Treatment
Histology of TENS
Early



Late
A lymphocytic infiltrate at the D-E junction
Necrosis of keratinocytes that may be full thickness
Infiltrate may be marked or very scant
SJS &TEN
Presentation:
 Fever and influenza-like symptoms often precede the eruption.
 Skin lesions appear on face and trunk and spread rapidly (within 4
days) to their maximum extent
 Initial lesions are macular and are followed by desquamation. May
also form atypical targets with purpuric centers that coalesce, form
bullae, then slough.
 Two or more mucosal surfaces are also eroded with oral and
conjunctiva being most frequently affected.
 Difficulty with swallowing, photophobia, painful urination, and
extensive respiratory and alimentary tract involvement.
Workup:
 Skin bx usually performed to exclude other diseases
 DDX: Paraneoplastic pemphigus (excluded with DIF). Graft-versus
host disease (hx) and SSSS ( superficial blister).
SJS
Skin and conjunctival
Involvement
SJS
TENS
Management

Similar to an extensive burn
– Fluid and electrolyte imbalances, bacteremia from loss of
protective skin barrier, hypercatabolism, and sometimes
ARDS
– Pts who are very ill or have > 30%- 50% loss of epidermis
should be transferred to burn unit

IVIG in 10 pts in doses up to 0.75 g/kg/day for 4 days
led to response in 48 hrs and skin healing within 1 week
– No adverse rxn’s where observed
– Blocking apoptosis through blockade of the death receptor
FAS(CD 95)
Management

Immunosuppressive TX (controversial)
– Benefit of immunosuppressive TX is to stop the process
very quickly to reduce the ultimate amount of skin lost
– Once most of skin loss has occurred,
immunosuppressive TX only adds to morbidity and
perhaps mortality.
– Immunosuppressive therapy it should be done quickly,
in adequate doses, given a short trial to see if the
process can be arrested, and then tapered.


In pts who survive, the average time for epidermal
re-growth is 3 weeks
Most common sequelae are ocular scarring and
vision loss
TEN
Three weeks of healing after receiving IVIG.
Radiation-Induced EM




Occurs if phenytoin is given prophylactically in
neurosurgical pts who are receiving wholebrain radiation therapy and systemic steroids
Presentation: Erythema and edema initially on
the head in the radiation ports, as a dose of
steroids is being reduced. Eruption spreads
caudad and mucosal involvement may occur
Evolves over 1-2 days to lesions clinically and
histologically similar to EM
Can rarely be seen with radiation therapy
alone.
Urticarial EM


Virtually always associated with antibiotic ingestion
Presentation:
– Skin lesions consist of urticarial papules and plaques, some of which clear
centrally forming annular lesions,but no true iris lesions
– Lesions can be distinguished from true urticaia in that they are fixed for
days.
– Pruritis is common
– Bullae are absent, and mucous membranes are uninvolved

Histologically, there is a superficial and deep dermal infiltrate
containing eosinophils with dermal edema. Epidermis is not
involved

Treatment: Response to systemic steroids is dramatic, with
clearing in 48-72 hrs
HIV Disease and Drug Reactions


Those with helper T-cell counts between 25-200,
are at increased risk for development of adverse
rxn to meds.
Morbilliform rxn’s to Bactrim occurs in 45% of
AIDS pts:
– Associated hepatitis or neutropenia may require
discontinuation of drug
– Low-dose re-challenge / desensitization may be
attempted. Works 50-80% of the time.
– A similar increased risk is seen in HIV pts receiving
Augmentin

Severe bullous rxn’s-SJS, TEN are 100-1000
times more common.
Adverse Reactions to
Chemotherapeutic Agents
Radiation Enhancement &
Recall Reactions



Radiation dermatitis: Erythema and vesiculation at
ports.
“Radiation recall” May occur if chemo agents are
administered up to a week or more after radiation
therapy
A similar reactivation of a sunburn after
methotrexate therapy.
Chemo-induced acral erythema

Common syndrome induced most frequently by 5-florouracil,
doxorubicin, cystosine arabinoside (up to 40% of pts). Dose
dependent.
– May appear with bolus short-term infusions or low-dose, long-term
infusions. May present days to months after treatments are started

Presentation:
– Initially, dysesthesia or tingling of the palms and soles
– This is followed by painful, symmetric erythema and edema most
pronounced over the distal pads of the digits
– May be accompanied by a morbilliform eruption
– Erythema becomes dusky develops areas of pallor, blisters, desquamates,
then reepithelializes

Etiology:
– Likely a direct toxic effect of chemotherapeutic agents on the skin
– Large number of sweat glands on the palms and soles that may concentrate
the chemotherapeutic agent explaining the localization of the toxicity
Chemo-induced acral erythema

Histology: Nonspecific.

Treatment:
– Pts usually recover without complications
– Most cases require only local supportive care
– Cold compresses and elevation are helpful; cooling of hands
during tx may reduce severity of rxn
– Modification of dose decreases the pain of fluorouracil
induced syndrome
Neutrophilic Eccrine Hidradenitis




Occurs in neutropenic pts with malignancies, usually
AML -most commonly associated with chemo,
especially cytoarabine
Presentation: After 7-10 days of tx, the patient
becomes febrile and erythematous papules, plaques
or nodules appear, localized to trunk, extremities,
axillae, or pubic area. May be generalized.
Histology: a neutrophilic infiltrate involving
glandular and ductal portions of the eccrine gland
Treatment:
– Bx performed to exclude infection, sweets syndrome.
– Skin lesions resolve in 10 days, but in severe cases may
be tx with corticosteroids
Neutrophilic
Eccrine
Hidradenitis
Chemotherapy-Induced Hyperpigmentation

Adriamycin causes marked hyperpigmentation of nails,
skin and tongue
– Most commonly seen in black pts

Cyclophosphamide causes transverse banding of nails
or diffuse nail hyperpigmentation
– Bleomycin and 5FU causes similar transverse bands



Busulfan and 5FU induce diffuse hyperpigmentation
that may be photoaccentuated
Bleomycin induces characteristic flagellate
erythematous urticarial wheals associated with pruritis
within hrs - days of infusion
Fluorouracil causes a serpentine hyperpigmentation
overlying veins of infusion.
A. - Ulceration due to
extravasation of doxorubicin.
B - Horizontal melanonychia
due to 5-fluorouracil.
C - Erythema of the ears due
to the cytarabine (cytosine
arabinoside), sometimes
referred to as ‘Ara-C ears’;
the petechiae are due to
thrombocytopenia.
D - Erythrodysesthesia due
to cytarabine with erythema
of the plantar surface.
E - Necrosis of psoriatic
plaques due to an ‘overdose’
of methotrexate.
F - Raynaud's phenomenon
and digital necrosis due to
systemic bleomycin.
Acrodynia




Caused by mercury poisoning, usually in infancy and has
pathognomonic skin changes.
Presentation: Painful swelling of hands and feet. Hands & feet
are dusky red, pink, cold & clammy Sometimes with pruritis.
Erythema is usually blotchy but may be diffuse. Hemorrrhagic
puncta are sometimes evident
Other signs:
– On trunk, a blotchy macular or papular erythema is usually
present
– Stomatitis and loss of teeth may occur
– Fever, irritability, photophobia, increased perspiration
– Always moderate upper respiratory inflammation and sore
throat
– Albuminuria and hematuria are usually present
Diagnosis is made by finding mercury in the urine
Acrodynia
Stomatitis
Sweeling of feet.
Acrodynia
Etiology:

Broken thermometers

Teething powders

Poisoned fish

Broken phosphorescent bulbs
Treatment:

Chelating agents - Dimercaprol
Bromoderma

Presentation:
– Most common is acneform erruption with inflammatory pustules in
hairy parts of body and butterfly area of face(must be differentiated
from rosacea). Vesicular lesions and bullae are common.
– Nodular lesions with a violaceous color are mistaken for malignant
lymphoma of skin


It may occur after a small dose or after protracted use of
bromides. Bromides are excreted in milk.
Treatment:
– Cessation of bromide ingestion with rapid resolution.
– In acute intoxication 2 to 4 g of sodium chloride by mouth, taken
daily, rapidly replaces the bromide in body fluids.
– In severe cases of intoxication in which the pt is badly confused,
ethacrynic acid rapidly decreases the bromide level, with clearing of
lesions
Bromoderma
Bromoderma
Bromide eruption on shin with bullae and
granulomas
Iododerma

Presentation - acneiform eruption with
numerous acutely inflamed follicular pustules,
surrounded by a ring of hyperemia. Swelling,
redness, and scaling of eyelids occurs.
– Bullous lesions are also common and may become
ulcerated and crusted
– Pruitus and urticaria may be only manifestations of
mild iodism


Acne vulgaris and rosacea are worsened by
iodine
Treatment is same as bromoderma
Iododerma
Edematous erythematous
papules on the buttocks
with central crusts
Only brief duration
distinguishes it clinically
from basal cell carcinoma.
Topical Corticosteroids

Appearance of these side effects depends on three
factors:
1. Strength of steroid
2. Area to which it is applied
3. The individual’s predisposition to certain side effects

Common Side effects:
– Atrophy, striae, telangiectasia, skin fragility, and
purpura are the most frequent changes seen. Hypo
pigmentation in dark skinned individuals.
– Telangiectasias in fair-skinned individuals using
fluorinated corticosteroids on the face may or may not
persist.
Topical Corticosteroids

Repeated application of corticosteroids to the face,
scrotum or vulva may lead to marked atrophy of
these tissues ( First marriage….Now This ! )
– Tissue becomes “addicted” to the topical steroid, so that
withdrawing it results in severe itching or burning.
– Difficult to manage

Treatment: Reduce strength of steroid, add topicals
like doxepin, pramoxine, or menthol and camphor.
– Also TIMS may help during taper.

Telangiectasiases usually disappear in a few months
after corticosteroid applications are stopped. Lasers
of hyfercation may be needed.
Topical Corticosteroids

Atopic children with more than 50% body
surface area involvement may have short
stature. Some believe this is related to
chronic steroid use.
– If used over a large area, sufficient topical steroids may
be absorbed to suppress the hypothalamic pituitary axis in
any patient.
– May affect growth of children with atopic dermatitis and
has led to Addisonian steroid dependency and also
Cushing’s syndrome.
– Bone mineral density is reduced in adults whose chronic
atopic dermatitis is severe enough to require steroids
stronger than hydrocortisone.
Topical Corticosteroids
Other Reactions:
 Topical corticosteroids may induce allergic
contact dermatitis (esp in stasis dermatitis
with long term use.)
– Consider this complication in any pt with an
eczematous dermatitis who becomes worse or
is refractory to topical steroid tx.
– Systemic corticosteroid administration may be
tolerated, but in some pts there is a cross
reaction manifested by whole-body allergic
dermatitis

Steroid Acne, perioral dermatitis
Side effects…

Atrophy and purpura caused
by prolonged applications of
corticosteroid preparations
Steroid Acne due to mid potency application to the face.
Injected Corticosteroids
Intralesional injection may produce subcutaneous atrophy at
site of injection and may migrate along lymphatics causing
not only local side effects but linear atrophic
hypopigmented hairless streaks
 These may take years to resolve
 To avoid these complications-inject directly into the lesion,
not into the fat, and use only minimal concentration and
volume
Intramuscular steroid injections should always be given in the
buttocks with a long needle (at least 1.5 inches in adults)
 Injection into deltoid muscle sometimes causes
subcutaneous atrophy
 Pt can be assured that this will fill in but it may take several
yrs
SE of Injected Corticosteriods
Lipoatrophy of the buttock
resulting from a corticosteroid
injection
Systemic
Corticosteroids
Side Effects
Systemic Corticosteroids Side Effects
Acneiform Erruption
Osteonecrosis of head of femur
How to combat side effects…

Bone loss can occur early in course of tx and is
important to manage preemptively:
– Supplement with calcium & vitamin D (1.0-1.5 g calcium
and 400-800 U of cholecalciferol daily)
– Stop smoking
– Decrease alcohol consumption
– Obtain bone mineral density at baseline (via DEXA scan)
& throughout tx period if long term steroid use is
anticipated (yearly?)
– Hypogonadism which contributes to osteoporosis can be
treated in men and women with testosterone and estrogen
respectively
– Calcitonin and bisphosphonates may be added to
management as needed
THE END