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Life-threatening erythroderma: diagnosing and

treating the bred manQ


Marti Jill Rothe, MD
*
, Megan L. Bernstein, BS, Jane M. Grant-Kels, MD
Department of Dermatology, University of Connecticut Health Center, Farmington, CT 06030, USA
Abstract Exfoliative erythroderma, or diffuse erythema and scaling of the skin, may be the
morphologic presentation of a variety of cutaneous and systemic diseases. Establishing the diagnosis
of the underlying disease is often difficult and, not uncommonly, erythroderma is classified as
idiopathic. Several cases are presented to demonstrate the diversity of presentation of this disease.
Laboratory findings are typically unhelpful in establishing the etiology of erythroderma. Clinical data
combined with multiple skin biopsies over time are necessary. Systemic complications of erythroderma
include infection, fluid and electrolyte imbalances, thermoregulatory disturbance, high output cardiac
failure, and acute respiratory distress syndrome. The initial approach to the management of
erythroderma of any etiology includes attention to nutrition, fluid and electrolyte replacement, and
the institution of gentle local skin care measures. Oatmeal baths and wet dressings to weeping or crusted
sites should be followed by application of bland emollients and low-potency topical corticosteroids.
Systemic dermatologic therapy may be required to maintain improvement achieved with local measures
or to control erythroderma refractory to local measures. The prognosis of erythroderma is dependent on
the underlying etiology.
D 2005 Published by Elsevier Inc.
Introduction
Exfoliative erythroderma, or diffuse erythema and
scaling of the skin, may be the morphologic presentation
of a variety of cutaneous and systemic diseases (Table 1).
The dermatologist is faced with multiple challenges when
caring for the patient with exfoliative erythroderma.
Establishing the diagnosis of the underlying disease is often
difficult and, not uncommonly, erythroderma is classified as
idiopathic. Exfoliative erythroderma places the patient at
high risk for secondary infection as well as cardiovascular
and respiratory compromise. Additional risks are posed by
systemic dermatologic therapy, which is often required to
control the disease. The following case summaries highlight
these clinical challenges.
Case presentations
Case 1
In March 2000, a 55-year-old man is referred for a
second opinion to the university for a 1-year history of
abrupt-onset erythroderma refractory to cyclosporine and
acitretin. The patient complains of fissuring of the palms
and soles and of being cold and pruritic but has been able to
continue his work as a financial analyst. No new med-
ications were initiated before the onset of erythroderma, and
0738-081X/$ see front matter D 2005 Published by Elsevier Inc.
doi:10.1016/j.clindermatol.2004.06.018
* Corresponding author. Tel.: +1 860 679 4176; fax: +1 860 679 1267.
E-mail address: rothe@nsol.uchc.edu (M.J. Rothe).
Clinics in Dermatology (2005) 23, 206217
discontinuation of medications was unhelpful. The patients
past medical history is significant for hypertension and
alcoholism in recovery. Personal and family history are
negative for psoriasis and atopy. Physical examination
shows a diffuse salmon-colored erythroderma of the skin
with only rare small spared areas, keratoderma, mild
ectropion, and scattered excoriations. Multiple biopsies
show spongiotic dermatitis; one biopsy shows focal
follicular plugging and focal parakeratosis alternating with
orthokeratosis, both horizontally and vertically (Fig. 1). A
presumptive diagnosis of pityriasis rubra pilaris is made.
The patient is referred to a hepatologist for clearance to
initiate methotrexate therapy. While awaiting results of the
hepatology evaluation, the patient develops new-onset pain
in his sacroiliac joints and fingers. He is evaluated by
rheumatology and the diagnoses of psoriatic arthritis and
probable psoriatic erythroderma are made. There is a
gradual response to methotrexate 25 mg weekly with only
few small residual psoriatic plaques. The patient is
ultimately able to taper off methotrexate with remission of
his joint and skin disease.
Case 2
In November 1998, a 26-year-old woman with a 5-year
history of psoriasis vulgaris is evaluated for worsening
disease failing to clear with topical steroids. A 30-treatment
trial of broadband ultraviolet B is ineffective. Psoralen-UV-
A therapy is initiated with an initial response followed by a
flare that eventuates into erythroderma. Multiple biopsies are
obtained and only one reveals the definitive changes of
psoriasis (Figs. 2 and 3). Over the course of 5 years the
erythroderma has waxed and waned but there has been only a
partial response to topical therapy, methotrexate, and
Table 1 Differential diagnosis
Dermatoses
Psoriasis
Atopic dermatitis
CTCL
Pityriasis rubra pilaris
Superficial pemphigus
Bullous pemphigoid
Contact dermatitis
Chronic actinic dermatitis
Pseudolymphoma
1
Hailey-Hailey
2
Infections
Dermatophyte
3,4
Norwegian scabies
Toxoplasmosis
5
Histoplasmosis
6,7
Leishmaniasis
8
HIV
Tuberculosis
9
Systemic
Subacute cutaneous lupus
10
Dermatomyositis
11-14
Acute graft-vs-host disease
15
Postoperative transfusion induced
16
Sarcoidosis
17,18
Thyrotoxicosis
19
Common variable hypogammaglobulinemia
20
Severe combined immune defect with Omenns syndrome
21
Leiners disease
Maple syrup urine disease
22
Histiocytosis
23
Hypercalcitonemia
24
Hematologic
Hodgkins lymphoma
3,25-27
B-cell lymphoma
28
Anaplastic large cell lymphoma
29
Acute myelomonocytic leukemia
30
Adult T-cell leukemia
31
Chronic lymphocytic leukemia
25
Reticulum cell sarcoma
32
Myelodysplasia
33
Chronic eosinophilic leukemia
34
Malignancy
Prostate
3,4
Lung
3,4,35
Thyroid
3
Liver
3,36
Breast
4
Ovary
4
Fallopian tube
37
Rectum
4
Esophagus
38
Stomach
35,39
Melanoma
4,40
Buschke-Loewenstein tumor (a verrucous carcinoma on anogenital
mucosal surfaces)
41
Fig. 1 Biopsy changes consistent with pityriasis rubra pilaris
demonstrating follicular plugging and alternating orthokeratosis
and parakeratosis (hematoxylin and eosin, original magnification
20 ).
Life-threatening erythroderma: diagnosing and treating the bred manQ 207
cyclosporine alone and in combination with mycophenolate
mofetil. The patients care is complicated by obesity,
underlying hypertension and diabetes, and noncompliance.
She is engaged to be married and interested in conceiving
within the next several years. She has required hospitaliza-
tion for secondary infection and shows partial improvement
of the erythroderma during the admission. The patients
internist has been reluctant to approve treatment with a
biologic agent because of poor control of the diabetes
secondary to noncompliance.
Case 3
A 40-year-old man reports the abrupt onset of near
erythroderma (Fig. 4) after treatment with clindamycin for a
dental abscess while on a golf trip to Florida in February
2003. There is no personal or family history of atopy or
psoriasis. Past medical history is significant for hypertension
and hyperlipidemia. There is no resolution of the eruption
upon discontinuation of his systemic medications, which are
subsequently restarted. Examination shows diffuse erythema
of the face with lichenified plaques of the forehead and
multiple excoriations of the scalp, widespread scaling and
erythema of the trunk and the extremities with some areas of
sparing, and circinate plaques with peripheral desquamation
affecting the thighs and buttocks. Biopsy reveals spongiotic
dermatitis and periodic acid-Schiff (PAS) stain is negative.
Direct immunofluorescence is negative. There is no improve-
ment with topical therapy and antihistamines, but there is
partial improvement while the patient is on a business trip to
South Carolina in the spring. The patient is reluctant to begin
empiric therapy with methotrexate and his internist believes
the patient requires ongoing treatment with atorvastatin,
which precludes concomitant treatment with cyclosporine.
Because of partial improvement with sun exposure, the
patient agrees to therapy with narrowband ultraviolet B in
June 2003. By October 2003, the lower extremities and
buttocks are completely clear, but there are residual small
plaques with silvery scale over the trunk and proximal
upper extremities and persistence of lichenified plaques
over the forehead. The patient declines biopsy of the residual
eruption but plans to continue phototherapy until a month-
long trip to Florida.
Case 4
A 42-year-old black woman with a history of atopic
dermatitis presented to her internist with weight loss,
fatigue, and erythroderma. Previously she had been healthy
and on no medications. Physical examination shows
erythroderma, diffuse alopecia of the scalp and loss of the
lateral eyebrows, peripheral lymphadenopathy, erosions of
the hard palate, punctate purpura affecting the pulps of
several fingers, and dilated vessels about the nail folds.
Fig. 2 Biopsy demonstrating psoriasis with epidermal hyperpla-
sia, hypogranulosis, and spongiform pustular formation (hematox-
ylin and eosin, original magnification 2.5 ).
Fig. 3 Higher magnification of spongiform pustule within the
epidermis (hematoxylin and eosin, original magnification 20 ).
Fig. 4 Patient in case 3 with widespread erythema and areas of
spared skin.
M.J. Rothe et al. 208
Laboratory examination reveals a decreased white blood cell
count and antinuclear antibody test is positive at 1:1280 rim
pattern. Skin biopsy shows an interface dermatitis (vacuolar
alteration and a superficial as well as interface lymphohis-
tiocytic infiltrate) (Fig. 5). Her erythroderma clears with
oatmeal baths and mid potency topical steroids. She was
referred to rheumatology for further workup and manage-
ment of her collagen vascular disease.
Case 5
A 60-year-old man with a long history of psoriasis
vulgaris was referred to the university in November 1993
for management of a flare refractory to topical therapy and
etretinate. Physical examination shows a shivering patient
with widespread salmon-colored erythema of the face,
trunk, and extremities with some clear areas. The margins
of plaques adjacent to spared areas show collarettes (Fig. 6).
Biopsy of lesional skin shows predominantly eosinophilic
spongiosis (Fig. 7) without definitive evidence of acanthol-
ytic keratinocytes. Direct immunofluorescence of perile-
sional skin is positive for intercellular IgG particularly
prominent in the superficial portion of the epidermis.
Pemphigus foliaceus clears with pulse steroids, and meth-
otrexate provides chronic control of his psoriasis and
pemphigus for the following 10 years.
Case 6
An 80-year-old woman with Alzheimers disease who
resides in a nursing home is referred to the university for
progressively worsening atopic dermatitis despite topical
and systemic steroid therapy. Physical examination reveals
widespread erythema (Fig. 8) sparing only her face and
Fig. 7 Histology demonstrated eosinophilic spongiosis (hema-
toxylin and eosin, original magnification 10 ).
Fig. 8 Elderly patient in case 6 with near erythroderma. Scabies
preparation with a burrow shows mites, eggs, and fecal material.
Fig. 5 Biopsy demonstrating an interface dermatitis (hematox-
ylin and eosin, original magnification 20 ).
Fig. 6 Clinically, collarettes are noted indicating a previously
ruptured blister.
Life-threatening erythroderma: diagnosing and treating the bred manQ 209
some areas over her chest, keratoderma, and fingernail
dystrophy. Closer examination of the primary lesions of her
chest shows coalescing burrows. Scabies preparation is
positive. The patient is successfully treated with several
courses of permethrin cream.
Epidemiologic and clinical features of
erythroderma
The above cases are illustrative of the varied clinical
presentations of erythroderma. There are multiple published
epidemiologic studies of erythrodermic patients.
3,4,25,
26,32,35,42-48
A male predominance has been observed, with
a male-to-female ratio ranging from 2:1 to 4:1. The average
reported age of affected patients is 41 to 61 years, with most
published series excluding children. The most commonly
diagnosed etiologies are psoriasis, spongiotic dermatitis, drug
Fig. 9 Patient with erythrodermic psoriasis and classic plaques
on elbows.
Table 2 Drugs implicated in erythroderma
Allopurinol
25,44,47,53
Amiodarone
54
Antimalarials
3,25,32,50,55
Arsenicals
54
Aspirin
54
Aztreonam
54
Barbiturates
55
Bromodeoxyuridine
56
Bupropion
57
Captopril
58
Carbamazepine
47,53,59
Carboplatin
60
Cefoxitin
61,62
Chlorpromazine
44
Chlorpropamide
54
Cimetidine
63
Cisplatin
64
Clodronate
65
Clofazimine
66
Codeine
3
Dapsone
67,68
Dideoxyinosine
69
Diltiazem
70
Doxycycline
71
Ephedrine
72
Epoprostenol
73
Etumine
47
Erythropoietin
74
Ethylenediamine
75
Fluindione
76
Fluorouracil
54
Gentamicin
77
Gold
3,32,44,53
Hypericum (St. Johns wort)
78
Indinavir
79
Interleukin-2
80
Iodine
3
Isoniazid
25,26,46
Isosorbide dinitrate
25
Lamotrigine
81
Lithium
82
Mercurials
3,26
Mexiletine
54
Minocycline
54
Neomycin
54
Nifedipine
83
Omeprazole
84
Penicillin
3,25,26,32
Phenobarbital
85
Phenolphthalein
3
Phenothiazines
54
Phenylbutazone
46
Phenytoin
25,35,51,86,87
Practolol
44
Propolis
88
Pseudoephedrine
89
Quinidine
32,53
Ranitidine
54
Retinoids
90
Rhus (lacquer)
91
Ribostamycin
92
Streptomycin
3,46
Sulfasalazine
52
Sulfonamide antibiotics
3,25
Sulfonylureas
54
Terbinafine
93
Terbutaline
25
Tetrachloroethylene
3
Thalidomide
94,95
Thiacetazone
46
Thiazide
25
Timolol eyedrops
96
Trimethoprim
44
Tumor necrosis factor-a
80
Vancomycin
97
Zidovudine
98
Table 2 (continued)
M.J. Rothe et al. 210
reactions, and cutaneous T-cell lymphoma (CTCL). Eryth-
roderma is classified as idiopathic in 9% to 47% of cases.
Erythroderma may be attributable to an exacerbation of a
preexisting dermatosis in more than half of patients.
49
Usually, patients with erythroderma secondary to psoriasis
or spongiotic dermatitis have a history of more localized
disease before the onset of erythroderma.
43
In a review of 50
patients with psoriatic erythroderma, Boyd and Menter
50
observed an average age of onset of 48 years, a male-to-
female ratio of 2:1, and an average of 14 years between the
onset of psoriasis and the development of erythroderma.
Triggers of psoriatic erythroderma include withdrawal of
topical or systemic corticosteroids; abrupt discontinuation of
methotrexate; topical irritants such as tars; systemic
medications such as antimalarials, lithium, and terbinafine;
phototherapy burns; infection, including HIV; pregnancy;
emotional stress; and systemic illness. Classic plaques of
psoriasis vulgaris may be evident in early and remitting
stages of erythroderma (Fig. 9). Psoriatic arthritis and
psoriatic nail changes may be present in some cases.
It is important to consider other possible etiologies even
in patients who may have a clear history of psoriasis or
atopic dermatitis or who may have features of psoriasis
vulgaris on examination. Eugster et al
49
describe 7 patients
with malignancy-related erythroderma, 5 of whom had a
history of preexisting dermatosis.
Onset of erythroderma due to drug reactions is typically
sudden and rapid and its resolution is typically faster than
cases of erythroderma due to other causes. A notable
exception occurs when erythroderma accompanies systemic
drug hypersensitivity reactions due to antibiotics, anticon-
vulsants, and allopurinol. Hypersensitivity develops within
2 to 5 weeks after the medication is started and may persist
for weeks despite discontinuation of the medication. Fever,
leukocytosis with eosinophilia, edema, lymphadenopathy,
organomegaly, and liver and renal dysfunction are charac-
teristic.
51,52
Table 2 provides a comprehensive list of drugs
implicated in drug-induced erythroderma.
Sezary syndrome is by definition manifested as eryth-
roderma, lymphadenopathy, hepatosplenomegaly, and cir-
culating Sezary cells. Pruritus is typically severe. Long-
standing disease is characterized by painful fissured
keratoderma (Fig. 10) and leonine facies secondary to
lymphomatous infiltration of the skin (Fig. 11).
99
Pityriasis rubra pilaris often begins as a seborrheic
dermatitis-like eruption of the scalp that quickly evolves,
especially after intense sun exposure, into a generalized
salmon-colored erythema with islands of sparing. Kerato-
derma is a prominent and early feature. Follicular pink
papules affecting the dorsal fingers, wrists, and elbows may
be present.
The diagnosis of erythroderma secondary to immuno-
bullous disease is most readily made when blisters and
erosions are present. Superficial pemphigus may show
impetigo-like erosions or collarettes indicative of a ruptured
blister. Tense blisters are usually, but not always, a feature of
erythrodermic bullous pemphigoid.
100
Pathognomonic features may facilitate the diagnosis of
erythrodermic dermatomyositis (eg, Gottrons papules,
heliotrope, poikiloderma, periungual telangiectasis, muscle
weakness),
12,13
chronic actinic dermatitis (eg, photoaccen-
tuation), erythrodermic sarcoidosis (eg, apple jelly
lesions),
17
and Norwegian scabies (eg, burrows).
Symptoms common to erythroderma of any etiology are
thermoregulatory disturbance, malaise, fatigue, and pruritus.
Lichenification, diffuse alopecia, dermatopathic lymphade-
nopathy, keratoderma, nail dystrophy, and ectropion are
signs common to long-standing erythrodermas of any Fig. 10 Patient with fissuring of Sezary.
Fig. 11 Histology demonstrating epidermotropism of enlarged
mononuclear cells with minimal spongiosis consistent with CTCL
(hematoxylin and eosin, original magnification 25 ).
Life-threatening erythroderma: diagnosing and treating the bred manQ 211
etiology
47
(Fig. 12). Pitting pretibial and pedal edema is
observed in 50% of erythrodermic patients.
73,94
Laboratory investigations
Laboratory findings are most often not diagnostic for
etiology of erythroderma. Common abnormalities found in
erythrodermic patients include leukocytosis, anemia, elevat-
ed erythrocyte sedimentation rate, lymphocytosis, eosino-
philia, and increased serum IgE.
3,25,32,43,44,46,47,53,101
In a
clinical study by Sigurdsson et al,
53
13 of 102 patients had
an erythrocyte sedimentation rate higher than 30 mm/h, 8 of
whom had idiopathic erythroderma. Other findings include
elevated creatinine level, elevated uric acid level, and
lowered serum protein levels.
26,47
Eosinophilia is not
diagnostic for etiology. Eosinophil count greater than 1.0
10
9
/L, however, was found in 20% of patients.
53
The
negative nitrogen balance found in chronic erythroderma
can lead to findings of hypoalbuminemia.
32
Sezary cell count analysis can be used for diagnosis of
Sezary syndrome. More than 20% circulating Sezary cells is
diagnostic for Sezary syndrome, whereas less than 10% is
nonspecific.
45,53
Sezary cells are found in these lower
numbers in many benign dermatoses, including atopic
dermatitis, psoriasis, lichen planus, discoid lupus, and
parapsoriasis.
102
Immunophenotyping of skin lymphocytes can be used to
differentiate Sezary syndrome from actinic reticuloid.
Sigurdsson et al
53
found predominance of CD8
+
lympho-
cytes in 7 of 12 patients with actinic reticuloid. Differen-
tiation between Sezary syndrome and actinic reticuloid can
also be accomplished via nuclear contour index of
peripheral blood lymphocytes.
103
Clinical data combined with multiple skin biopsies over
time are necessary. T-cell receptor b gene rearrangement on
peripheral blood smears is used for sensitive and specific
differentiation of Sezary syndrome from other benign forms
of erythroderma.
104
This technique has been applied to skin
biopsies as well; in recent studies, specificity has been 100%
Fig. 12 Diffuse alopecia in patient with chronic idiopathic
erythroderma.
Table 3 Histologic differential diagnosis of the erythrodermic patient
Disease Diagnostic histological clue
Actinic reticuloid Atypical mononuclear cells admixed in a superficial, lichenoid, and deep dermal infiltrate;
overlying lichen simplex chronicus with or without spongiosis
Atopic dermatitis Superficial perivascular dermal infiltrate containing eosinophils with overlying spongiosis;
can be seen with eosinophilic spongiosis; with or without lichen simplex chronicus
Contact dermatitis Same as atopic dermatitis
CTCL/Sezary Mononuclear cells within the epidermis (exocytosis) unassociated with significant spongiosis (Fig. 7)
Dermatomyositis/Subacute
cutaneous lupus erythematosus
Interface dermatitis with vacuolar alteration, often thickening of the basement membrane,
colloid bodies, increased dermal mucin
Dermatophytosis Hyphae within stratum corneum, mounds of parakeratosis
Drug eruption Interface dermatitis with necrotic keratinocytes
Acute graft-vs-host disease Vacuolar alteration often with bsatellite cell necrosisQ of keratinocytes (Fig. 8)
Ichthyoses Changes of the specific type of inherited ichthyosis (epidermolytic hyperkeratosis) or nondiagnostic changes
Idiopathic Nonspecific changes (usually subacute or chronic spongiotic dermatitis-like changes)
Lymphoproliferative diseases Superficial, deep, and interstitial dermal infiltrate of atypical mononuclear cells
Paraneoplastic Nonspecific changes
Pemphigoid Subepidermal bulla with dermal eosinophils and/or eosinophilic spongiosis (Fig. 9)
Pemphigus Intraepidermal bulla with acantholysis and/or eosinophilic or neutrophilic spongiosis
Paraneoplastic pemphigus Suprabasal acantholysis, dyskeratotic keratinocytes, vacuolar alteration with lichenoid inflammation
Pityriasis rubra pilaris Epidermal hyperplasia with horizontal and vertical alternating orthokeratosis
and parakeratosis; dilated plugged follicular infundibulum
Psoriasis Psoriasiform epidermal hyperplasia with mounds or confluent parakeratosis layered
with neutrophils, hypogranulosis, and dilated tortuous papillary blood vessels (Fig. 10)
Sarcoidosis Epithelioid dermal granulomas with little or no mantle of surrounding lymphocytes
Scabies Superficial and deep perivascular and interstitial inflammation with many eosinophils;
frequent spongiosis; stratum corneum with mite, excreta, crusting possible
Seborrheic dermatitis Spongiotic psoriasiform dermatitis with parakeratosis often with neutrophils at the lips of the follicular ostia
Stasis with autoeczematization Spongiotic dermatitis often with some eosinophils
M.J. Rothe et al. 212
when used in conjunction with clinical and histological
features.
105,106
Histopathology
The histopathology of erythroderma varies depending on
the underlying etiology (Table 3). Therefore, careful
examination of the epidermis and dermis from a punch
biopsy is recommended. In approximately one third of
erythrodermic patients, however, the biopsies fail to reveal
the diagnostic features of any specific disease. In addition,
only 50% of any specific biopsy submitted on these patients
are likely to reveal the underlying cause.
107,108
This is in
part because the specific features of the disease can be
masked by nonspecific features associated with the eryth-
roderma. Therefore, multiple simultaneous punch skin
biopsies are recommended to enhance the possibility that
one might show the distinctive changes of the underlying
disease process that has resulted in the patients erythro-
derma. In addition to routine histology, special stains,
immunoperoxidase studies, gene rearrangement studies, and
direct immunofluorescence have proven to be very helpful.
Algorithm of approach to the erythrodermic
patient
Erythrodermic patient presents to your office.
q
Obtain history of possible precipitating causes and
pertinent past medical history and family history. Check
medication history.
q
Full skin examination of patient for any telltale sign of
underlying skin diseases. Check nails and mucosa. Check
lymph nodes and rule out organomegaly. Take vital signs to
establish patient stability.
q
Perform multiple skin biopsies for routine histology.
Simultaneously initiate cool down topical therapies and
supportive care immediately.
q
If appropriate, biopsy enlarged lymph nodes.
If appropriate, evaluate complete blood cell count,
CD4:CD8 ratio, and antinuclear antibodies.
If appropriate order chest x-ray.
Consider patch testing if appropriate.
If appropriate, rebiospy for direct immunofluoresence to
rule out immunobullous disease and/or rebiopsy for gene
rearrangement studies to rule out lymphoproliferative
disease.
If no underlying etiology identified, refer to primary care
physician to rule out underlying systemic disease.
q
Onceunderlyingetiologyisestablished, treat appropriately.
Systemic complications
Systemic complications of erythroderma include infec-
tion, fluid and electrolyte imbalances, thermoregulatory
disturbance, high output cardiac failure,
109
acute respiratory
distress syndrome,
110
and gynecomastia. The inflamed,
fissured, and excoriated skin is susceptible to bacterial
colonization, and sepsis occurs occasionally. Staphylococcal
sepsis is especially a risk for patients with CTCL and HIV-
positive erythroderma.
110-112
Fluid and electrolyte imbal-
ances occur from loss of fluid, electrolytes, and protein from
leaky capillaries.
Increased perfusion of the skin is associated with high
output cardiac failure and temperature dysregulation. High
output cardiac failure is associated with the shunting of
blood through the inflamed skin, and is of particular concern
in elderly patients or patients with preexisting cardiac
conditions.
109
These leaky dilated capillaries also allow
evaporation of heat, which contributes to thermoregulatory
disturbance, in addition to inability to respond to changes in
temperature via vasoconstriction and vasodilation.
113
There
is also an increase in the basal metabolic rate, which
elevates the skin temperature.
50
Erythroderma increases protein loss by 25% to 30% in
psoriatic erythroderma, and 10% to 15% from nonpsoriatic
erythroderma.
114
This protein loss causes a negative
nitrogen balance that can be manifest by edema, muscle
wasting, and hypoalbuminemia.
Increased circulating levels of adhesion molecules
intercellular adhesion molecule-1, vascular cell adhesion
molecule-1, and E-selectin have been found in patients with
erythroderma secondary to psoriasis, eczema, and patients
with CTCL. The adhesion molecule expression on endo-
thelial cells was examined in patients with erythroderma,
and there were no differences found in adhesion molecule,
vascular cell adhesion molecule-1, intercellular adhesion
molecule-1, P-selectin, and E-selectin expression in differ-
ent types of erythroderma. Sezary syndrome was found to
have higher mean expression of all adhesion molecules than
patients with other forms of CTCL, but it was not
statistically significant. Sigurdsson et al
115
suggest that the
similarities in adhesion molecule expression in various types
of erythroderma may correlate with the similarities in the
clinical examination of patients with erythroderma of
diverse etiologies. Cytokine profiles in dermal infiltrates
show differences between types of erythroderma, with
benign erythroderma showing a T-helper 1 cytokine profile,
whereas Sezary syndrome shows a T-helper 2 cytokine
profile. This may indicate that there are different pathophy-
siogical mechanisms for development of erythroderma.
116
Treatment
The initial approach to the management of erythroderma
of any etiology includes attention to nutrition and fluid and
Life-threatening erythroderma: diagnosing and treating the bred manQ 213
electrolyte replacement and the institution of gentle local
skin care measures. Oatmeal baths and wet dressings to
weeping or crusted sites should be followed by application
of bland emollients and low-potency topical corticosteroids.
Higher potency topical corticosteroids are not recommended
because of risk for systemic absorption secondary to the
extensive body surface area and the enhanced cutaneous
permeability.
117
Similarly, increased absorption of topical
tacrolimus has been observed in a patient with leukemic
erythroderma, posing the risk for nephrotoxicity and
warranting monitoring of tacrolimus blood levels.
118
Topical immunomodulators may also be irritating and
poorly tolerated by the erythrodermic patient. Other skin
irritants such as tars and hydroxy acid moisturizers are also
avoided. A warm and humidified environment will increase
patient comfort, prevent hypothermia, and improve mois-
turizing of the skin. Sedating oral antihistamines are
prescribed to relieve pruritus and anxiety. Systemic
antibiotics are required for patients with secondary infec-
tion. In cases in which a drug-induced erythroderma has not
been excluded, consideration should be given to discontin-
uation of all nonessential medications. Diuretics may be
necessary when peripheral edema fails to respond to leg
elevation and local skin care. Patients with evidence of
cardiovascular or respiratory failure require hospitalization
for urgent care.
Systemic dermatologic therapy may be required to
maintain improvement achieved with local measures or to
control erythroderma refractory to local measures. Systemic
corticosteroids are recommended for patients with systemic
drug hypersensitivity reactions and should obviously be
avoided in patients with possible underlying psoriasis. Bio-
logics are an important therapeutic advance in the treatment of
labile psoriasis; published reports describe rapid and dramatic
control of erythrodermic and generalized pustular psoriasis
with infliximab. Infusions of 5 to 10 mg/kg infliximab have
been found to substantially completely clear erythrodermic
psoriasis in 3 to 4 weeks and may be an effective alternative to
conventional treatments for acutely ill patients.
119,120
When the specific cause of erythroderma remains
undiagnosed, empiric therapy can be considered with agents
such as systemic corticosteroids, methotrexate, cyclosporine,
mycophenolate mofetil, and acitretin. A strong but not
confirmed suspicion for the diagnosis of psoriasis should
preclude the use of systemic corticosteroids. Similarly,
immunosuppressive agents such as cyclosporine should be
avoided unless a diagnosis of CTCL has been excluded by the
most sophisticated and up-to-date laboratory testing
available.
Natural course of disease
The prognosis of erythroderma is dependent on the
underlying etiology. With the exception of severe systemic
hypersensitivity reactions, drug-induced erythroderma
clears readily with discontinuation of the causative
drug.
44,121
Erythroderma secondary to psoriasis and spongi-
otic dermatitis usually improves within several weeks to
several months, although cases of chronic psoriatic atopic
erythroderma are not uncommon. Erythrodermic psoriasis
may recur in 15% of patients after initial clearing.
50
Erythroderma secondary to CTCL or other malignancy is
often persistent and refractory. One third of patients with
idiopathic erythroderma have been observed to show
complete remission,
4,45
whereas 50% of patients demon-
strate partial remission.
45
Those with chronic idiopathic
erythroderma are at high risk to evolve to CTCL.
25,45,47
Early published series of erythroderma reported a
significant mortality rate from complications including
pneumonia, cardiac failure, and sepsis.
3,32,42
Deaths were
most common in patients with pemphigus foliaceus,
lymphoproliferative malignancy, severe drug reactions,
and idiopathic erythroderma.
32
More recent series have
found a decreased mortality rate with most deaths occurring
in patients with malignancy-related erythroderma.
25,44,53
Deaths have also been reported in patients with high output
cardiac failure.
47
Conclusions
The erythrodermic patient requires immediate attention.
Unfortunately, physical examination, routine laboratory
findings, and even initial biopsies may be nondiagnostic,
often making these patients challenging to diagnose and
treat. Multiple biopsies and, often, repeat biopsies may be
necessary to make a definitive diagnosis. Although death
from cardiac failure, sepsis, capillary leakage syndrome, and
even respiratory distress syndrome have been reported, early
medical intervention and newer dermatologic therapies have
improved the prognosis of this devastating dermatologic
condition.
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