Erythroderma (Generalized Exfoliative Dermatitis)
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Exfoliative dermatitis (ED) is a definitive term that refers to a scaling erythematous dermatitis involving 90% or more of the cutaneous surface. Exfoliative dermatitis is characterized by erythema and scaling involving the skin’s surface and often obscures the primary lesions that are important clues to understanding the evolution of the disease. Clinicians are challenged to find the cause of exfoliative dermatitis by eliciting the history of illness prior to erythema and scaling, by probing with biopsies, and by performing blood studies. See the images below.
The term red man syndrome is reserved for idiopathic exfoliative dermatitis, in which no primary cause can be found, despite serial examinations and tests. Idiopathic exfoliative dermatitis is characterized by marked palmoplantar keratoderma, dermatopathic lymphadenopathy, and a raised level of serum immunoglobulin E (IgE) and is more likely to persist than other types.
The term l’homme rouge refers to exfoliative dermatitis often secondary to cutaneous T-cell lymphoma. Erythrodermic mycosis fungoides should be distinguished from leukemic Sézary syndrome with erythroderma. [1] The historic classification of exfoliative dermatitis into Wilson-Brocq (a chronic process associated with exacerbation and remissions), Hebra or pityriasis rubra (relentlessly progressive disease), and Savill (self-limiting) types lacks any clinical significance.
An increased skin blood perfusion occurs in exfoliative dermatitis (ED) that results in temperature dysregulation (resulting in heat loss and hypothermia) and possible high-output cardiac failure. The basal metabolic rate rises to compensate for the resultant heat loss. Fluid loss by transpiration is increased in proportion to the basal metabolic rate. The situation is similar to that observed in patients following burns (negative nitrogen balance characterized by edema, hypoalbuminemia, loss of muscle mass).
A marked loss of exfoliated scales occurs that may reach 20-30 g/d. This contributes to the hypoalbuminemia commonly observed in exfoliative dermatitis. Hypoalbuminemia results, in part, from decreased synthesis or increased metabolism of albumin. Edema is a frequent finding, probably resulting from fluid shift into the extracellular spaces. Immune responses may be altered, as evidenced by increased gamma-globulins, increased serum IgE in some cases, eosinophil infiltration, and CD4+ T-cell lymphocytopenia in the absence of HIV infection. Oxidative stress is also associated with drug-induced erythroderma. [2]
Chronic erythroderma in elderly men may represent a unique condition distinct from adult atopic dermatitis. [3]
No racial predilection is reported for exfoliative dermatitis (ED).
Male-to-female ratio is 2-4:1.
Exfoliative dermatitis onset usually occurs in persons older than 40 years, except when the condition results from atopic dermatitis, seborrheic dermatitis, staphylococcal scalded skin syndrome, or a hereditary ichthyosis. Age of onset primarily is related to etiology. [4, 5]
The prognosis of exfoliative dermatitis depends largely on underlying etiology.
The disease course is rapid if it results from drug allergy, lymphoma, leukemia, contact allergens, or staphylococcal scalded skin syndrome.
A study [6] of pediatric patients (aged < 19 y) found that fever is a poor prognostic marker and may indicate a susceptibility to rapid deterioration. In this group, those with the following characteristics have a higher tendency to develop hypotension: age 3 years or younger, ill appearance, vomiting, glucose level of 110 mg/dL or less, calcium value of 8.6 mg/dL or less, platelet count of 300,000/μL or less, elevated creatinine value, polymorphonuclear leukocyte count of 80% or greater, and the presence of a focal infection. The risk of toxic shock syndrome is increased especially in children with erythroderma and fever who have the following additional features: age of 3 years or younger, ill appearance, elevated creatinine value, and hypotension upon arrival.
The disease course is gradual if it results from generalized spread of a primary skin disease (eg, psoriasis, atopic dermatitis).
The mean duration of illness typically is 5 years, with a median of 10 months.
Mortality varies according to the disease’s cause. In a study of 91 of 102 patients with exfoliative dermatitis by Sigurdsson et al, [7] a mortality rate of 43% was observed. Only 18% of the deaths were directly related to exfoliative dermatitis. In 74% of the deaths, causes unrelated to exfoliative dermatitis were implicated.
Educate patients on the specifics of the underlying cause of their exfoliative dermatitis (ED) and the importance of diligent follow-up management as indicated. Patients should be educated on the benefits of a healthy lifestyle and to immediately treat occurrences of erythroderma to better manage their diseases in the long term. Patients should be advised to avoid the use of and/or contact with of irritant soaps, lotions, detergents, and chlorine, and special considerations should be made for allergies, especially for patients with atopic dermatitis. [8] Excessive sweating should also be avoided.
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99mTC-sestamibi [13]
ACE inhibitors
Allopurinol
Aminoglutethimide
Amiodarone
Amitriptyline
Amoxicillin
Ampicillin
Angiogenetic inhibitors [14]
Arsenic
Aspirin
Atropine
Auranofin
Aurothioglucose
Barbiturates
Benactyzine
Beta-blockers
Beta carotene
Bumetanide
Bupropion
Butabarbital
Butalbital
Captopril
Carbamazepine
Carbidopa
Cephalosporins [15]
Chloroquine
Chlorpromazine
Chlorpropamide
Cimetidine
Ciprofloxacin
Cisplatin
Clofarabine [16]
Clofazimine
Clofibrate
Co-trimoxazole
Cromolyn
Cytarabine
Dapsone
Demeclocycline
Desipramine
Diazepam
Diclofenac
Diflunisal
Diltiazem
Doxorubicin
Doxycycline
Efavirenz [17]
Enalapril
Escitalopram [18]
Esomeprazole [19]
Ethambutol [20]
Etodolac
Fenofibrate [21]
Fenoprofen
Fluconazole
Fluindione [22]
Fluoxetine [23]
Fluphenazine
Flurbiprofen
Furosemide
Gemfibrozil
Gliclazide [24]
Glipizide [25]
Gold
Griseofulvin
Hydroxychloroquine
Imatinib [26]
Imipramine
Indomethacin
Intravenous immunoglobulin [27]
Intravesical mitomycin C [28]
Iodixanol [29]
Isoniazid
Isosorbide
Ketoconazole
Ketoprofen
Ketorolac
Leflunomide [30]
Lithium
Meclofenamate
Mefenamic Acid
Meprobamate
Methylphenidate
Midodrine [31]
Minocycline
Morphine sulfate [32]
Nalidixic Acid
Naproxen
Nevirapine [33]
Nitrazepam [25]
Nifedipine
Nitrofurantoin
Nitroglycerin
Nizatidine
Norfloxacin
Omeprazole
Pantoprazole [34]
Penicillamine
Penicillin
Pentobarbital
Perphenazine
Phenobarbital
Phenothiazines
Phenylbutazone
Phenytoin
Piroxicam
Primidone
Prochlorperazine
Propranolol
Pyrazinamide [20]
Pyrazolones
Quinapril
Quinidine
Quinine
Retinoids
Rifampin
Sorafenib [35]
Streptomycin
Strontium ranelate [36]
Sulfadoxine
Sulfamethoxazole
Sulfasalazine
Sulfisoxazole
Sulfonamides
Sulfonylureas
Sulindac
Terbinafine [37]
Tetracycline
Tobramycin
Tocilizumab [38]
Trazodone
Trifluoperazine
Trimethoprim
Vancomycin
Verapamil
Warfarin [39]
Sanusi H Umar, MD, FAAD Clinical Instructor of Medicine, Department of Medicine, Division of Dermatology, University of California, Los Angeles, David Geffen School of Medicine
Sanusi H Umar, MD, FAAD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Medical Association
Disclosure: Nothing to disclose.
A Paul Kelly, MD Chief, Clinical Professor, Department of Internal Medicine, Division of Dermatology, King/Drew Medical Center, Charles Drew University of Medicine and Science
A Paul Kelly, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, National Medical Association, Pacific Dermatologic Association
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society
Disclosure: Nothing to disclose.
Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Pennsylvania Academy of Dermatology
Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.
Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
James W Patterson, MD Professor of Pathology and Dermatology, Director of Dermatopathology, University of Virginia Medical Center
James W Patterson, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Dermatopathology, Royal Society of Medicine, Society for Investigative Dermatology, United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.
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