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Erythema Multiforme Toxic Epidermal Necrolysis and Homeopathy


© Dr. Rajneesh Kumar Sharma MD (Homoeopathy)

Alternate Names

EM, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, Lyell’s Syndrome


Erythema multiforme (EM) is a skin condition of unknown cause, mediated by deposition of immune complex (mostly IgM) (Psora/ Syphilis) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure.


It is a type of hypersensitivity (allergic) (Psora/ Sycosis/ Syphilis) reaction that occurs in response to medications, infections, or illness.

  • Medications associated with erythema multiforme include sulphonamides, penicillin, barbiturates, and phenytoin. (Causa occasionalis)
  • Associated infections include herpes simplex and mycoplasma infections.

The exact cause is unknown. The disorder is thought to involve damage to the blood vessels of the skin with subsequent damage to skin tissues (Psora/ Syphilis) . Approximately 90% of erythema multiforme cases are associated with herpes simplex or Mycoplasma infections. The syndrome occurs primarily in children and young adults.

Viral upper respiratory tract infections, Mycoplasma pneumonia, pharyngitis and Herpes simplex infection are also reported to cause erythema multiforme. The list of other possible etiologies is extensive, and includes systemic lupus erythematosus, histoplasmosis, pregnancy, malignancy and external-beam radiation. In most series, some cases remain idiopathic. Several authors have postulated an immunologic etiology for erythema multiforme, although no one has been able to demonstrate conclusively the pathogenesis of erythema multiforme.


It may present with a classic skin lesion with or without systemic symptoms (Psora++/ Syphilis+). In Stevens-Johnson syndrome, the systemic symptoms are severe and the lesions are extensive, involving multiple body areas (especially the mucous membranes). Toxic epidermal necrolysis (TEN syndrome, or Lyell’s syndrome) involves multiple large blisters that coalesce, followed by sloughing of all or most of the skin and mucous membranes (Psora+/ Syphilis++).


Skin lesion

  • Multiple (Psora)
  • Sudden onset and  may recur (Psora)
  • May spread (Psora/ Syphilis)
  • May appear as nodule, papule, or macule (Psora/ Syphilis)
  • Central lesion surrounded by concentric rings of pallor and redness (“target”, “iris”, “bull’s eye” shape) (Syphilis)

A typical Target Shape lesion

  • May have vesicles and bullae of various sizes (Psora/ Sycosis/ Syphilis)
  • Located on the legs, arms, palms, hands, or feet
  • May involve the face or lips
  • Trunk is usually not involved
  • Usually symmetrical (Psora)
  • Itching of the skin may be present (Psora)
  • Fever (Psora)
  • General ill feeling (Psora)
  • Joint aches (Psora)

Additional symptoms that may be-  

  • Vision abnormalities (Psora/Syphilis)
  • Dry eyes (Psora/ Sycosis)
  • Bloodshot eyes (Psora)
  • Eye pain (Psora)
  • Eye burning, itching and discharge (Psora/ Sycosis/ Syphilis)
  • Mouth sores (Psora/ Syphilis)

Stevens-Johnson syndrome

Stevens-Johnson syndrome has similar skin lesions with the additional involvement of no less than two mucous membranes, and fever (Psora). The appearance of the mucosal lesion is erythema and oedema (Psora/ Sycosis), which progresses to erosions and pseudomembrane formation (Syphilis). In addition to the target lesions, there is development of a characteristic maculopapular rash, usually early in the disease (Psora). Prodromal symptoms, such as fever, malaise, and cough are sometimes reported as a feature, and they usually occur seven to ten days prior to full-blown exhibition (Psora). The majority of cases of erythema multiforme and Stevens-Johnson syndrome are between ages 20 and 40, and 20% of cases occur in children and adolescents. The mortality of Stevens-Johnson syndrome is reported as 3 to 19%.

Toxic epidermal necrolysis (TEN)

It is distinguished by larger body surface area involvement, and the development of bullae (Psora/ Sycosis/ Syphilis). The epidermis of the skin peels off in sheets greater than 3 cm, and the skin becomes tender within 48 hours (Syphilis). TEN should be distinguished from staphylococcal scalded skin syndrome. Some permanent sequelae, most of which are ocular, or permanent skin pigmentary changes are seen. The most common cause of death is sepsis, mostly from Staphy aureus or Pseudomonas aeruginosa infections. The mortality rate is 30% to 70%.

Necrolysis of mucosa and skin in TEN

Differential Diagnosis

  • Kawasaki’s disease
  • Behcet’s syndrome
  • Small-vessel vasculitis syndromes
  • Lupus erythematosus, pemphigus
  • Pemphigoid, epidermolysis bullosa
  • Dermatitis herpetiformis.


The diagnostic criteria for erythema multiforme (EM) is individual “target” skin lesions less than 3 cm in diameter, less than 20% of body surface area involved, with minimal mucous membrane involvement, and biopsy compatible with EM. The cutaneous lesions are typically symmetric, and involve the extremities, with the dorsal hands and extensor aspects most commonly involved.

It is primarily based on the appearance of the skin lesion and its typical symmetrical distribution, especially if there is a history of risk factors or associated diseases.

There may be a positive Nikolsky’s sign. (The sign is positive when slight rubbing of the skin results in exfoliation of the outermost layer, forming a blister within minutes.)

A skin lesion biopsy and microscopic examination may be helpful to differentiate erythema multiforme from other disorders. Erythema multiforme may show tissue death and other changes. Microscopic examination of the tissue may also show antibody deposits.


Treatment includes control of the underlying causes or illnesses, treatment of the symptoms, and prevention of infection. Suspected medications should be discontinued.


Mild forms of erythema multiforme usually resolve without difficulty in 2 to 6 weeks, but they may recur. More severe forms may be difficult to treat. Stevens-Johnson syndrome and toxic epidermal necrolysis are associated with high death rates.


  • Permanent skin damage and scarring
  • Endorgans inflammation- Pneumonitis, Myocarditis, Nephritis, Hepatitis
  • Secondary skin infection (cellulitis)
  • Systemic infection, sepsis
  • Loss of body fluids, shock

Homoeopathic Treatment

Remedies in decreasing order of indication in EN.

Here, we see that skin manifestations of Thyroidinum, Kali iod, Arnica, Lac def, Syphilinum, Rannunculus bulbosus, Graphites, Nat carb, Clemetis, Sepia and many more given above are similar to those of Erythema multiforme. After addition of constitutional symptoms, the correct choice of remedy can be easily made for a perfact and sure cure.


28. Erythema Multiforme" height="57" border="0" width="45"> A. External Manifestations > 28. Erythema Multiforme Lichtman's Atlas of Hematology

Erythema Multiforme" height="53" border="0" width="39"> Chapter 123. The Vascular Purpuras > Erythema Multiforme Williams Hematology, 8e

Erythema Multiforme (Stevens–Johnson Syndrome)" height="54" border="0" width="42"> Chapter 15. Ocular Disorders Associated with Systemic Diseases > Erythema Multiforme (Stevens–Johnson Syndrome) Vaughan & Asbury's General Ophthalmology, 18e

Erythema Multiforme" height="53" border="0" width="42"> Chapter 15. Skin > Erythema Multiforme CURRENT Diagnosis & Treatment: Pediatrics, 21e

 Chapter 177. Erythema Multiforme, Stevens-Johnson Syndrome, and Toxic Epidermal Necrolysis The Color Atlas of Family Medicine, 2e

Erythema Multiforme ( Figure 20-6 )" height="51" border="0" width="39"> Chapter 20. Dermatopathology > Erythema Multiforme (Figure 20-6 ) Pathology: The Big Picture

Erythema Multiforme" height="53" border="0" width="40"> Chapter 245. Serious Generalized Skin Disorders > Erythema Multiforme Tintinalli's Emergency Medicine

Erythema multiforme" height="51" border="0" width="36"> Chapter 32. Viral & Rickettsial Infections > Erythema multiforme CURRENT Medical Diagnosis & Treatment 2014

Erythema Multiforme" height="53" border="0" width="38"> Chapter 32. Viral & Rickettsial Infections > Erythema Multiforme CURRENT Medical Diagnosis & Treatment 2014

Erythema Multiforme: Introduction" height="53" border="0" width="39"> Chapter 39. Erythema Multiforme > Erythema Multiforme: Introduction Fitzpatrick's  Dermatology in General Medicine, 8e

 Chapter 39. Erythema Multiforme Fitzpatrick's Dermatology in General Medicine, 8e

Stevens–Johnson Syndrome, Toxic Epidermal Necrolysis, and Erythema Multiforme" height="49" border="0" width="39"> Chapter 5. Conjunctiva & Tears > Stevens–Johnson Syndrome, Toxic Epidermal Necrolysis, and Erythema Multiforme Vaughan & Asbury's General Ophthalmology, 18e

Erythema Multiforme" height="54" border="0" width="40"> Chapter 6. Basic Pathologic Reactions of the Skin > Erythema Multiforme Fitzpatrick's Dermatology in General Medicine, 8e

Chapter 6. Dermatologic Disorders > Erythema Multiforme CURRENT Medical Diagnosis & Treatment 2014

Key Syndrome Erythema Multiforme" height="61" border="0" width="35"> Chapter 6. The Skin and Nails > Key Syndrome Erythema Multiforme DeGowin's Diagnostic Examination, 9e

Interface Dermatitis: Erythema Multiforme" height="53" border="0" width="40"> Chapter 8. Diseases of the Skin > Interface Dermatitis: Erythema Multiforme Pathophysiology of Disease, 6e

Encyclopedia Homoeopathica

Radar 10

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Comment by Dr Rajneesh Kumar Sharma MD(Hom) on February 24, 2014 at 11:47pm

Thanks Debby... You are always awesome....

Comment by Debby Bruck on February 24, 2014 at 11:42pm

Dear Dr Rajneesh. This disease looks quite frightening and one would be concerned about life and death outcome, plus how many people may be affected by this disease and the age ranges. How does one contract this illness and can nutrition in any way help? Was this topic of interest because you have seen one or more cases?

MedScape Reports |  Erythema multiforme (EM) is an acute, self-limited, and sometimes recurring skin condition that is considered to be a type IV hypersensitivity reaction associated with certain infections, medications, and other various triggers.[1]

Erythema multiforme may be present within a wide spectrum of severity. Erythema multiforme minor represents a localized eruption of the skin with minimal or no mucosal involvement. The papules evolve into pathognomonic target lesions or iris lesions that appear within a 72-hour period and begin on the extremities (see the following image). Lesions remain in a fixed location for at least 7 days and then begin to heal. Lesions may also appear as arcuate lesions (see the second image below). Precipitating factors include herpes simplex virus (HSV), Epstein-Barr virus (EBV), and histoplasmosis. Because this condition may be related to a persistent antigenic stimulus, recurrence is the rule rather than the exception, with most affected individuals experiencing 1-2 recurrences per year.


PubMed  Erythema multiforme, Stevens-Johnson syndrome and toxic epidermal n...


To review 10 years' experience in a tertiary care paediatric hospital of erythema multiforme (EM), Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). In addition, to apply a recently described classification system for EM, SJS and TEN in children.


Retrospective study of all children with a discharge diagnosis of EM, SJS or TEN over a 10-year period.


A university tertiary care paediatric hospital.


Sixty-one paediatric patients with a discharge diagnosis of EM, SJS or TEN.


Epidemiology, laboratory features, causative factors, treatment methods, complications and mortality of EM, SJS and TEN in this group of patients. Comparison of correlation with aetiology of old and new classification systems in a paediatric population.


Mucous membrane involvement was documented in 61% of patients. Ocular involvement was seen in 39%. Complications occurred in 21% cases, all of whom had SJS or TEN. Only one patient died as a result of their skin condition. Corticosteroids were used in 18% of cases; 95% of whom had a discharge diagnosis of SJS or TEN. The drugs most commonly identified as aetiological agents were sulphonamides and penicillins (26% each). The most frequently implicated infectious agent was herpes simplex virus (19.7%). Classification of study cases according to Bastuji-Garin et al. indicates a strong trend toward bullous EM cases being attributable to infection and SJS/TEN cases to drugs. There was no such clear trend with respect to aetiology when diagnosis was done without the classification system.


EM, SJS and TEN rarely cause mortality but significant morbidity is seen. Infectious agents, particularly herpes simplex virus, and drugs, especially the sulphonamides and penicillins, are the most common aetiological agents. The classification system proposed by Bastuji-Garin et al. correlates better with aetiology than the practice that preceded it.

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