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Year : 1990  |  Volume : 56  |  Issue : 3  |  Page : 196-199

Elucidation and management of 30 patients of drug induced toxic epidermal necrolysis (DTEN)

Correspondence Address:
Surrinder Kaur

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Thirty patients of drug induced toxic epidermal necrolysis (DTEN) were seen over a period of 7 years. They included 16 males and 14 females and their ages ranged from 5 months to 60 years with a mean of 23 years. The epidermal necrosis affected 20-100% of the body surface area. The oral, nasal and conjunctival mucosae were involved in all the cases. Antitubercular drugs were the most common offending agents (1/3rd of the patients) followed by anticonvuIsants, sulfonamides, butazones, and antibiotics. TEN proved fatal in 8 (27%) patients with septicemia being the most common predisposing factor. Other factors which contributed to fatal outcome were underlying severe disease in 2 patients and disseminated intravascular coagulation in one.

Keywords: Toxic epidermal necrolysis (TEN), Drugs, Corticosteroids, Complications.

How to cite this article:
Kaur S, Nanda A, Sharma K V. Elucidation and management of 30 patients of drug induced toxic epidermal necrolysis (DTEN). Indian J Dermatol Venereol Leprol 1990;56:196-9

How to cite this URL:
Kaur S, Nanda A, Sharma K V. Elucidation and management of 30 patients of drug induced toxic epidermal necrolysis (DTEN). Indian J Dermatol Venereol Leprol [serial online] 1990 [cited 2020 Oct 24];56:196-9. Available from:

Drug induced toxic epidermal necrolysis (DTEN) is a relatively rare, potentially life threatening, generalized mucocutaneous disorder with reported mortality ranging from 20-70%[0],[2],[3] A large number of reports on precipitating drugs, clinical course, treatment, and outcome have appeared from different parts of the world.[1],[4],[5],[6],[7],[8],[9] We present our experience with 30 patients of DTEN seen over last 7 years and managed in general skin wards.

  Materials and Methods Top

All the patients presenting with suspected drug induced toxic epidermal necrolysis (DTEN) between the years 1982 and 1989 were hospitalized. A detailed history of precipitating factors, especially the drugs, temporal correlation between the intake of drug(s) and onset of symptoms was elucidated. A detailed cutaneous and systemic examination was carried out. Percentage of body surface area involved was recorded. A complete hematological profile, urinalysis, serum biochemistry, skiagram of the chest, bacterial cultures from the skin, throat, eyes, and urine were carried out in all patients at the time of admission and thereafter weekly till discharge. Tzanck smear for exfoliative cytology, and biopsy specimens for histopathology from involved skin were taken in all the cases. Fungal cultures and serology was sent from all patients suspected of having septicemia or those who had persistent fever.

The patients having DTEN were given a corner bed of the cubicle having-,total of the 6 beds in general medical ward. A screen was kept around the patient and whenever required, a burn cage was arranged. Strict aseptic precautions were taken and only two resident doctors and a staff nurse were allowed to handle the patient. The treatment protocol comprised of stoppage of all the suspected drugs, frequent change of posture, maintenance of fluid and electrolyte balance, care of the eyes and oral cavity, potassium permanganate compresses (1:10,000 dilution) and paraffin gauge dressing of the denuded areas. Patients who reported within 7 days of the onset of symptoms of TEN were treated with prednisolone 1-2 mgs/kg body weight in a short course. All suspected infections and septicemias were treated with appropriate antibiotics. Prophylactic antibiotics were given when more than 60% of the body surface area was involved with large eroded area. Treatment of the basic disease, if necessary was continued with alternative unrelated drugs.

  Results Top

A total of 30 patients of drug induced TEN, 16 males and 14 females, were seen over a period of 7 years. They constituted 0.034% of 87518 dermatology out patients. The mean age of the patients was 23 years (range 5-60 years). The peak incidence was observed between second and fourth decade. Arititubercular drugs were among the most commonly (1/3rd of the total patients) encountered precipitating drugs followed by anticonvulsants, sulfonamides, butazones, and antibiotics [Table - 1].

The extent of skin involvement varied from 20% of body surface to almost total. Patients having more than 60% skin involvement were toxic and profoundly ill. Fever ranging from 38 to 41° C was recorded in 25 (83.3%) patients. Skin tenderness with positive Nikolsky's sign and mucosal involvement was present in all (100%) patients.

Tuberculosis was the underlying disease in 9 patients, including pulmonary tuberculosis in 5, disseminated tuberculosis in 3 (one also had biopsy proven renal amyloidosis), and tuberculous salpingitis in one. Another patient on antitubercular therapy from outside was infact suffering from subacute bacterial endocarditis. Grandmal epilepsy was present in 5 cases, and grade IV protein energy malnutrition with fungal colitis and bronchopneumonia was present in one case each. Rest of the patients (14) . took drugs for headache, ear-ache, sore throat, fever, and. joint pains etc.

The erythrocyte sedimentation rate was elevated in all the patients. Leukocytosis (leukocytic count more than 10,000/mm3) was present in 7 (23.3%), leukopenia (leukocytic countless than 3,000/mm3) in 6 (20%), and anemia in 10 (33.3%) patients. Transient proteinuria and microscopic hematuria was found in 7 (23.3%) patients.

Staphylococcus aureus was isolated from the skin of 7 (23.3%) patients at the first instance. Number of isolations increased subsequently from skin as well as other sites. Eleven (36.7%) patients were suspected to have septicemia during the hospital stay and the organisms were isolated in 6 patients. They included Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas seruginosa, and B.proteus. Two of these patients also showed rising antibody titre to Candida albicans and Aspergillus fumigatus respectively and were treated with ketoconazole.

Twenty one patients received systemic corticosteroids whereas 9 patients did not receive steroids. Secondary infection [Table - 2] was the most commonly observed complication seen in 11 (36.7%) patients. Incidence of secondary infection was higher in patients having more than 60% body surface area involvement with large eroded areas. An overall mortality of 27% (8 of 30 patients) was observed with a relatively higher (33.3%) incidence in patients managed without steroids versus those who received steroids (23.8%). However this figure was not statistically significant. No difference in complication rate (septicemia, bronchopneumonia, eye lesions etc.), between the two groups was noticed. Septicemia was the most common predisposing factor to fatal outcome. Other factors which contributed to bad prognosis included disseminated intravascular coagulation (DIC) in one patient, and severe underlying diseases including disseminated, tuberculosis with renal amyloidosis, grade IV protein energy malnutrition with fungal colitis and bronchopneumonia in one patient each.

The eye sequelae included panophthalmitis leading on to blindness, keratoconjunctivitis sicca, and corneal opacities in one patient each. Others included cicatricial alopecia (one patient), twenty nail dystrophy (2), and meatal stenosis (one).

  Comments Top

Contrary to most earlier reports where sulphonamides, anti convuIsants, antibiotics, and non-steroidal anti infIammatory drugs were commonly encountered offending drugs for TEN,[1],.[4],[5],[6] antitubercular drugs formed the major (1/3rd of the patients) group in the present series [Table - 1]. Tuberculosis is still one of the major health problems in India and antitubercular drugs are used frequently. This explains the difference in pattern of culprit drugs for TEN with us.[10],[11],[12]

The fatality rate in TEN has varied from 20-­70%.[1],[2],[3] A mortality of 33-50% was reported even when the patients were managed in the burn centres.[13],[14] Mortality rate of 27% in the present series of 30 patients, where they were managed in the general medical wards is comparable. If managed under proper aseptic precautions with nutritional care, and close monitoring for complications, a better survival rate can be achieved. In most recent series, the use of corticosteroids in DTEN has been questioned.[3],[4],[5] We found an apparently better survival rate in patients who received steroids versus those who did not. However, we do not recommend systemic corticosteroids for all patients of DTEN, as our groups were not matched in terms of age, sex extent of disease, underlying disorders and many other parameters. We feel that steroids may be of help if given in early stages of the disease. As some immunologic mechanism is responsible in pathogenesis of TEN[4], they may be exercising an irri,rnunomodulatory role. Recently, a better prognosis with use of plasmapheresis[15], cadaver's allografts and xenografts[3], and steroids pulse therapy[16] has been claimed and needs to be confirmed in large number of patients.

  References Top

1.Lyell A : A review of the toxic epidermal necrolysis in Britain. Brit J Dermatol, 1967; 79 : 662-671.  Back to cited text no. 1    
2.Fritsch PC and Elias PM : Toxic epidermal necrolysis, in : Dermatology in General Medicine. 3rd Ed, Editors, Fitzp atrick TB, Eisen AZ, Wolff K et al : Mc Graw Hill Book Company, New York, 1987; p 563.  Back to cited text no. 2    
3.Heimbach DM, Engram LH, Marvin JA et al : Toxic epidermal necrolysis : A step forward in treatment, JAMA, 1987; 257 . 21171-2175.  Back to cited text no. 3    
4.Hang MCY : Drug-induced toxic epidermal necrolysis, Brit J Dermatol, 1985; 113 : 597-600.  Back to cited text no. 4    
5.Ruiz-Maldonado R : Acute disseminated epidermal necrosis types 1, 2 and 3 : Study of sixty cases, J Amer Acad Dermatoi, 1985; 13 : 623-635.  Back to cited text no. 5    
6.Gullaume SC, Roujeau JC, Revuz J et al : The culprit drugs in 87 cases of toxic epidermal necrolysis (Lyell's syndrome), Arch Dermatol, 1987; 123 : 1166-1170.  Back to cited text no. 6    
7.Lyell A : Toxic epidermal necrolysis (The scalded skin syndrome) : A reapraisal, Brit J Dermatol, 1979; 100 : 69-86.  Back to cited text no. 7    
8.Peck GC, Herzig GP and Elias PM : TEN in a patient with Graft-Vs-host reaction, Arch Dermatol, 1972; 105 : 561-569.  Back to cited text no. 8    
9.Tagami H, Tatsuta K, Iwatski K et al : Delayed hypersensitivity in ampicillin-induced toxic epidermal necrolysis, Arch Dermatol, 1983; 119 : 910-913.  Back to cited text no. 9    
10.Bedi TR, Singh OP and Bhutani LK : Acute epidermal necrolysis (Lyell's syndrome), Ind J Chest Dis, 1974; 16 : 55-57.  Back to cited text no. 10    
11.Sehgal VN, Bahadur P, Ghosh SK et al : Toxic epidermal necrolysis as a result of anti-tubercular drugs, Ind J Chest Dis, 1973; 15 : 57-60.  Back to cited text no. 11    
12.Jain VK, Mathur KC, Shukla SN et al Toxic epidermal necrolysis (Lyell's syndrome) due to streptomycin, Ind J Chest Dis, 1980; 22 : 73-76.  Back to cited text no. 12    
13.Halebian PH, Madden MR, Finkleskin JL et al Improved burn center survival of patients with toxic epidermal necrolysis managed without steroids, Ann Surg, 1986; 204 : 503-511.  Back to cited text no. 13    
14.Kim PS, Goldfarb JN, Gaisford JC et al : Stevens­Johnson syndrome and toxic epidermal necrolysis : A pathologic review with recommendations for a treatment protocol, J Burn Care Rehabil, 1983; 4 : 91-100.  Back to cited text no. 14    
15.Kamanabroo D, Schmitz LW and Czarnetzki BM Plasmapheresis in severe drug induced toxic epidermal necrolysis, Arch Dermatol, 1985; 121 1548-1549.  Back to cited text no. 15    
16.Sheretz EF, Jegasothy BV and Lazarus GS Pehnytein hypersensitivity reaction presenting with toxic epidermal necrolysis and severe hepatitis, J Amer Acad Dermatol, 1985; 12 : 178-181.  Back to cited text no. 16    


[Table - 1], [Table - 2]

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