Indian Journal of Critical Care Medicine August 2014 Vol 18 Issue 8
is based on the 6 h rule; maximum recommended dose is 30 vials. Repeat doses for neurotoxic is based on the 1-2 h rule; maximum dose is 20 vials. Only the lyophilized polyvalent ASV is available in India.
Ofloxacin-induced toxic epidermal necrolysis
Anticholinesterase drugs have a variable, but potentially useful effect in patients with neurotoxic envenoming. Atropine sulfate (0.6 mg for adults; 50 g/kg for children) followed by neostigmine in a dose range of 0.01-0.04 mg/ kg every 1-3 h up to a maximum of 10 mg/24 h can be administered by intramuscular or intravenous route. Patients are observed over 30-60 min for improved neuromuscular transmission. Neostigmine appears to have no useful role in confirmed presynaptic envenoming, that is poisoning by common kraits and Russell’s viper. It is effective in postsynaptic neurotoxins such as those of cobra.[3] “anticholinesterase test” (e.g. “tensilon test”) needs to be performed first to check responsiveness of the patient to the drug as is performed for patients with suspected myasthenia gravis. The use of these drugs will help reduce the consumption of ASV, which is generally limited in a developing country like ours.[4] Awareness of the health care providers on this issue needs to be increased and comparative trials need to be done to quantify its dose sparing effect.
Sir, Toxic epidermal necrolysis (TEN) is a potentially life-threatening dermatologic disorder characterized by widespread erythema, necrosis, and bullous detachment of the epidermis and mucous membranes, resulting in exfoliation and possible sepsis and/or death. It is also known as Lyell’s syndrome. The drugs most commonly involved are antibiotics such as sulfonamides, beta-lactams tetracyclines, and quinolones. Anticonvulsants are such as phenytoin, phenobarbital and carbamazepine. Antiretroviral drugs, nonsteroidal anti-inflammatory drugs, and allopurinol.[1] Mycoplasma pneumoniae, herpes simplex, lupus erythematosus, aplastic anemia after allogeneic hematopoietic stem cell transplantation have also been reported as a cause of nondrug induced TEN.[2]
Vikas Saini, Dinesh Sardana, Tanvir Samra
Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Correspondence: Dr. Tanvir Samra, C-II/77 Moti Bagh 1, New Delhi - 110 021, India. E-mail: [email protected]
References 1. 2.
3.
4.
Raina S, Raina S, Kaul R, Chander V, Jaryal A. Snakebite profile from a medical college in rural setting in the hills of Himachal Pradesh, India. Indian J Crit Care Med 2014;18:134-8. National Snakebite Management Protocol, India. Directorate General of Health and Family Welfare, Ministry of Health and Family Welfare, India; 2008. Available from: http://www.mohfw.nic.in. [Last accessed on 2014 Jan 30] Watt G, Theakston RD, Hayes CG, Yambao ML, Sangalang R, Ranoa CP, et al. Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study. N Engl J Med 1986;315:1444-8. Anil A, Singh S, Bhalla A, Sharma N, Agarwal R, Simpson ID. Role of neostigmine and polyvalent antivenom in Indian common krait (Bungarus caeruleus) bite. J Infect Public Health 2010;3:83-7. Access this article online Quick Response Code: Website: www.ijccm.org
DOI: 10.4103/0972-5229.138164
A 42-year-old man presented with rapidly progressive generalized detachment of skin. Patient gave a history of abdominal pain and diarrhea for which he took tablets containing ofloxacin. After 2 days, he developed acute generalized erythematous rashes all over his body including face, trunk, upper, and lower extremities [Figure 1]. He also developed erosive lesions over oral mucosa and congestion of conjuntiva [Figure 2]. On examination, patient was febrile (39°C) and hypotensive (100/70 mm Hg). Generalized sheet like peeling of the skin involving >90% of body was present. Erosion and crusting over lip was present. Nikolsky sign was positive. There was no hepatosplenomegaly or lymphadenopathy. His total white blood cell count was 5.23 × 109/L. Platelet count was normal. Hemoglobin was 13.5 g/dl. Liver function tests showed mild elevation in aspartate aminotransferase (90 U/L) and alanine aminotransferase (70 U/L). Serum creatinine was 1.1 mg/dl. History and clinical findings were suggestive of TEN secondary to ofloxacin intake. Patient was treated with dexamethasone intravenously and fusidic acid antibiotic cream topically. Fluid management, symptomatic and supportive management had been done. Patient showed significant improvement within 2 week. Lesions totally resolved in a few weeks leaving postinflammatory pigmentation over body. 545
Indian Journal of Critical Care Medicine August 2014 Vol 18 Issue 8
or TEN in which a fluoroquinolone was the offending agent have been reported. Of these, 26 were associated with ciprofloxacin, whereas only one was associated with ofloxacin.[5] Here, we are reporting a patient with TEN induced by ingestion of oral ofloxacin which is not a common cause of TEN.
Gaurang Gupta
Department of dermatology, Om Premia Hospital, Palwal, Haryana, India
Correspondence: Dr. Gaurang Gupta, Department of Dermatology, Om Premia Hospital, 56 km stone, Palwal, Haryana India. Email: [email protected]
Figure 1: Sheet like peeling of skin
References 1. 2. 3. 4. 5.
Lissia M, Mulas P, Bulla A, Rubino C. Toxic epidermal necrolysis (Lyell’s disease). Burns 2010;36:152-63. Harr T, French LE. Toxic epidermal necrolysis and Stevens-Johnson syndrome. Orphanet J Rare Dis 2010;5:39. Correia O, Delgado L, Ramos JP, Resende C, Torrinha JA. Cutaneous T-cell recruitment in toxic epidermal necrolysis. Further evidence of CD8+lymphocyte involvement. Arch Dermatol 1993;129:466-8. Melde SL. Ofloxacin: A probable cause of toxic epidermal necrolysis. Ann Pharmacother 2001;35:1388-90. Van Bambeke F, Tulkens PM. Safety profile of the respiratory fluoroquinolone moxifloxacin: Comparison with other fluoroquinolones and other antibacterial classes. Drug Saf 2009;32:359-78. Access this article online
Figure 2: Crusting and erosive lesions over lip
Quick Response Code: Website: www.ijccm.org
The pathogenesis of Stevens-Johnson syndrome (SJS)/TEN is not fully understood, but is believed to be immune-mediated. The clinical, histopathological, and immunological findings in SJS/TEN support the concept, that SJS and TEN are specific drug hypersensitivity reactions in which cytotoxic T lymphocytes play a role in the initiation phase.[3] The histopathology of SJS/TEN lesions show that keratinocyte apoptosis followed by necrosis is the pathogenic basis of the widespread epidermal detachment observed in SJS/TEN.[2] The risk of death for patients with TEN can be accurately predicted by the TEN-specific severity-of-illness score. We calculated that our patient had a final score of 2 and a mortality risk of 12.1%. The frequency of fluoroquinolone use has been increasing owing to their broad antibacterial spectra and few adverse effects. Until now, these drugs have seldom been implicated in patients with TEN, but the incidence of fluoroquinolone-induced cutaneous reactions may be on the increase.[4] Until date, a total of 31 cases of SJS 546
DOI: 10.4103/0972-5229.138166
Internal jugular vein thrombosis from rhino-cerebral mucormycosis: Be careful before cannulation Sir, Rhino-cerebral mucormycosis is a relatively uncommon fungal infection of the nasal cavity and para-nasal
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
is based on the 6 h rule; maximum recommended dose is 30 vials. Repeat doses for neurotoxic is based on the 1-2 h rule; maximum dose is 20 vials. Only the lyophilized polyvalent ASV is available in India.
Ofloxacin-induced toxic epidermal necrolysis
Anticholinesterase drugs have a variable, but potentially useful effect in patients with neurotoxic envenoming. Atropine sulfate (0.6 mg for adults; 50 g/kg for children) followed by neostigmine in a dose range of 0.01-0.04 mg/ kg every 1-3 h up to a maximum of 10 mg/24 h can be administered by intramuscular or intravenous route. Patients are observed over 30-60 min for improved neuromuscular transmission. Neostigmine appears to have no useful role in confirmed presynaptic envenoming, that is poisoning by common kraits and Russell’s viper. It is effective in postsynaptic neurotoxins such as those of cobra.[3] “anticholinesterase test” (e.g. “tensilon test”) needs to be performed first to check responsiveness of the patient to the drug as is performed for patients with suspected myasthenia gravis. The use of these drugs will help reduce the consumption of ASV, which is generally limited in a developing country like ours.[4] Awareness of the health care providers on this issue needs to be increased and comparative trials need to be done to quantify its dose sparing effect.
Sir, Toxic epidermal necrolysis (TEN) is a potentially life-threatening dermatologic disorder characterized by widespread erythema, necrosis, and bullous detachment of the epidermis and mucous membranes, resulting in exfoliation and possible sepsis and/or death. It is also known as Lyell’s syndrome. The drugs most commonly involved are antibiotics such as sulfonamides, beta-lactams tetracyclines, and quinolones. Anticonvulsants are such as phenytoin, phenobarbital and carbamazepine. Antiretroviral drugs, nonsteroidal anti-inflammatory drugs, and allopurinol.[1] Mycoplasma pneumoniae, herpes simplex, lupus erythematosus, aplastic anemia after allogeneic hematopoietic stem cell transplantation have also been reported as a cause of nondrug induced TEN.[2]
Vikas Saini, Dinesh Sardana, Tanvir Samra
Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Correspondence: Dr. Tanvir Samra, C-II/77 Moti Bagh 1, New Delhi - 110 021, India. E-mail: [email protected]
References 1. 2.
3.
4.
Raina S, Raina S, Kaul R, Chander V, Jaryal A. Snakebite profile from a medical college in rural setting in the hills of Himachal Pradesh, India. Indian J Crit Care Med 2014;18:134-8. National Snakebite Management Protocol, India. Directorate General of Health and Family Welfare, Ministry of Health and Family Welfare, India; 2008. Available from: http://www.mohfw.nic.in. [Last accessed on 2014 Jan 30] Watt G, Theakston RD, Hayes CG, Yambao ML, Sangalang R, Ranoa CP, et al. Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study. N Engl J Med 1986;315:1444-8. Anil A, Singh S, Bhalla A, Sharma N, Agarwal R, Simpson ID. Role of neostigmine and polyvalent antivenom in Indian common krait (Bungarus caeruleus) bite. J Infect Public Health 2010;3:83-7. Access this article online Quick Response Code: Website: www.ijccm.org
DOI: 10.4103/0972-5229.138164
A 42-year-old man presented with rapidly progressive generalized detachment of skin. Patient gave a history of abdominal pain and diarrhea for which he took tablets containing ofloxacin. After 2 days, he developed acute generalized erythematous rashes all over his body including face, trunk, upper, and lower extremities [Figure 1]. He also developed erosive lesions over oral mucosa and congestion of conjuntiva [Figure 2]. On examination, patient was febrile (39°C) and hypotensive (100/70 mm Hg). Generalized sheet like peeling of the skin involving >90% of body was present. Erosion and crusting over lip was present. Nikolsky sign was positive. There was no hepatosplenomegaly or lymphadenopathy. His total white blood cell count was 5.23 × 109/L. Platelet count was normal. Hemoglobin was 13.5 g/dl. Liver function tests showed mild elevation in aspartate aminotransferase (90 U/L) and alanine aminotransferase (70 U/L). Serum creatinine was 1.1 mg/dl. History and clinical findings were suggestive of TEN secondary to ofloxacin intake. Patient was treated with dexamethasone intravenously and fusidic acid antibiotic cream topically. Fluid management, symptomatic and supportive management had been done. Patient showed significant improvement within 2 week. Lesions totally resolved in a few weeks leaving postinflammatory pigmentation over body. 545
Indian Journal of Critical Care Medicine August 2014 Vol 18 Issue 8
or TEN in which a fluoroquinolone was the offending agent have been reported. Of these, 26 were associated with ciprofloxacin, whereas only one was associated with ofloxacin.[5] Here, we are reporting a patient with TEN induced by ingestion of oral ofloxacin which is not a common cause of TEN.
Gaurang Gupta
Department of dermatology, Om Premia Hospital, Palwal, Haryana, India
Correspondence: Dr. Gaurang Gupta, Department of Dermatology, Om Premia Hospital, 56 km stone, Palwal, Haryana India. Email: [email protected]
Figure 1: Sheet like peeling of skin
References 1. 2. 3. 4. 5.
Lissia M, Mulas P, Bulla A, Rubino C. Toxic epidermal necrolysis (Lyell’s disease). Burns 2010;36:152-63. Harr T, French LE. Toxic epidermal necrolysis and Stevens-Johnson syndrome. Orphanet J Rare Dis 2010;5:39. Correia O, Delgado L, Ramos JP, Resende C, Torrinha JA. Cutaneous T-cell recruitment in toxic epidermal necrolysis. Further evidence of CD8+lymphocyte involvement. Arch Dermatol 1993;129:466-8. Melde SL. Ofloxacin: A probable cause of toxic epidermal necrolysis. Ann Pharmacother 2001;35:1388-90. Van Bambeke F, Tulkens PM. Safety profile of the respiratory fluoroquinolone moxifloxacin: Comparison with other fluoroquinolones and other antibacterial classes. Drug Saf 2009;32:359-78. Access this article online
Figure 2: Crusting and erosive lesions over lip
Quick Response Code: Website: www.ijccm.org
The pathogenesis of Stevens-Johnson syndrome (SJS)/TEN is not fully understood, but is believed to be immune-mediated. The clinical, histopathological, and immunological findings in SJS/TEN support the concept, that SJS and TEN are specific drug hypersensitivity reactions in which cytotoxic T lymphocytes play a role in the initiation phase.[3] The histopathology of SJS/TEN lesions show that keratinocyte apoptosis followed by necrosis is the pathogenic basis of the widespread epidermal detachment observed in SJS/TEN.[2] The risk of death for patients with TEN can be accurately predicted by the TEN-specific severity-of-illness score. We calculated that our patient had a final score of 2 and a mortality risk of 12.1%. The frequency of fluoroquinolone use has been increasing owing to their broad antibacterial spectra and few adverse effects. Until now, these drugs have seldom been implicated in patients with TEN, but the incidence of fluoroquinolone-induced cutaneous reactions may be on the increase.[4] Until date, a total of 31 cases of SJS 546
DOI: 10.4103/0972-5229.138166
Internal jugular vein thrombosis from rhino-cerebral mucormycosis: Be careful before cannulation Sir, Rhino-cerebral mucormycosis is a relatively uncommon fungal infection of the nasal cavity and para-nasal
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
