Indian Journal of Critical Care Medicine February 2015 Vol 19 Issue 2
guidewire. There was no backflow in all 3 lumens due to reverse bent of CVC at IJV valve. It is always better to do ultrasound screening of course and structure of IJV before CVC.
Monish S. Raut, Arun Maheshwari
2. 3. 4.
Department of Cardiac Anesthesia, Dharam Vira Heart Center, Sir Ganga Ram Hospital, New Delhi, India
Harmon JV Jr, Edwards WD. Venous valves in subclavian and internal jugular veins. Frequency, position, and structure in 100 autopsy cases. Am J Cardiovasc Pathol 1987;1:51‑4. Wu X, Studer W, Erb T, Skarvan K, Seeberger MD. Competence of the internal jugular vein valve is damaged by cannulation and catheterization of the internal jugular vein. Anesthesiology 2010;112:979. Fukazawa K, Aguina L, Pretto EA Jr. Internal jugular valve and central catheter placement. Anesthesiology 2010;112:979.
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Correspondence: Dr. Monish S. Raut, Department of Cardiac Anesthesia, Dharam Vira Heart Center, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi ‑ 110 060, India. E‑mail: [email protected]
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References 1.
Sir, Ratol paste, a commonly used rodenticide in Indian houses contain 3% yellow phosphorus. Yellow phosphorus is a general protoplasmic poison causing multiorgan failure. [1] Doses >1 mg/kg are almost invariably fatal. Ratol paste poisoning is either suicidal or accidental. The clinical course of ratol paste poisoning is different from that of most other poisons. The patients are usually asymptomatic during the initial 72 h of ingestion, or they may have signs and symptoms of gastrointestinal irritation. After 72 h they develop deranged liver function, acute hepatic failure, coagulopathy. Central nervous system effects include changes in mental status like confusion, psychosis, hallucinations, and coma. Cardiac toxicity includes hypotension, tachycardia, arrhythmias, and cardiogenic shock. Some patients may develop acute tubular necrosis and acute renal failure.[1‑3] Because of the initial asymptomatic phase few patients do not reveal about ratol paste ingestion and present late to the hospital. Patients who present late after consumption of the lethal dose develops fulminant hepatic failure with mortality of 100%.[2] In severe ingestions of ratol paste, patients do not have the initial asymptomatic stage, and they die due to shock and cardiopulmonary arrest in early stages itself.[4] There is no specific antidote for yellow phosphorus poisoning. Treatment is directed at removal of the poison and supportive therapy.[1‑3] 128
DOI: 10.4103/0972-5229.151025
Furukawa S, Wingenfeld L, Takaya A, Nakagawa T, Sakaguchi I, Nishi K, et al. Morphological variations of the internal jugular venous valve. Anat Physiol 2012;2:108.
Should ratol paste be banned?
Website:
Aluminum phosphide, zinc phosphide are the other rodenticides available. They are mainly used in agricultural fields[5] in contrast to ratol paste, which is used in houses. Also, ratol paste is commonly mistaken for toothpaste and consumed by children. And the product directions suggest that the paste be applied to bread to enable ingestion by rodents, thus making it appealing to children as well. [1] Hence, accidental poisoning is more common with ratol paste. This fatal poison is freely available over the counter in toxic doses at very cheaper prices.[3] Similar to any other poisoning, prevention strategies by restricting access to this poison, creating public awareness regarding the lethality of ratol paste and regulating the market sale of this compound should be helpful. However, this lethal ratol paste is easily available at cheaper costs and accidental poisoning is more common, especially among children. Hence, we call for a ban on market sales of ratol paste.
S. Khaja Mohideen, K. Senthil Kumar
Department of Anaesthesiology and Critical Care, Kauvery Hospitals, Trichy, Tamil Nadu, India
Correspondence: Dr. S. Khaja Mohideen, 228, Periyar Nagar, Rajagopalapuram, Pudukkottai ‑ 622 003, Tamil Nadu, India. E‑mail: [email protected]
References 1.
2.
Mauskar A, Mehta K, Nagotkar L, Shanbag P. Acute hepatic failure due to yellow phosphorus ingestion. Indian J Pharmacol 2011;43:355‑6. Kafeel SI, Chandrasekaran VP, Eswaran V. Role of N‑acetyl cystine in
Indian Journal of Critical Care Medicine February 2015 Vol 19 Issue 2
3.
4. 5.
outcome of patients with YP poisoning‑An observational study. Natl J Emerg Med 2012;1:35‑40. Saoji AA, Lavekar AS, Salkar HR, Pawde GB, Tripathi SS. A case on suicidal poisoning associated with ratol and a perspective on yellow phosphorus poisoning. Int J Recent Trends Sci Technol 2014;10:223‑5. Simon FA, Pickering LK. Acute yellow phosphorus poisoning. “Smoking stool syndrome”. JAMA 1976;235:1343‑4. Bumbrah GS, Krishan K, Kanchan T, Sharma M, Sodhi GS. Phosphide poisoning: A review of literature. Forensic Sci Int 2012;214:1‑6.
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Website: www.ijccm.org
DOI: 10.4103/0972-5229.151026
Potassium permanganate toxicity: A rare case with difficult airway management and hepatic damage
transplantation.[5] Use of NAC has shown good outcome in above mentioned toxicities, which are oxidizing agents like KMnO4.
Sir, We read case report “potassium permanganate (KMnO4) toxicity: A rare case with difficult airway management and hepatic damage” by Agrawal et al.[1] with great interest. We would like to discuss some points regarding the management of the patient.
Correspondence: Dr. Atul Jindal, Department of Pediatrics, All India Institute of Medical Sciences, Raipur ‑ 492 099, Chhattisgarh, India. E‑mail: [email protected]
Potassium permanganate is a powerful oxidizing agent. Free radicals generated due to absorbed permanganate ion overwhelm reduced tissue glutathione stores and causes liver injury. Its clinical course closely resembles that of paracetamol poisoning.[2] Hepatic injury due to a similar mechanism is also seen in toxicities due to carbon tetrachloride, chloroform, clove oil and amanita mushroom. N‑acetylcysteine (NAC) acts as an antioxidant, both directly as a glutathione substitute and indirectly as a precursor for glutathione. It also causes vasodilatation by increasing cyclic guanosine monophosphate level, inhibits platelet aggregation, acts as a sulfydryl donor to regenerate endothelial derived relaxing factor and reduce interleukin‑8 and tumor necrosis factor‑alpha production.[3] It improves transplant free survival in early stage nonacetaminophen acute liver failure [4] and also of great benefit in centers without facility for liver
Hence, we suggest an early use of NAC in KMnO4 poisoning to prevent or reduce hepatic injury as also suggested by Young et al.[2]
Chinmay Barik, Atul Jindal
Department of Pediatrics, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India
References 1.
2. 3. 4.
5.
Agrawal VK, Bansal A, Kumar R, Kumawat BL, Mahajan P. Potassium permanganate toxicity: A rare case with difficult airway management and hepatic damage. Indian J Crit Care Med 2014;18:819‑21. Young RJ, Critchley JA, Young KK, Freebairn RC, Reynolds AP, Lolin YI. Fatal acute hepatorenal failure following potassium permanganate ingestion. Hum Exp Toxicol 1996;15:259‑61. Atkinson MC. The use of N‑acetylcysteine in intensive care. Crit Care Resusc 2002;4:21‑7. Lee WM, Hynan LS, Rossaro L, Fontana RJ, Stravitz RT, Larson AM, et al. Intravenous N‑acetylcysteine improves transplant‑free survival in early stage non‑acetaminophen acute liver failure. Gastroenterology 2009;137:856‑64, e1. Mumtaz K, Azam Z, Hamid S, Abid S, Memon S, Ali Shah H, et al. Role of N‑acetylcysteine in adults with non‑acetaminophen‑induced acute liver failure in a center without the facility of liver transplantation. Hepatol Int 2009;3:563‑70.
Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.151027
129
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.
guidewire. There was no backflow in all 3 lumens due to reverse bent of CVC at IJV valve. It is always better to do ultrasound screening of course and structure of IJV before CVC.
Monish S. Raut, Arun Maheshwari
2. 3. 4.
Department of Cardiac Anesthesia, Dharam Vira Heart Center, Sir Ganga Ram Hospital, New Delhi, India
Harmon JV Jr, Edwards WD. Venous valves in subclavian and internal jugular veins. Frequency, position, and structure in 100 autopsy cases. Am J Cardiovasc Pathol 1987;1:51‑4. Wu X, Studer W, Erb T, Skarvan K, Seeberger MD. Competence of the internal jugular vein valve is damaged by cannulation and catheterization of the internal jugular vein. Anesthesiology 2010;112:979. Fukazawa K, Aguina L, Pretto EA Jr. Internal jugular valve and central catheter placement. Anesthesiology 2010;112:979.
Access this article online
Correspondence: Dr. Monish S. Raut, Department of Cardiac Anesthesia, Dharam Vira Heart Center, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi ‑ 110 060, India. E‑mail: [email protected]
Quick Response Code:
www.ijccm.org
References 1.
Sir, Ratol paste, a commonly used rodenticide in Indian houses contain 3% yellow phosphorus. Yellow phosphorus is a general protoplasmic poison causing multiorgan failure. [1] Doses >1 mg/kg are almost invariably fatal. Ratol paste poisoning is either suicidal or accidental. The clinical course of ratol paste poisoning is different from that of most other poisons. The patients are usually asymptomatic during the initial 72 h of ingestion, or they may have signs and symptoms of gastrointestinal irritation. After 72 h they develop deranged liver function, acute hepatic failure, coagulopathy. Central nervous system effects include changes in mental status like confusion, psychosis, hallucinations, and coma. Cardiac toxicity includes hypotension, tachycardia, arrhythmias, and cardiogenic shock. Some patients may develop acute tubular necrosis and acute renal failure.[1‑3] Because of the initial asymptomatic phase few patients do not reveal about ratol paste ingestion and present late to the hospital. Patients who present late after consumption of the lethal dose develops fulminant hepatic failure with mortality of 100%.[2] In severe ingestions of ratol paste, patients do not have the initial asymptomatic stage, and they die due to shock and cardiopulmonary arrest in early stages itself.[4] There is no specific antidote for yellow phosphorus poisoning. Treatment is directed at removal of the poison and supportive therapy.[1‑3] 128
DOI: 10.4103/0972-5229.151025
Furukawa S, Wingenfeld L, Takaya A, Nakagawa T, Sakaguchi I, Nishi K, et al. Morphological variations of the internal jugular venous valve. Anat Physiol 2012;2:108.
Should ratol paste be banned?
Website:
Aluminum phosphide, zinc phosphide are the other rodenticides available. They are mainly used in agricultural fields[5] in contrast to ratol paste, which is used in houses. Also, ratol paste is commonly mistaken for toothpaste and consumed by children. And the product directions suggest that the paste be applied to bread to enable ingestion by rodents, thus making it appealing to children as well. [1] Hence, accidental poisoning is more common with ratol paste. This fatal poison is freely available over the counter in toxic doses at very cheaper prices.[3] Similar to any other poisoning, prevention strategies by restricting access to this poison, creating public awareness regarding the lethality of ratol paste and regulating the market sale of this compound should be helpful. However, this lethal ratol paste is easily available at cheaper costs and accidental poisoning is more common, especially among children. Hence, we call for a ban on market sales of ratol paste.
S. Khaja Mohideen, K. Senthil Kumar
Department of Anaesthesiology and Critical Care, Kauvery Hospitals, Trichy, Tamil Nadu, India
Correspondence: Dr. S. Khaja Mohideen, 228, Periyar Nagar, Rajagopalapuram, Pudukkottai ‑ 622 003, Tamil Nadu, India. E‑mail: [email protected]
References 1.
2.
Mauskar A, Mehta K, Nagotkar L, Shanbag P. Acute hepatic failure due to yellow phosphorus ingestion. Indian J Pharmacol 2011;43:355‑6. Kafeel SI, Chandrasekaran VP, Eswaran V. Role of N‑acetyl cystine in
Indian Journal of Critical Care Medicine February 2015 Vol 19 Issue 2
3.
4. 5.
outcome of patients with YP poisoning‑An observational study. Natl J Emerg Med 2012;1:35‑40. Saoji AA, Lavekar AS, Salkar HR, Pawde GB, Tripathi SS. A case on suicidal poisoning associated with ratol and a perspective on yellow phosphorus poisoning. Int J Recent Trends Sci Technol 2014;10:223‑5. Simon FA, Pickering LK. Acute yellow phosphorus poisoning. “Smoking stool syndrome”. JAMA 1976;235:1343‑4. Bumbrah GS, Krishan K, Kanchan T, Sharma M, Sodhi GS. Phosphide poisoning: A review of literature. Forensic Sci Int 2012;214:1‑6.
Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.151026
Potassium permanganate toxicity: A rare case with difficult airway management and hepatic damage
transplantation.[5] Use of NAC has shown good outcome in above mentioned toxicities, which are oxidizing agents like KMnO4.
Sir, We read case report “potassium permanganate (KMnO4) toxicity: A rare case with difficult airway management and hepatic damage” by Agrawal et al.[1] with great interest. We would like to discuss some points regarding the management of the patient.
Correspondence: Dr. Atul Jindal, Department of Pediatrics, All India Institute of Medical Sciences, Raipur ‑ 492 099, Chhattisgarh, India. E‑mail: [email protected]
Potassium permanganate is a powerful oxidizing agent. Free radicals generated due to absorbed permanganate ion overwhelm reduced tissue glutathione stores and causes liver injury. Its clinical course closely resembles that of paracetamol poisoning.[2] Hepatic injury due to a similar mechanism is also seen in toxicities due to carbon tetrachloride, chloroform, clove oil and amanita mushroom. N‑acetylcysteine (NAC) acts as an antioxidant, both directly as a glutathione substitute and indirectly as a precursor for glutathione. It also causes vasodilatation by increasing cyclic guanosine monophosphate level, inhibits platelet aggregation, acts as a sulfydryl donor to regenerate endothelial derived relaxing factor and reduce interleukin‑8 and tumor necrosis factor‑alpha production.[3] It improves transplant free survival in early stage nonacetaminophen acute liver failure [4] and also of great benefit in centers without facility for liver
Hence, we suggest an early use of NAC in KMnO4 poisoning to prevent or reduce hepatic injury as also suggested by Young et al.[2]
Chinmay Barik, Atul Jindal
Department of Pediatrics, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India
References 1.
2. 3. 4.
5.
Agrawal VK, Bansal A, Kumar R, Kumawat BL, Mahajan P. Potassium permanganate toxicity: A rare case with difficult airway management and hepatic damage. Indian J Crit Care Med 2014;18:819‑21. Young RJ, Critchley JA, Young KK, Freebairn RC, Reynolds AP, Lolin YI. Fatal acute hepatorenal failure following potassium permanganate ingestion. Hum Exp Toxicol 1996;15:259‑61. Atkinson MC. The use of N‑acetylcysteine in intensive care. Crit Care Resusc 2002;4:21‑7. Lee WM, Hynan LS, Rossaro L, Fontana RJ, Stravitz RT, Larson AM, et al. Intravenous N‑acetylcysteine improves transplant‑free survival in early stage non‑acetaminophen acute liver failure. Gastroenterology 2009;137:856‑64, e1. Mumtaz K, Azam Z, Hamid S, Abid S, Memon S, Ali Shah H, et al. Role of N‑acetylcysteine in adults with non‑acetaminophen‑induced acute liver failure in a center without the facility of liver transplantation. Hepatol Int 2009;3:563‑70.
Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.151027
129
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.
