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Recent Advances in Management of Aluminium Phosphide Poisoning

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Recent Advances in Management of Aluminium Phosphide Poisoning Int. J. Curr. Res. Med. Sci. (2017). 3(4): 73-76 International Journal of Current Research in Medical Sciences ISSN: 2454-5716 P-ISJN: A4372-3064, E -ISJN: A4372-3061 www.ijcrims.com Update Article Volume 3, Issue 4 -2017 DOI: http://dx.doi.org/10.22192/ijcrms.2017.03.04.011 Recent Advances in Management of Aluminium Phosphide Poisoning N.S Neki*, Gagandeep Singh Shergill**, Amritpal Singh***, Amanpreet Kaur****, Sharique Nizami*****, Taranjit Singh******, Jatinderpal Singh Pannu******* *Professor, **Junior Resident, ***Senior Resident, Department of Medicine, Govt. Medical college and Guru Nanak Dev Hospital, Amritsar, India ****Consultant Gynaecologist, Civil Hospital, Fatehgarh Sahib, Punjab *****Senior Resident, Department of Surgery, Mata Gujari Memorial Medical College and LSK hospital, Kishanganj, Bihar, India. ******Registrar, Medical Oncology & Haematology, Artemis Hospital, Gurgaon, Haryana ******* Medical Officer, PCMS-1, distt. Taran Taran, Punjab *Corresponding author: [email protected] Abstract Aluminium phosphide (AlP), commonly known as celphos is a household name in villages of Punjab. This cheap solid fumigant and a highly toxic pesticide is commonly used for grain preservation. The post “green revolution” era saw alarmingly increased mortality by consumption of celphos for suicidal intent. Till date, there is no specific antidote for its intoxication and the poisoning carries extremely high mortality. The article will throw some light upon the recent advances that have been made regarding the management of acute aluminium sulphide poisoning (AAlPP). Keywords: Aluminium phosphide poisoning; Celphos poisoning; AAlPP; ECMO; boric acid as an antidote to AAlPP Introduction AlP, a mitochondrial poison, exerts its toxicity and instantaneous. The mortality ranges from due to deadly phosphine gas that is liberated when 45% to 100%. it reacts with water or hydrochloric acid in the stomach. Phosphine gas (PH3), the active Discussion pesticide component of AlP, is rapidly absorbed by inhalation, ingestion, and skin or mucosal In Northern India, when it comes to choosing a contacts. The mechanism of toxicity includes poison for suicidal intent, celphos is perhaps the cellular hypoxia due to the effect on favourite choice of victims- way ahead of barbiturates, organophosphorus or copper mitochondria, inhibition of cytochrome C oxidase 1 and formation of highly reactive hydroxyl sulphate . Upon contact with moisture in the radicals. The signs and symptoms are nonspecific environment, AlP undergoes a chemical reaction 73 Int. J. Curr. Res. Med. Sci. (2017). 3(4): 73-76 yielding phosphine gas. Phosphine inhibits Specific therapy and recent advances: cellular oxygen utilization and can induce lipid peroxidation. In the case of oral intake, the The clinical management of intoxication from phosphine gas released is absorbed by the AlP is mainly supportive. In one study, gastrointestinal tract with simple diffusion and is intravenous magnesium has shown significant mainly excreted by the kidneys and lungs. improvement in indicators of oxidative stress and Phosphine, like cyanide, inhibits mitochondrial a lower incidence of mortality (20%) in cytochrome oxidase and cellular oxygen comparison to control subjects (44% mortality) 17. utilization 2,3,4. It can rapidly perturb Oral administration of the anti-ischemic drug mitochondrial conformation and inhibit oxidative trimetazidine, which works through a metabolic respiration by 70%. This situation results a severe mechanism of decreasing the production of decrease in mitochondrial membrane potential 3. oxygen-derived free radicals and stimulating the AlP generates cellular superoxide and peroxide oxidative metabolism of glucose has been radicals, which trigger cellular damage by lipid suggested to decrease mortality14,15. peroxidation . The direct toxic effects of Administration of sorbitol solution (at a dose of 1- phosphine 5 and phosphides 6on cardiac myocytes, 2 ml/kg) as a cathartic and vegetable oils and fluid loss and adrenal gland can induce profound liquid paraffin as inhibitor of phosphine release circulatory collapse. Death is usually a resultant from the overdosed AlP has been suggested17. of refractory myocardial depression, resistant coconut oil has been shown to have a role in hypotension, severe metabolic acidosis and acute managing acute AlP poisoning even 6 h post respiratory distress syndrome. ingestion 18. Digoxin has been suggested for treatment of cardiogenic shock induced by acute Traditionally, the management of AAlPP is AlP intoxication19. largely symptomatic as there is no specific antidote available. Gastric lavage with potassium Case reports and studies are available which permanganate (1:10,000) is done as it oxidizes suggest the treatment with various agents by PH to form non-toxic phosphate7. Activated various regimens with varying results. N-omega- 3 nitro-L-arginine methyl ester (L-NAME)20, N- charcoal (approximately 100 g) given through a 20 21 2+ nasogastric tube to delay the absorption. Liquid acetylcysteine , hyperbaric oxygen , 25Mg - carrying nanoparticles 22, intragastric irrigation paraffin, that accelerate the excretion of AlP and 22 8 with sweet almond oil , combination of vitamin phosphine is often used . For symptomatic relief 23 from severe gastritis, antacids and proton pump C and methylene blue , extensive gastric lavage blockers are employed. As AlPP is often with coconut oil and sodium bicarbonate solution with simultaneous aspiration24, intra-aortic associated with hypoglycaemia, correction of 25 plasma glucose level with glucose containing balloon pump , have all been used in isolation or fluids is done. Circulatory shock is dealt with 24 in conjucnction with one another. hr low dose dopamine (4–6 μg/kg/min) and 9 However, above all of them, Extracorporeal intravenous fluids . Hydrocortisone 200–400 mg membrane oxygenation (ECMO) seems to hold every 4–6 hr has been reported to be used with good results10. Patients who land up in ARDS the maximum promise regarding success require intensive care monitoring and mechanical management of this lethal poisoning. ECMO is a modified "heart-lung" machine to provide ventilation. If systolic blood pressure is >90 mm Hg, Diuretics may be used to enhance excretion temporary cardiorespiratory support. Timely as the main route of elimination of phosphine is intervention with ECMO in patients with AlP renal 11. Arrhythmias are common and they are poisoning-induced severe metabolic acidosis and managed just as any other situation. Metabolic refractory cardiogenic shock has shown acidosis requires administration of intravenous significant improvement in overall survival in sadium bicarbonate. Dialysis may be required for several trials and studies. Although EMCO is severe acidosis and acute renal failure. associated with significant complication rates of its own, it might come up as a promising 74 Int. J. Curr. Res. Med. Sci. (2017). 3(4): 73-76 “bridge therapy” in cases with intractable 4. Proudfoot AT. Aluminium and zinc phosphide cardiorespiratory failure caused by AlP poisoning poisoning. Clin Toxicol (Phila) 2009; 47:89– who are not responding to conventional 100. treatment.26,28,29 5. Almasieh M, Lieven CJ, Levin LA, Di Polo A. A cell-permeable phosphine-borane Soltani etal have purposed a very interesting complex delays retinal ganglion cell death hypothesis stating Boric acid as a “trapping after axonal injury through activation of the agent” for deadly phosphine gas and hence, pro-survival extracellular signal-regulated purposes it be a specific antidote. Boric acid is a kinases 1/2 pathway. J Neurochem. 2011; non-toxic Lewis acid which efficiently traps PH3 118:1075–86. gas. In this reaction, boric acid acts as a Lewis 6. Hsu CH, Quistad GB, Casida JE. Phosphine- acid and phosphine acts as a Lewis base. The induced oxidative stress in Hepa 1c1c7 resulted polar reaction product which has H and cells. Toxicol Sci 1998; 46:204–10. OH groups can form hydrogen bonds with water 7. Grover A, Bansal S. Aluminium phosphide molecules and hence can be excreted in urine by poisoning. Manual of medical 30 the body . Though the idea appears very practical emergencies. New Delhi: M M Healthcare; in theory, the hypothesis is yet to be tested for In 1997. 64:532–539. vitro and in vivo studies. 8. Chugh SN, Arora V, Kaur S, Sood AK. Toxicity of exposed aluminium phosphide. J Conclusion Assoc Phys Ind 1993; 41:569–70. 9. Chugh SN, Chugh K, Ram S, Malhotra KC. Although there is no specific treatment for AAlPP Electrocardiographic abnormalities in as yet, various agents have been used with aluminium phosphide poisoning with special reasonable success. EMCO has proved to be a reference to its incidence, pathogenesis, game changer. Boric acid could be the answer for mortality and histopathology. J Indian Med the future. Assoc 1991; 89:32–35. 10. Gurjar M, Baronia AK, Azim A, Sharma K. Financial Support and Sponsorship: Nil Managing aluminum phosphide poisonings. J Emerg Trauma and Shock 2011; 4:378-84. Conflicts of Interest: There are no conflicts of 11. Shadnia S, Rahimi M, Pajoumand A, Rasouli interest MH, Abdollahi M. Successful treatment of acute aluminium phosphide poisoning: References possible benefit of coconut oil. Hum Exp Toxicol 2005; 24:215–18. 12. Siwach SB, Jagdish K, Katyal VK, Dhall A, 1. Singh D, Dewan I, Pandey AN, Tyagi S. Bhardwaj G. Prognostic indices in aluminium Spectrum of unnatural fatalities in the phosphide poisoning observations on acidosis Chandigarh zone of north-west India
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