ORIGINAL_ARTICLE
Effectiveness of High Dose Pralidoxime for Treatment of Organophosphate Poisoning
Background: For effective treatment of organophosphate (OP) poisoning, development of a standardized protocol with flexible dose regimen for atropine and pralidoxime is an essential step. In this study, we aimed to assess the protocol devised in our setting; Bach Mai Hospital Poison Treatment Center, for treatment of OP poisoning that included a higher dose regimen of pralidoxime (2PAM). Methods: A protocol for treatment of OP poisoning was developed during 1995 to 1996, which included an atropinization scoring scale and a modification of 2PAM dose regimen. In this study, OP poisoned patients who were treated during 1997 to 2002 with the new protocol (study group or cases) were compared with historical control group which included OP poisoned patients treated between 1993 and 1994 prior to establishment of the new protocol. Results: One-hundred and eight cases and 54 controls were included. The cases and controls were not significantly different according to age, gender and plasma cholinesterase activity on admission from each other. There was no significant difference of mean duration of 2PAM therapy between the two groups. The controls received mean total 2PAM dose of 7.2±4.1 g, while the patients in the study group received 20.0±12.7 g which was 2.77 times higher than the dose for control group (P<0.001). Patients in the study group received significantly lower doses of atropine (100.2±119.1 vs. 231.8±225.5, P<0.001). Patients in the study group required a shorter duration of hospital stay compared to controls (6.2±4.8 vs. 8.2±5.8, P=0.035). In addition, morality rate decreased significantly (P=0.004) from 13% to 1.9% by application of the new protocol. Conclusion: The new protocol was more effective for patients with OP toxicity as it reduced the morbidities and mortality. A flexible regimen of 2PAM therapy for OP poisoning is recommended to be implemented.
https://apjmt.mums.ac.ir/article_3377_42f41dd37fc929da18f2e2d3292018bc.pdf
2014-09-01
97
103
10.22038/apjmt.2014.3377
Atropine
Clinical Protocols
Organophosphate Poisoning
Pralidoxime Compounds
Therapeutic Human Experimentation
Pham
Due
phamduehanoi@gmail.com
1
Director, Poison Control Center, Bach Mai hospital, Hanoi, Vietnam. Associate Professor, Deputy Head of Critical Care Department, Bach Mai Hospital, Hanoi Medical University, Hanoi, Vietnam
LEAD_AUTHOR
Eddleston M. Patterns and problems of deliberate selfpoisoning in the developing world. QJM 2000;93:715-31.
1
Dewan G. Analysis of Recent Situation of Pesticide Poisoning in Bangladesh: Is There a Proper Estimate? Asia Pac J Med Toxicol 2014;3:76-83.
2
Mahesh M, Gowdar M, Venkatesh CR. A Study on Two Dose Regimens of Pralidoxime in the Management of Organophosphate Poisoning. Asia Pac J Med Toxicol 2013;2:121-5.
3
Tuan NV, Dalman C, Thiem NV, Nghi TV, Allebeck P. Suicide attempts by poisoning in Hanoi, Vietnam: methods used, mental problems, and history of mental health care. Arch Suicide Res 2009;13:368-77.
4
Buckley NA, Eddleston M, Li Y, Bevan M, Robertson J. Oximes for acute organophosphate pesticide poisoning. Cochrane Database Syst Rev 2011;(2):CD005085.
5
Due P. Rational Use of Atropine in Treatment of Organophosphate Poisoning. [Research Project] Hanoi: Bach Mai University; 1994. p. 196-202. (In Vietnamese)
6
Eddleston M, Eyer P, Worek F, Juszczak E, Alder N, Mohamed F, et al. Pralidoxime in acute organophosphorus insecticide poisoning--a randomised controlled trial. PLoS Med 2009;6:e1000104.
7
Roberts DM, Aaron CK. Management of acute organophosphorus pesticide poisoning. BMJ 2007;334:629-34.
8
Thunga G, Pandey S, Nair S, Mylapuri R, Vidyasagar S, Kunhikatta V, et al. Comparative Study of continuous pralidoxime infusion versus intermittent dosing: Applicationof high-performance liquid chromatography method on serum of organophosphate poisoned patients. Asia Pac J Med Toxicol 2013;2:105-10.
9
Due P, Nguyen NT. The Achievements of the Poison Control Center of Bach Mai Hospital, Vietnam. Asia Pac J Med Toxicol 2013;2:118.
10
Knedel M, Böttger R. A kinetic method for determination of the activity of pseudocholinesterase (acylcholine acyl-hydrolase 3.1.1.8.). KlinWochenschr 1967;45:325-7. (In German)
11
Senanayake N, Karalliedde L. Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome. N Engl J Med 1987;316:761-3.
12
Yang CC, Deng JF. Intermediate syndrome following organophosphate insecticide poisoning. J Chin Med Assoc 2007;70:467-72.
13
de Silva HJ, Wijewickrema R, Senanayake N. Does pralidoxime affect outcome of management in acute organophosphorus poisoning? Lancet 1992;339:1136-8.
14
Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet 2008;371:597-607.
15
Due P. The change of plasma cholinesterase in acute organophosphate poisoning patients. Abstract presented at the 6th APAMT congress; 2007 Dec 12-14; Bangkok, Thailand.
16
Konickx LA, Worek F, Jayamanne S, Thiermann H, Buckley NA, Eddleston M. Reactivation of plasma butyrylcholinesterase by pralidoxime chloride in patients poisoned by WHO class II toxicity organophosphorus insecticides. Toxicol Sci 2013;136:274-83.
17
Lucyk S, Vilensky D, Fok PT, Nelson LS. Reactivation of plasma butyrylcholinesterase by pralidoxime chloride in patients poisoned by WHO class II toxicity organophosphorus insecticides. Toxicol Sci. 2014;138:482.
18
Pawar KS, Bhoite RR, Pillay CP, Chavan SC, Malshikare DS, Garad SG. Continuous pralidoxime infusion versus repeated bolus injection to treat organophosphorus pesticide poisoning: a randomised controlled trial. Lancet 2006;368:2136-41.
19
Shivakumar S, Raghavan K, Ishaq RM, Geetha S. Organophosphorus poisoning: a study on the effectiveness of therapy with oximes. J Assoc Physicians India 2006;54:250-1.
20
Cherian MA, Roshini C, Visalakshi J, Jeyaseelan L, Cherian AM. Biochemical and clinical profile after organophosphoruspoisoning--a placebo-controlled trial using pralidoxime. J Assoc Physicians India 2005;53:427-31.
21
Sungur M, Güven M. Intensive care management of organophosphate insecticide poisoning. Crit Care 2001;5:211-5.
22
Johnson S, Peter JV, Thomas K, Jeyaseelan L, Cherian AM. Evaluation of two treatment regimens of pralidoxime (1 gm single bolus dose vs 12 gm infusion) in the management of organophosphorus poisoning. J Assoc Physicians India 1996;44:529-31.
23
ORIGINAL_ARTICLE
Methadone Related Poisoning on the Rise in Tehran, Iran
Background: In Iran, methadone has been used for methadone maintenance treatment (MMT) as well as analgesic treatment in pain clinics. Recently, there are some reports regarding accidental and intentional methadone poisonings and deaths. The aim of this study was to evaluate the trend of methadone poisonings and deaths during a 10-year period in Tehran, Iran. Methods: This was a retrospective cross-sectional study over 2000 to 2010. Patients with a documented methadone poisoning who were admitted in Loghman Hakim Hospital Poison Center in Tehran, Iran were identified and included in the study. The data including patients’ age, gender, ingested dose, co-ingestants, intention of ingestion and outcome were extracted from the patients’ medical records. Results: During the study period, 1426 cases of methadone poisoning were recorded, of which, 1041 cases (73%) were men. Thirty-six cases (2.5%) died. Mean age of the patients was 29.9 ± 17 years. In 476 cases, the intention of poisoning could not be determined, and in the remaining, the intention was misuse (n = 273, 28.7%), suicide (n = 254, 26.7%), accidental (n = 245, 25.8%) and abuse (n = 178, 18.8%). Mean of the ingested dose of methadone was 120.6 ± 306.8 mg. The incidence of acute methadone poisoning per one million population of Tehran was 0.43 in 2000 that rose to 37.62 in 2010. Conclusion: The results indicate that methadone poisoning and deaths have increased in Tehran. MMT clinics should be strictly run according to the national guideline to prevent methadone poisoning. With regard to high frequency of poly-drug use in methadone poisoning, it seems important to warn health care providers against prescription of other drugs with methadone.
https://apjmt.mums.ac.ir/article_3378_04ca5bf5699d791aac5f891c9560d240.pdf
2014-09-01
104
109
10.22038/apjmt.2014.3378
death
incidence
Iran
methadone
Poisoning
Kambiz
Soltaninejad
1
Legal Medicine Research Center, Legal Medicine Organization of Iran, Tehran, Iran
AUTHOR
Hossein
Hassanian-Moghaddam
hassanian@sbmu.ac.ir
2
Excellent Center of Clinical Toxicology, Toxicology Research Center, Department of Clinical Toxicology, Loghman Hakim Hospital, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Shahin
Shadnia
shahin1380@yahoo.com
3
Excellent Center of Clinical Toxicology, Toxicology Research Center, Department of Clinical Toxicology, Loghman Hakim Hospital, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Joseph H, Stancliff S, Langrod J. Methadone maintenance treatment (MMT): a review of historical and clinical issues. Mt Sinai J Med 2000;67:347-64.
1
Clausen T, Anchersen K, Waal H. Mortality prior to, during and after opioid maintenance treatment (OMT): A national prospective cross-registry study. Drug Alcohol Depend 2008;94:151-7.
2
Bell J, Zador D. A risk-benefit analysis of methadone maintenance treatment. Drug Saf 2000;22:179-90.
3
Caplehorn JR, Dalton MS, Haldar F, Petrenas AM, Nisbet JG. Methadone maintenance and addicts' risk of fatal heroin overdose. Subst Use Misuse 1996;31: 177-96.
4
Marsch LA. The efficacy of methadone maintenance interventions in reducing illicit opiate use, HIV risk behavior and criminality: A meta-analysis. Addiction 1998;93:515-32.
5
Metrebian N, Shanahan W, Wells B, Stimson GV. Feasibility of prescribing injectable heroin and methadone to opiate-dependent drug users: Associated health gains and harm reductions. Med J Aust 1998;168:596-600.
6
Ministry of Health and Medical Education. Statistics of methadone production (In Persian). Tehran: Ministry of Health and Medical Education; 2013.
7
Graham NA, Merlo LJ, Goldberger BA, Gold MS. Methadone- and heroin-related deaths in Florida. Am J Drug Alcohol Abuse 2008;34:347-53.
8
Luty J, O'Gara C, Sessay M. Is methadone too dangerous for opiate addiction? BMJ 2005;331:1352-3.
9
Wolff K. Characterization of methadone overdose: Clinical considerations and the scientific evidence. Ther Drug Monit 2002;24:457-70.
10
Glaizal M, Gazin V, Aymard I, Messina-Gourlot C, Richard N, Mallaret M, et al. Suicidal poisonings with methadone in France: Results of a two year national survey by the Toxicovigilance Network. Clin Toxicol 2012;50:841-6.
11
Gheshlaghi F, Izadi-Mood N, Mardani A, Piri-Ardekani MR. Dose-Dependent Effects of Methadone on QT interval in Patients under Methadone Maintenance Treatment. Asia Pac J Med Toxicol 2013;2:6-9.
12
Aghabiklooei A, Shadnia S, Hassanian-Moghaddam H, Zamani N. Acute respiratory distress syndrome caused by methadone syrup. Arh Hig Rada Toksikol 2013;64:439-43.
13
Shadnia S, Soltaninejad K, Heydari K, Sasanina G, Abdollahi M. Tramadol intoxication: a review of 114 cases. Hum Exp Toxicol 2008;27:201-5.
14
Madden ME, Shapiro SL. The methadone epidemic: Methadone-related deaths on the rise in Vermont. Am J Forensic Med Pathol 2011;32:131-5.
15
Bernard JP, Havnes I, Slørdal L, Waal H, Mørland J, Khiabani HZ. Methadone-related deaths in Norway. Forensic Sci Int 2013;224:111-6.
16
Momtazi S, Rawson R. Substance abuse among Iranian high school students. Curr Opin Psychiatry 2010;23:221-6.
17
Karrari P, Mehrpour O, Afshari R, Keyler D. Pattern of illicit drug use in patients referred to addiction treatment centres in Birjand, Eastern Iran. J Pak Med Assoc 2013;63:711-6.
18
Cerdá M, Ransome Y, Keyes KM, Koenen KC, Tracy M, Tardiff KJ, et al. Prescription opioid mortality trends in New York City, 1990-2006: Examining the emergence of an epidemic. Drug Alcohol Depend 2013;132:53-62.
19
Gagajewski A, Apple FS. Methadone-related deaths in Hennepin County, Minnesota: 1992-2002. J Forensic Sci 2003;48:668-71.
20
Afshari R. Non-medical Use of Medications in Middle and Low Income Countries. Asia Pac J Med Toxicol 2014;3:49.
21
Shadnia S, Rahimi M, Hassanian-Moghaddam H, Soltaninejad K, Noroozi A. Methadone toxicity: Comparing tablet and syrup formulations during a decade in an academic poison center of Iran. Clin Toxicol 2013;51:777-82.
22
Corkery JM., Schifano F, Ghodse AH, Oyefeso A. The effects of methadone and its role in fatalities. Hum Psychopharmacol 2004;19:565-76.
23
Khodabandeh F, Kahani S, Shadnia S, Abdollahi M. Comparison of the efficacy of methadone maintenance therapy vs. narcotics anonymous in the treatment of opioid addiction: A 2-year survey. Int J Pharmacol 2012;8:445-9.
24
Mostafazadeh B, Farzaneh E. Risks and risk factors of repeated suicidal attempt: Study on unconscious poisoned patients. Asia Pac J Med Toxicol 2013;2:28-31
25
ORIGINAL_ARTICLE
Spirometric Findings in TNT Factory Workers Compared with Unexposed Controls
Background: Trinitrotoluene (TNT) is one of the most well-known and oldest explosive agents. In the recent decade, bioenvironmental, biochemical, and biological effects of TNT exposure have been more in the spotlight. In this study, we aimed to evaluate spirometric parameters in workers of a TNT factory exposed to TNT and other related fumes and dusts compared with the unexposed controls. Methods: In this case-control study, spirometry was done for TNT factory workers (cases) and matched healthy controls, and their results were compared with each other. Matched controls were selected from workers who worked in the same geographic area without any history of TNT or other chemical materials exposure. Spirometric studies were done during the early hours of day. Results: Overall, 90 subjects (47 TNT exposed cases and 43 controls) were included. The two groups showed no significant difference in demographic characteristics and smoking habits. In spirometry, it was found that the cases had significantly lower forced vital capacity (91.4 ± 13.7% vs. 100.2 ± 13.0%, P = 0.002), forced expiratory volume in 1 second (98.0 ± 14.9% vs. 104.7 ± 12.5%, P = 0.024) and peak expiratory flow (98.4 ± 17.3% vs. 107.9 ± 21.7%, P = 0.025) compared with controls. According to spirometric findings, 10 cases (21.3%) and no controls had restrictive pattern, which means TNT factory workers had 1.27 (CI: 1.09-1.47, P = 0.001) fold risk for development of restrictive patterns. Conclusion: Chronic exposure to TNT or prolonged working in TNT factories may predispose the workers to respiratory disorders. In addition to regular screening programs, preventive measures and devices should be considered for TNT factory workers to reduce the harms.
https://apjmt.mums.ac.ir/article_3379_1ae39d0e957c7621f7d2b735d9aab8a4.pdf
2014-09-01
110
114
10.22038/apjmt.2014.3379
Lung Diseases
occupational exposure
Solvents
Spirometry
Trinitrotoluene
Majid
Shohrati
1
Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Bita
Najafian
2
Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Amin
Saburi
aminsaburi@yahoo.com
3
Health Research Center, Baqiyatallah University of medical sciences, Tehran, Iran
AUTHOR
Ensiyeh
Vahedi
4
Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Mostafa
Ghanei
mghaneister@gmail.com
5
Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Choodum A, Kanatharana P, Wongniramaikul W, Nicdaeid N. Rapid quantitative colourimetric tests for trinitrotoluene (TNT) in soil. Forensic Sci Int 2012;222:340-5.
1
Lewis TA, Newcombe DA, Crawford RL. Bioremediation of soils contaminated with explosives. J Environ Manage 2004;70:291-307.
2
Sabbioni G, Liu YY, Yan H, Sepai O. Hemoglobin adducts, urinary metabolites and health effects in 2,4,6-trinitrotoluene exposed workers. Carcinogenesis 2005;26:1272-9.
3
Sabbioni G, Rumler R. Biomonitoring of workers cleaning up ammunition waste sites. Biomarkers 2007;12:559-73.
4
Kruse A, Hertel M, Hindsholm M, Viskum S. Trinitrotoluene (TNT)-induced cataract in Danish arms factory workers. Acta Ophthalmol Scand 2005;83:26-30.
5
Shimizu H, Kumada T, Nakano S, Kiriyama S, Sone Y, Honda T, et al. Liver dysfunction among workers handling 5-nitro-o-toluidine. Gut 2002;50:266-70.
6
Qu GC. Nation-wide investigation of occupational poisonings by lead, benzene, mercury, organic phosphorus, and trinitrotoluene, with an analytical study of their aetiology. J Ind Hyg Occup Dis 1984:25-30.
7
Yan C, Wang Y, Xia B, Li L, Zhang Y, Liu Y. The retrospective survey of malignant tumor in weapon workers exposed to 2,4,6-trinitrotoluene. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 2002;20:184-8. (In Chinese)
8
Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. 18thed. New York, NY: McGraw-Hill Professional; 2011.
9
Wang L, He X, Bi Y, Ma Q. Stem cell and benzene-induced malignancy and hematotoxicity. Chem Res Toxicol 2012;25:1303-15.
10
Naziroglu M, Karaoglu A, Aksoy AO. Selenium and high dose vitamin E administration protects cisplatin-induced oxidative damage to renal, liver and lens tissues in rats. Toxicology 2004;195:221-30.
11
Kumagai Y, Wakayama T, Lib S, Shinohara A, Iwamatsu A, Sun G, et al. Zeta-crystallin catalyzes the reductive activation of 2,4,6-trinitrotoluene to generate reactive oxygen species: a proposed mechanism for the induction of cataracts. FEBS Lett 2000;478:295-8.
12
Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease [Internet]. 2014 [updated 2014 Jan 1; cited 2014 Aug 10]. Available from: http://www.goldcopd.org/guidelines-global-strategy-for-diagnosis-management.html
13
Letzel S, Goen T, Bader M, Angerer J, Kraus T. Exposure to nitroaromatic explosives and health effects during disposal of military waste. Occup Environ Med 2003;60:483-8.
14
Naderi M, Ghanei M, Shohrati M, Saburi A, Babaei M, Najafian B. Systemic complications of trinitrotoluene (TNT)
15
ORIGINAL_ARTICLE
Prevalent Poisonings in Adolescents and Adults in Dubai: A Compendium from Rashid Hospital
Background: Profile of acute poisonings varies from country to country depending on the ease of availability of substances and socio-economic condition of people; however, very little information from the United Arab Emirates (UAE) have been published, so far. This study was designed to find out the most common causes of overdose and poisoning in patients admitted to the emergency department of Rashid Hospital (RH), Dubai, UAE. Methods: In this retrospective cross sectional study, medical records of poisoned patients admitted to RH from 1st January 2012 to 31st December 2012 were reviewed. Demographic data, types of substances used, intention, length of hospital stay and outcomes were recorded in pre-designed checklists. Results: Overall, 163 patients were studied that among them gender distribution was relatively equal (male: female = 1.04: 1). Mean age of patients was 30.3 ± 11.5 and most patients were in the age group of 20 to 29 years age old (41.7%). Rgarding the type of poisons, the majority of patients were poisoned with pharmaceuticals (55.8%) followed by chemical substances (23.3%). In pharmaceutical poisonings, most cases were due to multi-drug ingestion (22.6%), followed by ingestion of paracetamol (14.1%) and benzodiazepines (4.3%). Considering the gender distribution, women were significantly more involved with pharmaceutical poisoning (P = 0.046), while venomous envenomation occurred only in men indicating a significant difference (P = 0.004). In chemical poisoning, most cases were due to ingestion of corrosive agents (19%). Suicidal poisoning was significantly more common in women (P < 0.001), while abuse was significantly more common in men (P < 0.001). Length of hospital stay averaged on 8.1 days. Only 3 patients died during the admission (mortality rate: 1.8%). Conclusion: Study on, training for and prevention of poisoning should receive more attention in the UAE. Over-the-counter drugs especially paracetamol should be prescribed in a more controlled manner.
https://apjmt.mums.ac.ir/article_3380_c12e63d811ff12b34b08244eb7f0f6fc.pdf
2014-09-01
115
119
10.22038/apjmt.2014.3380
Drug Overdose
Epidemiologic Studies
Hospital Emergency Service
Poisoning
United Arab Emirates
Fahad Akhtar
Hameed
fahad.hameed316@gmail.com
1
Resident, PGY3, Emergency Department, Rashid Hospital Trauma Centre, Dubai Health Authority (DHA), Dubai, United Arab Emirates
LEAD_AUTHOR
Humaira Kamil
Ansari
humaira.kamil@gmail.com
2
Resident, PGY3, Emergency Department, Rashid Hospital Trauma Centre, Dubai Health Authority (DHA), Dubai, United Arab Emirates
AUTHOR
Firas Jaafar
Al-Najjar
3
Consultant Emergency Medicine Specialist, Rashid Hospital Trauma Centre, Dubai Health Authority (DHA), Dubai, United Arab Emirates
AUTHOR
Lund C, Teige B, Drottning P, Stiksrud B, Rui TO, Lyngra M, et al. A one-year observational study of all hospitalized and fatal acute poisonings in Oslo: epidemiology, intention and follow-up. BMC Public Health 2012;12:858.
1
Afshari R, Majdzadeh R, Balali-Mood M. Pattern of acute poisonings in Mashhad, Iran 1993-2000. J Toxicol Clin Toxicol 2004;42:965-75.
2
Kara H, Bayir A, Degirmenci S, Kayis SA, Akinci M, Ak A, et al. Causes of poisoning in patients evaluated in a hospital emergency department in Konya, Turkey. J Pak Med Assoc 2014;64:1042-8.
3
Patil A, Peddawad R, Verma VCS, Gandhi H. Profile of Acute Poisoning Cases Treated in a Tertiary Care Hospital: a Study in Navi Mumbai. Asia Pac J Med Toxicol 2014;3:36-40.
4
Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012;380:2095-128.
5
Koronfel AA. Suicide in Dubai, United Arab Emirates. J Clin Forensic Med 2002;9:5-11.
6
Terris J. Profile of Poisonings in Dubai. Abstract presented at the 4th Mediterranean Emergency Medicine Congress; 2007 Sep 15-19; Sorrento, Italy.
7
Bharwani S, Hashim MJ, Raheel H, Rahim M, Sharif Y. Role of a poison center in reducing unintentional childhood ingestion by targeting pre-event risk factors. Pediatr Emerg Care 2013;29:296-300.
8
Sharif Y, El Ghandour S, Safarini M. Household Products Survey - HAAD Poison and Drug Information Center. Middle East J Fam Med 2010;8:20-5.
9
Prajapati T, Prajapati K, Tandon R, Merchant S. Acute Chemical and Pharmaceutical Poisoning cases Treated in Civil Hospital, Ahmedabad: One Year study. Asia Pac J Med Toxicol 2013;2:63-7.
10
Sarkar D, Shaheduzzaman M, Hossain MI, Ahmed M, Mohammad N, Basher A. Spectrum of Acute Pharmaceutical and Chemical Poisoning in Northern Bangladesh. Asia Pac J Med Toxicol 2013;2:2-5.
11
Afshari R. Non-medical Use of Medications in Middle and Low Income Countries. Asia Pac J Med Toxicol 2014;3:49.
12
Patel MJ, Shahid M, Riaz M, Kashif W, Ayaz SI, Khan MS, et al. Drug overdose: a wake up call! Experience at a tertiary care centre in Karachi, Pakistan. J Pak Med Assoc 2008;58:298-301.
13
Asghar A, Anees M, Mahmood KT. Accidental Poisoning In Children. J Biomed Sci Res 2010;2:284-9.
14
Jesslin J, Adepu R, Churi S. Assessment of prevalence and mortality incidences due to poisoning in a South Indian tertiary care teaching hospital. Indian J Pharm Sci 2010;72:587-91.
15
Mostafazadeh B, Farzaneh E. Risks and Risk Factors of Repeated Suicidal Attempt: Study on Unconscious Poisoned Patients. Asia Pac J Med Toxicol 2013;2:28-31.
16
Hovda KE, Bjornaas MA, Skog K, Opdahl A, Drottning P, Ekeberg O, et al. Acute poisonings treated in hospitals in Oslo: a one-year prospective study (I): pattern of poisoning. Clin Toxicol (Phila) 2008;46:35-41.
17
Dadpour B, Shafahi A, Monzavi SM, Zavar A, Afshari R, Khoshdel AR. Snakebite Prognostic Factors: Leading Factors of Weak Therapeutic Response Following Snakebite Envenomation. Asia Pac J Med Toxicol 2012;1:27-33.
18
Mondal RN, Chowdhury FR, Rani M, Mohammad N, Islam MM, Haque MA, et al. Pre-Hospital and Hospital Management Practices and Circumstances behind Venomous Snakebite in Northwestern Part of Bangladesh. Asia Pac J Med Toxicol 2012;1:18-21.
19
Sarmin S, Amin MR, Al-Mamun H, Rahman R, Faiz MA. Clinical Aspects of Green Pit Viper Bites in Bangladesh: A Study on 40 Patients. Asia Pac J Med Toxicol 2013;2:96-100.
20
ORIGINAL_ARTICLE
Pharmacokinetic Studies on Oximes in Organophosphate Poisoning: A Mini Review
Organophosphate (OP) poisoning is one of the most common causes of poisoning in developing countries especially in Southeastern Asia. Poisoning with phosphorus-containing organic chemicals or OP compounds can be managed with antidotes like oximes which are potential reactivators of acetylcholinesterase (AChE). The efficacy of oxime therapy in OP poisoned patients mainly depends upon various factors such as different dose plans, infusion rate of oximes, genetic differences of patients, type of oxime used and chemical nature of the OP compound ingested. Studies on pralidoxime kinetics in OP poisoned patients have shown that reactivation of AChE depends on the plasma concentration of oximes as well as OP compounds. The plasma concentration of oximes mainly depends on the dose plan from intermittent injection to continuous infusion after a loading dose. The incontrovertible fact is that the intermittent dosing of oximes results in deep troughs in blood pralidoxime/oxime levels (BPL) whereas continuous infusion of oximes maintains steady state plasma concentrations. Many published literature also highlighted pralidoxime via continuous infusion results in better outcomes with minimum fluctuation in BPL compared to intermittent dosing. At therapeutic doses, adverse effects of oximes are reported to be minimal. But high BPL is associated with some common adverse effects including dizziness, blurred vision and diastolic hypertension. Considering all the facts, it is important to note that kinetic studies of oximes are useful not only in deciding the dose regimen, but also in predicting the possible side-effects.
https://apjmt.mums.ac.ir/article_3381_ce224e5171391837c84ad8d3dcd18f79.pdf
2014-09-01
120
123
10.22038/apjmt.2014.3381
Organophosphate Poisoning
Oximes
Pharmacokinetics
Pralidoxime Compounds
Girish
Thunga
girishthunga77@gmail.com
1
Department of Pharmacy Practice, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, India
LEAD_AUTHOR
Sureshwar
Pandey
2
The School of Pharmacy, The University of the West Indies, ST Augustine, Trinidad and Tobago
AUTHOR
Sreedharan
Nair
3
Department of Pharmacy Practice, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, India
AUTHOR
Rama
Mylapuri
4
Department of Pharmacy Practice, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, India
AUTHOR
Sudha
Vidyasagar
5
Department of Medicine, Kasturba Medical College, Manipal University, Manipal, India
AUTHOR
Vijayanarayana
Kunhikatta
6
Department of Pharmacy Practice, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, India
AUTHOR
Akriti
Kaura
7
Department of Pharmacy Practice, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, India
AUTHOR
Eddleston M, Szinicz L, Eyer P, Buckley N. Oximes in acute organophosphorus pesticide poisoning: a systematic review of clinical trials. QJM 2002;95:275-83.
1
Thunga G, Sam KG, Khera K, Pandey S, Sagar SV. Evaluation of incidence, clinical characteristics and management in organophosphorus poisoning patients in a tertiary care hospital. J Toxicol Environ Health Sci 2010;2:73-6.
2
Dewan G. Analysis of Recent Situation of Pesticide Poisoning in Bangladesh: Is There a Proper Estimate? Asia Pac J Med Toxicol 2014;3:76-83.
3
Thunga G, Sam KG, Khera K, Xavier V, Verma M. Profile of acute mixed organophosphorus poisoning. Am J Emerg Med 2009;27:628.e1-3.
4
Mégarbane B. Toxidrome-based Approach to Common Poisonings. Asia Pac J Med Toxicol 2014;3:2-12.
5
Wilson IB, Ginsburg B. A powerful reactivator of alkylphosphate-inhibited acetylcholinesterase. Biochim Biophys Acta 1955;18:168-70.
6
Worek F, Bäcker M, Thiermann H, Szinicz L, Mast U, Klimmek R, et sl. Reappraisal of indications and limitations of oxime therapy in organophosphate poisoning. Hum Exp Toxicol 1997;16:466-72.
7
Worek F, Eyer P, Szinicz L. Inhibition, reactivation and aging kinetics of cyclohexylmethylphosphonofluoridate-inhibited human cholinesterases. Arch Toxicol 1998;72:580-7.
8
Pawar KS, Bhoite RR, Pillay CP, Chavan SC, Malshikare DS, Garad SG. Continuous pralidoxime infusion versus repeated bolus injection to treat organophosphorus pesticide poisoning: a randomised controlled trial. Lancet 2006;368:2136-41.
9
Mahesh M, Gowdar M, Venkatesh CR. A Study on Two Dose Regimens of Pralidoxime in the Management of Organophosphate Poisoning. Asia Pac J Med Toxicol 2013;2:121-5.
10
Due P. Effectiveness of High dose Pralidoxime for Treatment of Organophosphate Poisoning. Asia Pac J Med Toxicol 2014;3:97-103.
11
Eddleston M, Eyer P, Worek F, Juszczak E, Alder N, Mohamed F, et al. Pralidoxime in acute organophosphorus insecticide poisoning--a randomised controlled trial. PLoS Med 2009;6:e1000104.
12
Cherian MA, Roshini C, Visalakshi J, Jeyaseelan L, Cherian AM. Biochemical and clinical profile after organophosphoruspoisoning--a placebo-controlled trial using pralidoxime. J Assoc Physicians India 2005;53:427-31.
13
Buckley NA, Eddleston M, Li Y, Bevan M, Robertson J. Oximes for acute organophosphate pesticide poisoning. Cochrane Database Syst Rev. 2011;(2):CD005085.
14
Willems JL, De Bisschop HC, Verstraete AG, Declerck C, Christiaens Y, Vanscheeuwyck P, et al. Cholinesterase reactivation in organophosphorus poisoned patients depends on the plasma concentrations of the oxime pralidoxime methylsulphate and of the organophosphate. Arch Toxicol 1993;67:79-84.
15
Worek F, Diepold C, Eyer P. Dimethylphosphoryl-inhibited human cholinesterases: inhibition, reactivation, and aging kinetics. Arch Toxicol 1999;73:7-14.
16
Worek F, Thiermann H, Szinicz L, Eyer P. Kinetic analysis of interactions between human acetylcholinesterase, structurally different organophosphorus compounds and oximes. Biochem Pharmacol 2004;68:2237-48.
17
Willems JL, Langenberg JP, Verstraete AG, De Loose M, Vanhaesebroeck B, Goethals G, et al. Plasma concentrations of pralidoxime methylsulphate in organophosphorus poisoned patients. Arch Toxicol 1992;66:260-6.
18
Ríos JC, Repetto G, Galleguillos I, Jos A, Peso AD, Repetto M. High concentrations of pralidoxime are needed for the adequate reactivation of human erythrocyte acetylcholinesterase inhibited by dimethoate in vitro. Toxicol In Vitro 2005;19:893-7.
19
Jovanović D. Pharmacokinetics of pralidoxime chloride. A comparative study in healthy volunteers and in organophosphorus poisoning. Arch Toxicol 1989;63:416-8.
20
Peter JV, Moran JL, Graham P. Oxime therapy and outcomes in human organophosphate poisoning: an evaluation using meta-analytic techniques. Crit Care Med 2006;34:502-10.
21
Medicis JJ, Stork CM, Howland MA, Hoffman RS, Goldfrank LR. Pharmacokinetics following a loading plus a continuous infusion of pralidoxime compared with the traditional short infusion regimen in human volunteers. J Toxicol Clin Toxicol 1996;34:289-95.
22
Casey PB, Gosden E, Blakely L, Thompson JP, Vale JA. Plasma pralidoxime concentrations following bolus injection and continuous infusion. Przegl Lek 1995;52:203-4.
23
Thunga G, Pandey S, Nair S, Mylapuri R, Vidyasagar S, Kunhikatta V, et al. Comparative Study of Continuous Pralidoxime Infusion versus Intermittent Dosing: Application of High-Performance Liquid Chromatography Method on Serum of Organophosphate Poisoned Patients. Asia Pac J Med Toxicol 2013;2:105-10.
24
Eyer P. The role of oximes in the management of organophosphorus pesticide poisoning. Toxicol Rev 2003;22:165-90.
25
Kassa J. Review of oximes in the antidotal treatment of poisoning by organophosphorus nerve agents. J Toxicol Clin Toxicol 2002;40:803-16.
26
Howland MA. Antidotes in depth (A33): Pralidoxime. In: Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE, editors. Goldfrank’s Toxicologic Emergencies. 9th ed. New York, NY: McGraw Hill; 2011. p.1467-72.
27
Schexnayder S, James LP, Kearns GL, Farrar HC. The pharmacokinetics of continuous infusion pralidoxime in children with organophosphate poisoning. J Toxicol Clin Toxicol 1998;36:549-55.
28
Scott RJ. Repeated asystole following PAM in organophosphate self-poisoning. Anaesth Intensive Care 1986;14:458-60.
29
Xue SZ, Ding XJ and Ding Y. Clinical observation and comparison of the effectiveness of several oxime cholinesterase reactivators. Scand J Work Environ Health 1985;11:46-8.
30
ORIGINAL_ARTICLE
Structural Findings in the Brain MRI of Patients with Acute Carbon Monoxide Poisoning
Background: Carbon monoxide (CO) poisoning may lead to hypoxic/anoxic injury and eventually ischemic encephalopathy. Magnetic resonance imaging (MRI) has a well-recognized role in assessment of the severity of brain damage caused by CO poisoning. In this study, we aimed to present and analyze the structural abnormalities in the brain MRI and especially in diffusion weighted MRI (DWI) images in a series of patients with acute CO poisoning. Methods: This cross-sectional observational study was performed on patients with moderate to severe CO poisoning admitted to Mashhad Medical Toxicology Center of Imam Reza Hospital, Mashhad, Iran, during autumn and winter 2013. After stabilization, patients underwent brain MRI. T1 weighted, T2 weighted and FLAIR images in sagittal, axial and coronal sections, and DWI in axial sections were performed for each patient. Results: Eighteen patients (77.8% men) were enrolled in this study with median age of 29.5 years. Eleven patients (61.1%) had abnormal MRI signals and in 7 cases no abnormality or nonspecific abnormalities were detected. The most common involved region in brain MRI was white matter (38.9%) followed by globus pallidus (33.3%). Patients with signal abnormality in brain MRI had significantly longer duration of exposure to CO compared to those without signal changes (10.6 ± 6.2 h vs. 3.4 ± 2.8 h, P = 0.011). Nine patients had restricted diffusion in DWI. Patients with restricted diffusion in DWI had also longer duration of exposure to CO compared to patients with normal DWI (12.1 ± 5.5 h vs. 3.5 ± 2.9 h, P = 0.001). Conclusion: The white matter and globus pallidus were the most common affected regions in brain following acute CO poisoning. Signal abnormalities and restricted diffusion in MRI were correlated with duration of exposure to CO but not with the carboxyhemoglobin levels.
https://apjmt.mums.ac.ir/article_3382_d12c0ef76422fef182ba784c4d433adc.pdf
2014-09-01
124
129
10.22038/apjmt.2014.3382
Brain
Carbon Monoxide
magnetic resonance imaging
Poisoning
Yasmin
Davoudi
davoudiy@mums.ac.ir
1
Assistant Professor, Department of Radiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Bita
Dadpour
dadpourb@mums.ac.ir
2
Assistant Professor, Department of Internal Medicine, Medical Toxicology Centre, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Reza
Afshari
afsharireza@yahoo.com
3
Associate Professor, Department of Internal Medicine, Medical Toxicology Centre, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Naser
Hasaniyeh
4
Resident, Department of Radiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Nassim
Matin
nsmatn@yahoo.com
5
Student, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mahboobeh
Rahimi-Doab
6
Psychologist, Cardiac Anesthesia Research Center, Imam Reza Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Afshari R, Majdzadeh R, Balali-Mood M. Pattern of acute poisonings in Mashhad, Iran 1993-2000. J Toxicol Clin Toxicol 2004;42:965-75.
1
Tahouri A, Lyoussi B, Achour S. Carbon Monoxide Poisoning in the Region of Fez-Boulemane, Morocco: Epidemiological Profile and Risk Factors (2009-2012). Asia Pac J Med Toxicol 2013;2:131-5.
2
Rhalem N, Aghandous R, Chaoui H, Eloufir R, Badrane N, Windy M, et al. Role of the Poison Control Centre of Morocco in the Improvement of Public Health. Asia Pac J Med Toxicol 2013;2:82-6.
3
Iseki K, Hayashida A, Shikama Y, Goto K, Tase C. An Outbreak of Carbon Monoxide Poisoning in Yamagata Prefecture Following the Great East Japan Earthquake. Asia Pac J Med Toxicol 2013;2:37-41.
4
Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review. J Neurol Sci 2007;262:122-30.
5
O'Donnell P, Buxton P, Pitkin A, Jarvis L. The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning. Clin Radiol 2000;55:273-80.
6
Chu K, Jung K-H, Kim H-J, Jeong S-W, Kang D-W, Roh J-K. Diffusion-weighted MRI and 99mTc-HMPAO SPECT in delayed relapsing type of carbon monoxide poisoning: evidence of delayed cytotoxic edema. Eur Neurol 2004;51:98-103.
7
Beppu T. The role of MR imaging in assessment of brain damage from carbon monoxide poisoning: a review of the literature. AJNR Am J Neuroradiol 2014;35:625-31.
8
Kinoshita T, Sugihara S, Matsusue E, Fujii S, Ametani M, Ogawa T. Pallidoreticular damage in acute carbon monoxide poisoning: diffusion-weighted MR imaging findings. AJNR Am J Neuroradiol 2005;26:1845-8.
9
Silver D, Cross M, Fox B, Paxton R. Computed tomography of the brain in acute carbon monoxide poisoning. Clin Radiol 1996;51:480-3.
10
Lo CP, Chen SY, Lee KW, Chen WL, Chen CY, Hsueh CJ, et al. Brain injury after acute carbon monoxide poisoning: early and late complications. AJR Am J Roentgenol 2007; 189:W205-11.
11
Weaver LK, Valentine KJ, Hopkins RO. Carbon monoxide poisoning: risk factors for cognitive sequelae and the role of hyperbaric oxygen. Am J Respir Crit Care Med 2007; 176:491-7.
12
Kao LW, Nañagas KA. Carbon monoxide poisoning. Emerg Med Clin North Am 2004;22:985-1018.
13
Sener RN. Acute carbon monoxide poisoning: diffusion MR imaging findings. AJNR Am J Neuroradiol 2003;24:1475-7.
14
Martindale JL. Imaging abnormalities associated with carbon monoxide toxicity. J Emerg Med 2013;44:1140-1.
15
Stephen RA, Donal SW, Siobhain OB, Michael CR, Daniel CJ. Carbon monoxide poisoning: Novel magnetic resonance imaging pattern in the acute setting. Int J Emerg Med 2012;5:30.
16
Teksam M, Casey SO, Michel E, Liu H, Truwit CL. Diffusion-weighted MR imaging findings in carbon monoxide poisoning. Neuroradiology 2002;44:109-13.
17
Chang KH, Han MH, Kim HS, Wie BA, Han MC. Delayed encephalopathy after acute carbon monoxide intoxication: MR imaging features and distribution of cerebral white matter lesions. Radiology 1992;184:117-22.
18
Kim JH, Chang KH, Song IC, Kim KH, Kwon BJ, Kim HC, et al. Delayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions. AJNR Am J Neuroradiol 2003;24:1592-7.
19
Prockop LD, Naidu KA. Brain CT and MRI findings after carbon monoxide toxicity. J Neuroimaging 1999;9:175-81.
20
Parkinson RB, Hopkins RO, Cleavinger HB, Weaver LK, Victoroff J, Foley JF, et al. White matter hyperintensities and neuropsychological outcome following carbon monoxide poisoning. Neurology 2002;58:1525-32.
21
Pavese N, Napolitano A, De Iaco G, Canapicchi R, Collavoli PL, Lucetti C, et al. Clinical outcome and magnetic resonance imaging of carbon monoxide intoxication. A long-term follow-up study. Ital J Neurol Sci 1999;20:171-8.
22
Hossmann KA. The hypoxic brain. Insights from ischemia research. Adv Exp Med Biol 1999;474:155-69.
23
ORIGINAL_ARTICLE
Acute Copper Sulfate Poisoning: Case Report and Review of Literature
Background: Copper sulfate ingestion is a relatively popular method for committing suicide in Indian subcontinent. It causes a high mortality rate, and so a growing concern has been raised to identify the severe alarming signs suggestive of poor prognosis and to improve treatment approaches. Case report: A 22-year-old unmarried man working as a painter was found unconscious at his friend residence. The patient developed hypotension, hemorrhagic gastroenteritis with hematemesis and melena, renal and hepatic failure, severe metabolic acidosis and intravascular hemolysis during admission at hospital. His signs were refractory to treatment with fluid replacement therapy, vasoactive drugs, antiemetic drugs, ranitidine, furosemide, methylene blue and 2,3 dimercaptopropane-1-sulphonate. He died six hours post-admission. In post-mortem examinations, there were multiple sub-pleural and sub-epicardial hemorrhages and the gastrointestinal mucosa was congested, hemorrhagic, and greenish blue in color. The liver, on histological examination, showed sub-massive hepatic necrosis. On toxicological analyses, copper sulfate was detected in preserved viscera and results for other heavy metals were negative. Conclusion: Hypotension, cyanosis, uremia and jaundice can be considered as signs of poor prognosis in copper sulfate poisoning. Copper sulfate ingestion is life-threatening due to its deleterious effects on the upper GI, kidneys, liver and blood. Having no time to waste, aggressive treatments should be immediately instituted and signs of poor prognosis should be kept in mind.
https://apjmt.mums.ac.ir/article_3383_35ff4fc78b565c4c721f6f369aab1fac.pdf
2014-09-01
130
133
10.22038/apjmt.2014.3383
Copper sulfate
Forensic Toxicology
Gastrointestinal hemorrhage
Hemolysis
Poisoning
Mahesh Chand
Meena
drmahe2012@gmail.com
1
Department of Forensic Medicine and Toxicology, Lady Hardinge Medical College, New Delhi, India
LEAD_AUTHOR
Mukesh Kumar
Bansal
2
Department of Forensic Medicine and Toxicology, Lady Hardinge Medical College, New Delhi, India
AUTHOR
Blundell S, Curtin J, Fitzgerald D. Blue lips, coma and haemolysis. J Paediatr Child Health 2003;39:67-8.
1
Naha K, Saravu K, Shastry BA. Blue vitriol poisoning: a 10-year experience in a tertiary care hospital. Clin Toxicol (Phila) 2012;50:197-201.
2
James LP, Stowe CD, Argao E. Gastric injury following copper sulphate ingestion. Pediatr Emerg Care 1999;15:429-31.
3
Saravu K, Jose J, Bhat MN, Jimmy B, Shastry BA. Acute ingestion of copper sulphate: A review on its clinical manifestations and management. Indian J Crit Care Med 2007;11:74-80.
4
Bhowmik D, Mathur R, Bhargava Y, Dinda AK, Agarwal SK, Tiwari SC, et al. Chronic interstitial nephritis following parenteral copper sulfate poisoning. Ren Fail 2001;23:731-5.
5
Behera C, Rautji R, Dogra TD. An unusual suicide with parenteral copper sulphate poisoning: a case report. Med Sci Law 2007;47:357-8.
6
Sinkovic A, Strdin A, Svensek F. Severe acute copper sulphate poisoning: a case report. Arh Hig Rada Toksikol 2008;59:31-5.
7
Ellenhom MJ, Schonwold S, Ordag G. Metals and related compounds. Ellenhorn MJ. Ellenhorn's Medical Toxicology: Diagnosis and treatment of human poisoning. 2nd ed. Baltimore: Williams and Wilkins; 1997.
8
Gamakaranage CS, Rodrigo C, Weerasinghe S, Gnanathasan A, Puvanaraj V, Fernando H. Complications and management of acute copper sulphate poisoning; a case discussion. J Occup Med Toxicol 2011;6:34.
9
Oldenquist G, Salem M. Parenteral copper sulphate poisoning causing acute renal failure. Nephrol Dial Transplant 1999;14:441-3.
10
Sood N, Verma P. Life-threatening haemolysis in a patient with acute copper sulphate poisoning. Indian J Anaesth 2011;55:204-5.
11
Yang CC, Wu ML, Deng JF. Prolonged hemolysis and methemoglobinemia following organic copper fungicide ingestion. Vet Hum Toxicol 2004;46:321-3.
12
Valsami S, Stamoulis K, Lydataki E, Fountoulaki-Paparizos L. Acute copper sulphate poisoning: a forgotten cause of severe intravascular haemolysis. Br J Haematol 2012;156:294.
13
Sweni S, Meenakshisundaram R, Sakthirajan R, Rajendiran C, Thirumalaikolundusubramanian P. Acute renal failure in acute poisoning: prospective study from a tertiary care centre of South India. J Ren Care 2012;38:22-8.
14
Agarwal SK, Tiwari SC, Dash SC. Spectrum of poisoning requiring haemodialysis in tertiary care hospital in India. Int J Artif Organs. 1993;16:20-22.
15
Chen Z, Meng H, Xing G, Chen C, Zhao Y, Jia G, et al. Acute toxicological effects of copper nanoparticles in vivo. Toxicol Lett 2006;163:109-20.
16
Malik M, Mansur A. Copper Sulphate poisoning and exchange tranfusion. Saudi J Kidney Dis Transpl. 2011; 22:1240–1242.
17
Bradberry S. Copper. Medicine 2007;35:608.
18
Cai L, Li XK, Song Y, Cherian MG. Essentiality, toxicology and chelation therapy of zinc and copper. Curr Med Chem 2005;12:2753-63.
19
Prajapati T, Prajapati K, Tandon R, Merchant S. Acute Chemical and Pharmaceutical Poisoning cases Treated in Civil Hospital, Ahmedabad: One Year study. Asia Pac J Med Toxicol 2013;2:63-7.
20