A study on electrolyte abnormalities following consumption of poisoning compound
Corresponding Author(s) : Manjunathan N
International Journal of Allied Medical Sciences and Clinical Research,
Vol. 2 No. 4 (2014): 2014 Volume 2- Issue -4
Abstract
Background
The introduction of insecticides for agricultural and household insecticidemenace the toxicological aspects of Organophosphorus compound, Organochlorine compound , carbamatesbecame important tothephysician. In addition to the accidental exposure from use of these compounds as agricultural insecticides these agents are frequently used for suicidal and homicidal purposes because of their low cost and easy availability. .Most of the poisoning agents cause severe cell damage which results in disturbed homeostasis in the extra cellular fluid and often reflected in the blood by alteration in biochemical parameters. Electrolyte imbalance is a serious but readily correctable condition
Aim
To assess and evaluate the type of electrolyte abnormality in poisonings.
Methodology
After permission from ethical committee the present study was conducted in 50 adults patient, of either sex aged 14- 70 years with history of consumption of poisonous compounds between the periods of Jan 2013 to June 2014.Patient who consume the following compounds will be taken for this study are Organophosphorus poisoning ,Organochlorine poisoning ,Oleander poisoning ,Dhatura poisoning ,Aluminum and zinc phosphide poisoning .Age less than 14 years ,Corrosive poisoning ,Patients with pre-existing cardiac disorder , renal disorder ,uncontrolled hypertension ,endocrine disorders ,established hematological disorder are excluded from the study .
Results
76% of study patients were survived and 24% of the study patients were expired. Out of 24% who were expired ,16% death were due nature of poison consumed . Remaining 8% deaths were due to electrolyte abnormalities. Serumelectrolyteswerenormalinmostofthepatient.Hypokalemiafollowedbyhyponatremia were most common electrolyte derangementsinthestudy. Mortality rate was more in elderly group.
Conclusion
At admission 16% of patients had hyponatremia , 54% of patients had normal serum sodium level and 30% of patients had hyprenatremia. At admission 8% of patients had Hypokalemia , 60% of patients had normal potassium and 32% of patients had hyperkalemia. Mortality rate was more in elderly group.
Keywords
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX
-
[1] Kurzbaum A, Simsolo C, Kvasha L, Blum A. Toxic delirium due to Daturastramonium. Isr Med Assoc J. 2001;3:538–9
[2] Chang SS, Wu ML, Deng JF, Lee CC, Chin TF, Liao SJ. Poisoning by Datura leaves used as edible wild vegetables. Vet Hum Toxicol. 1999;41:242–5
[3] Spina SP, Taddei A. Teenagers with Jimson weed (Daturastramonium) poisoning. CJEM.2007;9:467–8
[4] Wiebe TH, Sigurdson ES, Katz LY. Angel's Trumpet (Daturastramonium) poisoning and delirium in adolescents in Winnipeg, Manitoba: Summer 2006. Paediatr Child Health. 2008;13:193–6
[5] Djibo A, Bouzou SB. Acute intoxication with "sobi-lobi" (Datura). Four cases in Niger. Bull SocPatholExot. 2000;93:294–7
[6] Eddleston M, Ariaratnam CA, Meyer PW,? et al. Epidemic of self-poisoning with seeds of the yellow oleander tree (Thevetiaperuviana) in northern Sri Lanka. Trop Med Int Health 1999; 4:266–73
[7] Eddleston M, Sheriff MHR, Hawton K. Deliberate self-harm in Sri Lanka: an overlooked tragedy in the developing world. Br Med J 1998; 317:133–5.
[8] Management of acute yellow oleander poisoning.” Eddleston, M and Warrell, DA. Q J Med 1999; 92: 483-485
[9] Safadi R, Levy I, Amitai Y, Caraco Y. Beneficial effects of digoxin-specific Fab antibody fragments in oleander intoxication. Arch Intern Med 1995; 155:2121–5
[10] Eddleston M. Patterns and problems of deliberate self-poisoning in the developing world. Q J Med 2000; 93: 715
[11] Bronstein AC, Spyker DA, Cantilena LR, et al. 2010 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 28th Annual Report. Clinical Toxicology 2011; 49: 910
[12] Bajaj R, Agarwal R, Wasir HS, Bhatia ML. (1988) Clinical toxicity and intensive haemodynamic monitoring in patients of aluminium phosphide poisoning. J AssocPhysInd, 36: 23
[13] Christophers AJ, Singh S, Goddard DG (2002) Dangerous bodies: a case of fatal aluminium 21 phosphide poisoning. MJA ,176 (8): 403
[14] S.BSiwach and A.Gupta,1995 , “The profile of acute poisoning in harayana-RohtakStudy” ,The Journal Of the Association Of Physicians Of India , vol 43,no.11, pp 756-759, pp 302-307,2010.
[15] T.Proudfoot,2009 ,”Aluminium and zinc phosphide poisoning ,Clinical Toxicology ,vol 47,n0.2,pp 89-100.
[16] M.Orak ,M.UstUndug and M.B.Sayhan,2008, Severe metabolic acidosis secondary to zinc phosphide poisoning, “ Journal Of The Pakisthan Medical Association , vol 58 ,pp 289-290.
[17] Mathai and M S Bhanu , 2007 ,Acute Aluminium phosphide poisoning : can we predict mortality ? “ Indian journal of Anaesthesia “ vol 54 pp 23-28.
References
[2] Chang SS, Wu ML, Deng JF, Lee CC, Chin TF, Liao SJ. Poisoning by Datura leaves used as edible wild vegetables. Vet Hum Toxicol. 1999;41:242–5
[3] Spina SP, Taddei A. Teenagers with Jimson weed (Daturastramonium) poisoning. CJEM.2007;9:467–8
[4] Wiebe TH, Sigurdson ES, Katz LY. Angel's Trumpet (Daturastramonium) poisoning and delirium in adolescents in Winnipeg, Manitoba: Summer 2006. Paediatr Child Health. 2008;13:193–6
[5] Djibo A, Bouzou SB. Acute intoxication with "sobi-lobi" (Datura). Four cases in Niger. Bull SocPatholExot. 2000;93:294–7
[6] Eddleston M, Ariaratnam CA, Meyer PW,? et al. Epidemic of self-poisoning with seeds of the yellow oleander tree (Thevetiaperuviana) in northern Sri Lanka. Trop Med Int Health 1999; 4:266–73
[7] Eddleston M, Sheriff MHR, Hawton K. Deliberate self-harm in Sri Lanka: an overlooked tragedy in the developing world. Br Med J 1998; 317:133–5.
[8] Management of acute yellow oleander poisoning.” Eddleston, M and Warrell, DA. Q J Med 1999; 92: 483-485
[9] Safadi R, Levy I, Amitai Y, Caraco Y. Beneficial effects of digoxin-specific Fab antibody fragments in oleander intoxication. Arch Intern Med 1995; 155:2121–5
[10] Eddleston M. Patterns and problems of deliberate self-poisoning in the developing world. Q J Med 2000; 93: 715
[11] Bronstein AC, Spyker DA, Cantilena LR, et al. 2010 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 28th Annual Report. Clinical Toxicology 2011; 49: 910
[12] Bajaj R, Agarwal R, Wasir HS, Bhatia ML. (1988) Clinical toxicity and intensive haemodynamic monitoring in patients of aluminium phosphide poisoning. J AssocPhysInd, 36: 23
[13] Christophers AJ, Singh S, Goddard DG (2002) Dangerous bodies: a case of fatal aluminium 21 phosphide poisoning. MJA ,176 (8): 403
[14] S.BSiwach and A.Gupta,1995 , “The profile of acute poisoning in harayana-RohtakStudy” ,The Journal Of the Association Of Physicians Of India , vol 43,no.11, pp 756-759, pp 302-307,2010.
[15] T.Proudfoot,2009 ,”Aluminium and zinc phosphide poisoning ,Clinical Toxicology ,vol 47,n0.2,pp 89-100.
[16] M.Orak ,M.UstUndug and M.B.Sayhan,2008, Severe metabolic acidosis secondary to zinc phosphide poisoning, “ Journal Of The Pakisthan Medical Association , vol 58 ,pp 289-290.
[17] Mathai and M S Bhanu , 2007 ,Acute Aluminium phosphide poisoning : can we predict mortality ? “ Indian journal of Anaesthesia “ vol 54 pp 23-28.