Serum Transaminases Level in Rodenticide Poisoning
Abstract
Rat killer poison consumption cases are among the second most common poisoning in developing countries. It is associated with significant morbidity and mortality. They develop varied complications including bleeding manifestations, hepatic and renal failure, encephalopathy and metabolic acidosis. However, some patients recover completely without any consequences and this is probably because of variability of the rodenticide content. So, the chemical content of the rat killer poison decides the morbidity and mortality. A retrospective analysis of serum transaminases level in patients with rat killer poisoning was performed. In our study, it is shown that the early rise in transaminases level significantly associated with outcome of patient. An AST cut off value of 697 IU/ Lon the fifth day post ingestion with 100% sensitivity and 100% specificity is an independent predictor for mortality. Absence of timely antidote administration and rapid onset of multi organ dysfunction (MODS) causes high mortality rate in acute rodenticide poisoning1.
Full Text:
PDFReferences
Orak M, Ustundag M, Sayhan MB. Severe metabolic acidosis secondaryto zinc phosphide poisoning. J Pak Med Assoc 2008; 58: 289-90.
Perry HE. Rodenticides. In: Shannon MW, Borron SW, Burns MJ, editors. Haddad and Winchester’s clinical management of poisoning and drugoverdose. Philadelphia, PA: Saunders – Elsevier; 2007. p. 1225-6.
Soltani M, Shetab-Boushehri SF, Mohammadi H, Shetab-Boushehri SV. Proposing boric acid as an antidote for aluminium phosphide poisoning by investigation of the chemical reaction between boric acid and phosphine. Journal of Medical Hypotheses and Ideas. 2013;7(1):21-24.
Proudfoot, A. T. 2009. Aluminium and zinc phosphidepoisoning.Clin.Toxicol.(Phila.) 47:89–100.
Chugh SN, Arora V, Sharma A, Chugh K. Free radical scavengers and lipid peroxidation in acute aluminium phosphide poisoning. Indian J Med Res 1996; 104: 190-3.
Chugh SN, Arora V, Sharma A, Chugh K. Free radical scavengers & lipidperoxidation in acute aluminium phosphide poisoning. Indian J Med Res1996; 104: 190-3.
Perry HE. Rodenticides. In: Shannon MW, Borron SW, Burns MJ, editors. Haddad and Winchester’s clinical management of poisoning and drug overdose. Philadelphia, PA: Saunders – Elsevier; 2007. p. 1225-6.
Ahmad SH, Fakhir S, Gupta S, Singh RK. Celphos poisoning. Indian Pediatr1991; 28: 300-1.Eurasian J Emerg Med 2016; 15: 39-43
Prasad.S et al. Banjaj R, Wasir HS. Epidemic aluminium phosphide poisoning in Northern India. Lancet 1988; 1: 820-1.
Konradsen F, van der Hoek W, Cole DC, Hutchinson G, Daisley H, Singh S, et al. Reducing acute poisoning in developing countries–-options for restricting the availability of pesticides. Toxicology 2003; 192: 249-61.
McCarron MM, Gaddis GP, Trotter AT. Acute yellow phosphorus poisoning from pesticide pastes. Clin Toxicol 1981;18:693-711.
Saleki S, Ardalan FA, Javidan-Nejad A. Liver histopathology of fatal phosphinepoisoning. Forensic SciInt 2007; 166: 190-3.
Santos O, Restrepo JC, Velásquez L, et al. Acute liver failure due to white phosphorus ingestion. Ann Hepatol. 2009;8: 162–5.
O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989;97:439–45.
Acharya SK, Dasarathy S, Kumer TL, et al. Fulminant hepatitis in a tropical population: clinical course, cause, and early predictors of outcome. Hepatology. 1996;23:1448–55.
Refbacks
- There are currently no refbacks.
This work is licensed under a Creative Commons Attribution-NoDerivatives 4.0 International License.
An initiative of The Tamil Nadu Dr M.G.R. Medical University