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VOLUME 24 , ISSUE 5 ( May, 2020 ) > List of Articles
Shivkumar Gopalakrishnan, Sangeetha Kandasamy, Ramya Iyyadurai
Keywords : Mortality, Rodenticide poisoning, Yellow phosphorus
Citation Information : Gopalakrishnan S, Kandasamy S, Iyyadurai R. Rodenticide Poisoning: Critical Appraisal of Patients at a Tertiary Care Center. Indian J Crit Care Med 2020; 24 (5):295-298.
License: CC BY-NC 4.0
Published Online: 27-07-2020
Copyright Statement: Copyright © 2020; The Author(s).
Importance: Rodenticide poisoning is a common occurrence in India. Of the different classes of rodenticides available, yellow phosphorus is considered highly toxic. There are scarce epidemiological data regarding the ingestion of yellow phosphorus in the subcontinent. Objectives: This study aimed to identify the clinical profile of rodenticide-poisoned patients and delineate mortality predictors. Design: Prospective observational study. Setting and participants: Study was conducted at the Department of Internal Medicine, Government Villupuram Medical College and Hospital. All adult inpatients with a history of rodenticide poison exposure were eligible participants. A total of 99 patients completed the study protocol. Main outcome: Survival with or without morbidity and death. Results: In all, 90.91% of patients consumed the paste formulation of rodenticide [yellow phosphorus (67.2%) and yellow phosphorus + zinc phosphide (24%)].The time to resuscitation showed significance to mortality. Survival rate among patients instituted gastric decontamination within 2 hours of exposure (97.87%) was significantly higher than those who were not (84.62%) (p = 0.033). The clinical picture revealed conspicuous absence of signs and symptoms during the first 24 hours. In all, 72.73% (n = 72) manifested with toxidrome after a lag period of 24–36 hours (range 18–72 hours). The dominant clinical manifestations included abdominal pain (52.53%), jaundice (22.21%), coagulopathy (15.15%), encephalopathy (10.10%), shock (10.10%), acute kidney injury (AKI; 7.08%), and multi-organ failure (17.17%). Laboratory data showed elevated aspartate transaminase (AST; 48.47%), alanine aminotransferase (ALT; 49.50%), bilirubin levels (22.21%), metabolic acidosis (10.12%), serum creatinine (7.08%), prothrombin time prolongation (PT/INR; 15.15%), and activated partial thromboplastin time (aPTT) (3.30%). The mortality was 9.1% (n = 9) of which 77.78% (n = 7) died of fulminant hepatic failure. The mean time for death was 4.22 days since exposure (range 2–8 days). Conclusion: Rodenticide poisoning in Southern India is dominated by yellow phosphorus. In this study, we identified delayed resuscitation, jaundice, hepatic encephalopathy, elevation of AST and ALT to >1000 IU/L, metabolic acidosis, and refractory shock as reliable predictors of bad outcome in this patient population. The common mode of death was fulminant hepatic failure. Relevance: Rodenticide poisoning ranks second in mortality hierarchy at our institute, and systematic analysis of this patient population is an urgent need.
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