Management of rodenticide poisoning Dr Sunil Karanth MD, FNB, EDIC, FCICM CHAIRMAN OF CRITICAL CARE SERVICES MANIPAL HEALTH ENTERPRISES (P) LTD MANIPAL HOSPITAL, BANGALORE ADJUNT PROFESSOR IN CRITICAL CARE MEDICINE MANIPAL UNIVERSITY

introduction Common source of poisoning in this part of the world Safety for other animals and humans Toxicity of agent Concentration of the active ingredient Bioaccumulation and persistence in the body tissues TWO CLINICAL TYPES Extremely potent and toxic Sodium fluoroacetate, fluoroacetamide, strychnine, crimidine, yellow phosphorous, zine phosphide, thallium sulphide Less toxic to humans Anticoagulants, red squill, indandiones

Coumarins and indandiones Warfarin and related compounds 2 types First generation – Hydroxy coumarin derivatives – Warfarin, coumachor, coumatetralyl Second generation – superwarfarins – bromodiolone, brodifacoum, difenacoum Decrease hepatic synthesis of Vitamin K-dependant factors Prothrombin time used for diagnosis and monitoring – increases in 24 hours and peaks at about 72 hours

coumarins Presents early or late with bleeding manifestations PT may remain high for days to weeks Treatment: Vitamin K1(Phytonadione) – 10-50 mg, 2-4 times per day Orally preferable because of a better adverse effect profile Sometimes, may be needed to be given for months Consider transfusion of FFPS if active bleeding present at admission

Inorganic rodenticides

Yellow phosphorous Dermal burns possible Oral ingestion 3 stages Gastrointestinal Period of relative improvement Myocardial, hepatic and CNS involvement – progressing on to multiorgan failure Toxic hepatitis with hepatic failure Myocarditis with cardiogenic shock Mechanism: PHOSPHENE GAS RELEASE

Yellow phosphorous MANAGEMENT DECREASE ABSORPTION Gastric lavage with potassium permanganate – controversial because of the corrosive nature of yellow phosphorus Gastric lavage with activated charcoal and mineral oil cathartic HEPATO-PROTECTION N-Acetyl cysteine Dose of 150mg/kg over 1 hour followed by 50 mg/kg over 4 hours and 100mg/kg over 15 hours SUPPORTIVE MEASURES Fluid resuscitation Organ specific support Hepatic encephalopathic measures High volume plasma exchange – may have a role? Liver transplantation

Zinc phosphide Highly toxic rodenticide Mechanism of action: - Release of phosphene gas Clinical profile - similar to yellow phosphorous 3 stages Lesser corrosive than Yellow phosphorus III stage Hepatic, CNS and myocardial involvement Hepatic failure, shock , CNS manifestations Multisystem organ failure Risk of hepatic failure

Zinc phosphide MANAGEMENT Supportive care Cardiovascular support Vasopressors to ECMO if needed Renal replacement therapy Liver support Osmotherapy Anti-encephalopathic measures High volume plasma exchange – may decrease transplant free survival Consider for transplant if appropriate

THALIUM SULFATE Absorbed from the gut and skin rapidly Slow onset of action in comparison to Phosphides Symptoms start over days CNS, GI, Hepatic, Renal and integumentary systems affected Alopecia seen after 2 weeks – more often seen in chronic poisoning Confirmation by the use of Urinary 24 hour levels which will be elevated TREATMENT General supportive care Role for Hemodialysis in faster elimination of thalium Use of Prussian blue (potassium ferric ferrocyanide) to enhance faecal excretion of thalium

Severe multiorgan metabolic toxicants

Sodium fluoroacetate and fluoroacetamide Readily absorbed from the gut Forms fluorocitrate in the body causing disruption of the Kreb’s urea cycle blocking intracellular respiration CNS, Cardiovascular, Metabolic predominantly involved Management Largely supportive Administer large dose of IV calcium gluconate guided by the serum calcium levels

STRYCHNINE, CRIMIDINE, TETRAMETHYLENE DISULFOTETRAMINE (TETS) Seizures and neurotoxicity are the predominant symptoms Strychnine can also cause severe muscle spasms of the diaphragm and intercostal muscles mimicking tetanus Potentially powerful CNS toxins Aggressive control of seizures Treatment is largely supportive

miscellaneous RED SQUILL No longer used as a rodenticide Generally safe on humans Cardiac glycoside – induces intense vomiting, hence very poorly absorbed CHOLECALCIFEROL All signs of hypercalcemia Polyuria, polydipsia, Nephrocalcinosis, Hypertension, proteinuria BROMETHALIN CNS toxin Uncoupling of oxidative phosphorylation in the neurons Cerebral edema, seizures, altered senosrium

summary Rodenticide poisoning Problem for many years now Different levels of toxicity Developing world – more potent toxins – high levels of mortality Most lethal toxins require multi-organ support Common toxins require various forms of liver support Early data suggest liver transplant as one of the modalities of definitive treatment

Thank you