Continuing Education Activity

Clinicians participating in this CME activity gain essential knowledge and skills for managing rodenticide toxicity. Specifically, they learn to identify and differentiate the diverse mechanisms of action and clinical presentations of various rodenticides, ranging from anticoagulant-induced bleeding to neurological and metabolic disturbances. This training also emphasizes the importance of promptly identifying the specific rodenticide involved through detailed history-taking, physical examination, and searching for packaging or other indicators. Participants can also assess and implement immediate stabilization techniques, apply specific antidotes, and provide supportive care. They also gain proficiency in interpreting laboratory and diagnostic test results and recognizing abnormalities associated with rodenticide ingestion.

This activity reviews the critical role of consultation with poison control centers and toxicologists for treatment guidance. Clinicians learn to develop and strategize effective treatment plans, incorporating collaboration with multidisciplinary teams to enhance patient outcomes. By the end of the activity, clinicians are also better prepared to coordinate follow-up care and recommend preventive measures to reduce accidental rodenticide exposures. This comprehensive approach improves clinicians' ability to provide timely and accurate diagnosis and management of rodenticide toxicity, ultimately enhancing patient care and safety.

Objectives:

• Identify the diverse mechanisms of action and clinical presentations of various rodenticides.
• Screen patients for potential rodenticide exposure through detailed history-taking and physical examination.
• Select appropriate laboratory and diagnostic tests to confirm rodenticide ingestion and identify associated abnormalities.
• Collaborate with multidisciplinary teams to develop and strategize effective treatment plans for rodenticide toxicity.

Introduction

Rodenticide toxicity is a significant public health concern due to the diverse mechanisms of action and the variety of available rodenticides. Most commonly, human exposure to rodenticides is accidental, often occurring in young children. The clinical presentation of rodenticide toxicity varies widely. Common symptoms range from anticoagulant-induced bleeding to neurological and metabolic disturbances. Prompt identification of the ingested rodenticide is critical for effective treatment and involves obtaining a detailed history, performing a thorough physical examination, and searching for packaging or other indicators of the specific rodenticide(s) involved. Management of rodenticide toxicity focuses on stabilizing the patient and providing specific antidotes or supportive care. Consultation with poison control centers or toxicologists is essential for guidance on appropriate treatment of rodenticide toxicity.

Etiology

Although anticoagulants are the most commonly used rodenticides today, many other rodenticide agents are available. Thus, symptoms of rodenticide poisoning vary depending on the specific agent(s) ingested. Rodenticide registration, distribution, sale, and use are regulated by the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), which is enforced by the Environmental Protection Agency (EPA).[1] FIFRA regulates the labeling of rodenticides and requires the prominent display of specific information, including a signal word that indicates an agent's degree of toxicity.

Rodenticides labeled with the signal word danger are highly toxic and include thallium, sodium monofluoroacetate (SMFA, fluoroacetate), strychnine, zinc phosphide, aluminum phosphide, elemental phosphorus, arsenic, and barium carbonate. Rarely used or banned agents with this labeling include tetramethylenedisulfotetramine (TETS or tetramine), aldicarb, alpha-chloralose, and pyrinuron. Rodenticides labeled with the signal word warning are moderately toxic and include alpha-naphthylthiourea and cholecalciferol. Finally, rodenticides labeled with the signal word caution pose low to very low risks for toxicity and include superwarfarin, warfarin, norbormide, bromethalin, and red squill.

Epidemiology

According to the 2022 Annual Report of the American Association of Poison Control Centers, more than 8000 rodenticide ingestions were reported in the United States.[2] More than half of these rodenticide ingestions were in children younger than 6. Anticoagulant rodenticides were identified as the ingested agents in more than 3000 cases. Bromethalin was the second most commonly ingested agent and was identified in 1681 cases.[2] 

Pathophysiology

Rodenticides consist of a wide variety of xenobiotics with different mechanisms of action. The pathophysiologic effects of several common rodenticides are summarized below.

Thallium

Thallium is a tasteless and odorless powder that can be absorbed through inhalation or the skin. This chemical acts by substituting for potassium in sodium-potassium adenosine triphosphatase and the sulfhydryl or thiol group of mitochondrial membranes. Thallium inhibits pyruvate kinase and succinate dehydrogenase, which disrupts the Krebs cycle, oxidative phosphorylation, and energy production.[3] Please see StatPearls' companion resource, "Thallium Toxicity," for more information.

Fluoroacetamide (Compound 1080) and Sodium Monofluoroacetate

Both fluoroacetamide and SMFA are metabolized into monofluoroacetyl coenzyme A, which is subsequently converted into fluorocitrate. Fluorocitrate irreversibly binds aconitase and inhibits the citric acid cycle. Inhibition of the citric acid cycle leads to lactic acidosis and the buildup of substrates that are otherwise broken down by aconitase, including citrate.[4] The buildup of citrate can bind cations and lead to electrolyte abnormalities, including clinically relevant hypocalcemia.[5] In addition, inhibition of fatty acid oxidation can lead to ketosis. Hyperammonemia may also result from associated inhibition of the urea cycle.[6]

Strychnine

Strychnine is an odorless and colorless powder. Strychnine toxicity commonly causes involuntary muscle contraction, resulting from strychnine's competitive inhibition of glycine receptors of postsynaptic and motor neurons within the spinal cord.[7] Please see StatPearls' companion resource, "Strychnine Toxicity," for more information.

Zinc and Aluminum Phosphide

When zinc or aluminum phosphide is ingested, gastric acid releases phosphine gas, which is absorbed into the bloodstream. Zinc and aluminum phosphides inhibit the cytochrome C oxidase system, which disrupts the formation of adenosine triphosphate (ATP).[8] 

Elemental Phosphorus

Elemental phosphorus exists in red or white forms, with white phosphorus used as a rodenticide. White phosphorus is very toxic and can cause damage both locally and systemically. When ingested, it causes direct tissue damage through exposure to phosphoric acid and phosphorus pentoxide. In circulation, phosphorous binds to calcium and can lead to clinically significant hypocalcemia.[9]

Arsenic

Arsenic is a toxic, inorganic compound whose exact mechanism of action is unknown. Proposed toxic mechanisms of arsenic include inhibition of hexokinase in glycolysis, inhibition of pyruvate dehydrogenase in the Krebs cycle, and aberrant vasodilation due to the formation of sulfhydryl compounds.[10] Please see StatPearls' companion resource, "Arsenic Toxicity," for more information.

Barium Carbonate

Barium carbonate dissolves easily in water and is highly toxic. The barium ion inhibits potassium diffusion out of cells, which can result in clinically significant hypokalemia.[11]

Tetramethylenedisulfotetramine (Tetramine)

Tetramine is odorless, colorless, and tasteless and is a reversible and noncompetitive antagonist of the gamma-aminobutyric acid type A (GABA-A) receptor.[12] Through antagonism of the GABA-A receptor, tetramine may induce seizures and other neurotoxic effects. 

Aldicarb

Originating from Latin America, aldicarb is also known as tres pasitos, which refers to the 3 little steps mice take before aldicarb causes death. Aldicarb is a potent cholinesterase inhibitor and causes a cholinergic toxidrome.[13]

Alpha-chloralose

Originating from Europe, alpha-chloralose is used as a veterinary anesthetic and rodenticide. Alpha-chloralose's mechanism of action is not clearly defined but is believed to be similar to that of barbiturates.[14]

Pyriminil

Pyriminil causes swift destruction of pancreatic beta cells through nicotinamide antagonism and impairment of NAD and NADH synthesis.[15][16]

Cholecalciferol (Vitamin D3)

Cholecalciferol mobilizes calcium from the bones and increases intestinal calcium absorption, which causes hypercalcemia.[17][18] Large ingestions of cholecalciferol may cause clinically significant hypercalcemia, leading to dehydration, anorexia, renal failure, and calcification of vital organs.

Anticoagulants (Superwarfarins and Warfarin)

Superwarfarins, including brodifacoum, difenacoum, bromadiolone, and chlorophacinone, are anticoagulant rodenticides that are structurally similar to warfarin but contain terminal phenyl groups instead of terminal methyl groups. Substituting a terminal phenyl group makes superwarfarins 100-fold more potent compared to warfarin.[19] Warfarin and superwarfarins are competitive inhibitors of the vitamin K epoxide reductase complex 1 (VKORC1). VKORC1 inhibition prevents the synthesis of clotting factors II, VII, IX, and X. Please see StatPearls' companion resource, "Warfarin Toxicity," for more information.

Norbormide

Norbromide causes extreme peripheral vasoconstriction, leading to ischemia, organ failure, and death. However, it is not toxic to humans.[20] 

Bromethalin

Bromethalin uncouples oxidative phosphorylation, leading to decreased ATP production. This lack of ATP causes edema around neuron sheaths, leading to toxic effects in the central and peripheral nervous systems. Bromethalin is rarely toxic to humans because it takes significant ingestion to exert toxic effects.[21]

Red Squill (Urginea maritima or Drimia maritima)

Red squill contains scillaren A and B, which are cardioactive glycosides.[22] Thus, red squill's mechanism of toxicity is very similar to digoxin and involves inhibition of the sodium-potassium ATPase pump. Inhibition of the sodium-potassium ATPase pump leads to gastrointestinal, cardiac, and central nervous system toxicity.[23]

History and Physical

Children are more susceptible to rodenticide toxicity due to accidental ingestion, whereas adults who attempt suicide with rodenticides represent a significant subset of affected patients.[24] The most common rodenticides used in the United States are anticoagulants. Symptoms consistent with ingesting anticoagulant rodenticides include hematuria, hemoptysis, epistaxis, flank pain, bruising, and petechiae under the blood pressure cuff.[25] However, the symptoms of rodenticide toxicity vary depending on the rodenticide(s) involved. Because of the wide range of potential toxicities, every effort should be made to identify the rodenticide(s) exposed to the patient. Accurate and timely identification of rodenticides may involve having friends or family of the patient or law enforcement search the patient's last known location to find rodenticide packaging or other indicators of what specific rodenticide(s) were involved in the exposure.

The toxicity of rodenticides is categorized by the amount of poison required to cause death in 50% of those animals exposed, which is known as lethal dose 50 (LD50). In some regions, including the United States, the toxicity of a rodenticide is denoted by signal words on product labels, such as danger, warning, or caution. Rodenticides labeled as danger are considered to be very toxic (LD50 is 0-50 mg/kg). Rodenticides labeled as warning are considered to be toxic (LD50 is 50-500 mg/kg). Finally, rodenticides labeled as caution are considered to be less toxic (LD50 is 500-5000 mg/kg).

Symptoms of toxicity for specific rodenticides are described below:

Thallium

Acute exposure to thallium can cause acute gastroenteritis, cranial nerve dysfunction, painful peripheral neuropathy, seizures, alopecia, and hyperpigmentation. Chronic exposure to thallium can cause tremors, ataxia, distal motor weakness, diplopia, nystagmus, seventh cranial nerve palsy, and ocular lens opacities.[3][26]

Fluoroacetamide (Compound 1080) and Sodium Monofluoroacetate 

Exposure to compound 1080 and SMFA may cause seizures, metabolic acidosis, shock, dysrhythmias, and hypocalcemia. Acute kidney injury, hepatic dysfunction, and cerebral or cerebellar atrophy may develop as late complications of compound 1080 or SMFA exposure.

Strychnine

Exposure to strychnine may cause muscle spasms, trismus, risus sardonicus, opisthotonos, lactic acidosis, and hyperthermia. Rhabdomyolysis may also develop due to muscle damage caused by strychnine exposure.[27]

Zinc and Aluminum Phosphide

Exposure to zinc and aluminum phosphide may cause acute gastroenteritis, acid-base disorders, cardiac arrhythmias, renal failure, hemorrhagic pulmonary edema, respiratory failure, hepatotoxicity, and intravascular hemolysis with methemoglobinemia.[28][28]

Elemental Phosphorus

Symptoms of elemental phosphorus toxicity include acute gastroenteritis, burns on the skin or mucosa, phosphorescent emesis or feces (smoking stools), dysrhythmias, renal failure, and hepatotoxicity.[29][30]

Arsenic

Symptoms of arsenic exposure include garlic taste, vomiting, bloody diarrhea, hypotension, prolonged QTc, acute kidney injury, delirium, and seizures. Arsenic may also cause coma in patients with significant exposure.[31][32]

Barium Carbonate

Exposure to barium carbonate may cause gastroenteritis, hypertension, arrhythmias, shortness of breath, and muscle paralysis.[33]

Tetramethylenedisulfotetramine (Tetramine)

Symptoms of TETS or tetramine exposure include gastroenteritis, arrhythmias, and convulsions. TETS or tetramine may cause respiratory failure or coma in patients with significant exposure.[12]

Aldicarb

Exposure to aldicarb may cause cholinergic symptoms, including excessive salivation, lacrimation, urination, and diarrhea. Aldicarb also commonly causes gastrointestinal upset and emesis.[34][35]

Alpha-chloralose

Symptoms of alpha-chloralose toxicity include convulsions, hypothermia, and respiratory depression.[36]

Pyriminil

Symptoms of pyriminil toxicity include hypoglycemia, Kussmaul breathing, hypotension, lethargy, and encephalopathy.

Cholecalciferol (Vitamin D3)

Exposure to toxic doses of cholecalciferol may cause polyuria, polydipsia, abdominal pain, vomiting, renal failure, and encephalopathy.[18]

Anticoagulants (Superwarfarins and Warfarin)

Symptoms of superwarfarin and warfarin toxicity include hematuria, hemoptysis, epistaxis, flank pain, and bruising. Some patients can experience intracranial bleeding as a result of toxic superwarfarin or warfarin exposures.

Norbormide

Evidence suggests that norbormide is safe in non-rat species, given its rat-selective mechanism of toxicity.[37][20] There are no reported cases of toxicity in humans.

Bromethalin

Symptoms of bromethalin exposure may include altered mental status and delirium that are secondary to severe cerebral edema.[38]

Red Squill (Urginea maritima or Drimia maritima)

Similar to digitalis toxicity, exposure to red squill can cause abdominal pain, vomiting, seizures, hyperkalemia, and cardiac arrhythmias.

Evaluation

Accurate and timely identification of the ingested rodenticide(s) is crucial when assessing patients suspected of rodenticide toxicity. Laboratory or diagnostic tests may be ordered to help identify or confirm the effects of an ingested rodenticide. However, abnormalities that laboratory or diagnostic tests detect may not be specific to a singular rodenticide. Thus, in the setting of unknown rodenticide ingestion, abnormal laboratory or diagnostic test results cannot definitively identify or confirm the ingested rodenticide. Commonly associated test abnormalities and their corresponding testing modalities are listed below.

Comprehensive Metabolic Panel

A comprehensive metabolic panel can detect hypoglycemia induced by zinc or aluminum phosphide; hyperglycemia caused by pyriminil; hypocalcemia caused by ingesting white phosphorus, SMFA, or fluoroacetamide; hypokalemia caused by barium carbonate, zinc phosphide, or aluminum phosphide; elevated blood urea nitrogen or creatinine caused by thallium, arsenic, white phosphorus, zinc phosphide, or aluminum phosphide; or elevated liver enzymes caused by thallium, arsenic, white phosphorous, zinc phosphide, or aluminum phosphide.[33][4]

Serum Phosphate

A serum phosphate can detect hyperphosphatemia caused by ingesting white phosphorus.

Creatine Phosphokinase

An elevated creatine phosphokinase may provide evidence of strychnine-induced muscle damage.[39]

Serum Lactate

An elevated serum lactate level can detect lactatemia. Along with an arterial blood gas showing anion gap metabolic acidosis, it may provide evidence of SMFA- or fluoroacetamide-induced lactic acidosis.[4]  

Serum Lipase

Elevated serum lipase levels may signify the ingestion of pyriminil.

Troponin

Elevated troponin levels may signify cardiac myocyte damage caused by zinc and aluminum phosphide.

Complete Blood Count

A complete blood count can detect anemia caused by zinc or aluminum phosphide.

International Normalized Ratio and Activated Partial Thromboplastin Time

Elevated international normalized ratio (INR) and activated partial thromboplastin time (aPTT) may signify ingesting anticoagulant rodenticides, including warfarin and superwarfarins.

12-Lead Electrocardiogram

A 12-lead electrocardiogram can detect QTc interval prolongation caused by SMFA, fluoroacetamide, white phosphorous, or arsenic.[40]

Chest and Abdominal X-Rays

Chest and abdominal x-rays may show the presence of radiopaque rodenticides, including barium carbonate, arsenic, and thallium.

Treatment / Management

Initial Care

Immediate management of rodenticide toxicity involves supporting the patient's airway, breathing, and circulation. Once stabilized, the patient's clothing should be removed, and the skin should be washed with water to remove any residual rodenticide. In addition, consultation with a poison control center or toxicologist should be initiated immediately after stabilization. Gastric decontamination strategies, including gastric lavage, activated charcoal, and whole bowel irrigation, should not be used before consultation with a regional poison control center or a medical toxicologist. Only limited data show that these interventions decrease mortality. Other essential treatments to consider after the patient is stabilized include isotonic fluid repletion for dehydration, cooling for hyperthermia, and antiemetic medication administration, such as ondansetron, for nausea or vomiting. Patients experiencing cholinergic toxicities after aldicarb exposure may benefit from the early administration of anticholinergic agents such as atropine, glycopyrrolate, and pralidoxime. 

Specific Medical Treatment

After initial treatment of rodenticide toxicity, further treatment is largely supportive. However, medical treatments that should be considered for specific rodenticide poisonings are reviewed below.

Renal replacement therapy: Hemodialysis, continuous renal replacement, or charcoal hemoperfusion may benefit patients with heavy metal poisonings from thallium, arsenic, or barium.

British anti-Lewisite/dimercaprol: British anti-Lewisite may be an effective chelator for patients with arsenic poisoning.[41] 

Meso-2,3-dimercaptosuccinic acid or 2,3-dimercapto-1-propane sulfonate: These medications may be effective chelators for patients with chronic arsenic poisoning.[41] 

Prussian blue: Prussian blue may be used as an ion exchanger in patients with thallium poisoning.[42][43]

Sodium or magnesium sulfate: Sodium and magnesium sulfates may be used for acute barium carbonate ingestion. These compounds render barium carbonate as a non-absorbable barium sulfate compound.[11]

Benzodiazepines: Benzodiazepines may be effective in treating muscle spasms and seizures caused by strychnine poisoning.[44]

Nicotinamide: Intravenous nicotinamide may be used in cases of pyriminil poisoning to replenish NAD and NADH for cellular energy metabolism.[16] 

Mineralocorticoids: Mineralocorticoid drugs, including fludrocortisone, may be used to treat orthostatic hypotension caused by pyriminil poisoning.

Digoxin immune fab: Digoxin immune fab binds cardiac glycoside agents and may be used to treat patients with red squill poisoning.[23]

Differential Diagnosis

Patients with rodenticide toxicity can have a wide range of clinical presentations. If rodenticide exposure is confirmed and the patient experiences symptoms consistent with rodenticide exposure, treatment for rodenticide toxicity should begin immediately. If rodenticide exposure is uncertain or unconfirmed, clinicians should work to rule out other conditions that may be the cause of the patient's symptoms, including acute viral gastroenteritis, Clostridioides difficile infection, foodborne toxin exposure, acute hepatitis, alcohol withdrawal, opioid withdrawal, diabetic ketoacidosis, disseminated intravascular coagulation, organophosphate or carbamate toxicity, epilepsy, intracranial hemorrhage, stroke, or rattlesnake bite.

Prognosis

The prognosis of rodenticide toxicity depends on the specific rodenticide and the amount ingested. Patients who receive treatment for acute rodenticide toxicity early have a better prognosis compared to those for whom treatment is delayed. The benefit of early treatment of rodenticide toxicity again underscores the importance of a detailed history, a thorough physical examination, and prompt rodenticide identification. Chronic rodenticide toxicity is associated with more morbidity compared to acute toxicity. However, large, acute rodenticide exposures are associated with high rates of death.

Complications

The complications of rodenticide toxicity vary depending on the rodenticide ingested. Severe complications of rodenticide toxicity include renal and hepatic failure, permanent neurological damage, and death.

Consultations

Consultation with a regional poison control center or medical toxicologist is vitally crucial to the effective diagnosis and management of rodenticide toxicity. Toxicology experts can help determine to which rodenticide(s) the patient was exposed and can assist clinicians in determining whether the patient needs to be admitted to the hospital. Additionally, toxicology experts can assist with determining the most effective treatment(s) for the patient, including the role of gastric decontamination, extracorporeal toxin elimination, and toxin-specific treatments.

Deterrence and Patient Education

When using rodenticides, instructions should always be followed, and steps should be taken to avoid exposing humans to them. All rodenticides should be kept out of reach of children and pets and stored in appropriate containers with sufficient labeling. Unfortunately, some rodenticides are brightly colored and may be mistaken for food. In addition, tamper-resistant rodent traps should be used to prevent accidental rodenticide ingestion. Poisoned rodents should be placed in secure bins, and individuals disposing of these rodents should always use gloves to avoid contact with rodenticides.

Enhancing Healthcare Team Outcomes

Rodenticide toxicity requires an integrated approach by healthcare professionals to enhance patient-centered care, outcomes, safety, and team performance. Clinicians, advanced practitioners, pharmacists, and other healthcare providers must develop skills in promptly identifying the ingested rodenticide through detailed history-taking, physical examinations, and identifying packaging or other indicators. They should strategize effective management plans that focus on stabilizing the patient and administering specific antidotes or supportive care. Responsibilities include ordering and interpreting laboratory and diagnostic tests, which provide critical information for patient management.

Interprofessional communication is essential, involving consultation with poison control centers and toxicologists for guidance on diagnosis and treatment protocols. Care coordination ensures that each team member understands their role in the patient's care, from initial assessment and stabilization to ongoing monitoring and support. This collaborative approach improves patient safety by avoiding delays in treatment and ensuring that all aspects of the patient's condition are addressed comprehensively. By working together, healthcare teams can improve patient outcomes and enhance team performance in managing rodenticide toxicity.

Review Questions

• Access free multiple choice questions on this topic.
• Comment on this article.

References

1.

Wogalter MS, Jarrard SW, Simpson SN. Influencing of warning label signal words on perceived hazard level. Hum Factors. 1994 Sep;36(3):547-56. [PubMed: 7989055]

2.

Gummin DD, Mowry JB, Beuhler MC, Spyker DA, Rivers LJ, Feldman R, Brown K, Pham NPT, Bronstein AC, DesLauriers C. 2022 Annual Report of the National Poison Data System^® (NPDS) from America's Poison Centers^®: 40th Annual Report. Clin Toxicol (Phila). 2023 Oct;61(10):717-939. [PubMed: 38084513]

3.

Zavaliy LB, Petrikov SS, Simonova AY, Potskhveriya MM, Zaker F, Ostapenko YN, Ilyashenko KK, Dikaya TI, Shakhova OB, Evseev AK, Rezaee R, Goroncharovskaya IV. Diagnosis and treatment of persons with acute thallium poisoning. Toxicol Rep. 2021;8:277-281. [PMC free article: PMC7848287] [PubMed: 33552926]

4.

DeLey Cox VE, Hartog MA, Pueblo E, Racine M, Jennings L, Tressler J, Tuet WY, Stone S, Pierce SA, Thompson L, Dukes A, Hoard-Fruchey H, Wong B, McCranor BJ. Methylene blue and monosodium glutamate improve neurologic signs after fluoroacetate poisoning. Ann N Y Acad Sci. 2020 Nov;1479(1):196-209. [PMC free article: PMC7554062] [PubMed: 32285953]

5.

Wang R, Zhuo L, Wang Y, Ren L, Liu Q, Liu L. Lessons learned from poisoning cases caused by 2 illegal rodenticides: Tetramine and fluoroacetamide. Medicine (Baltimore). 2016 Oct;95(41):e5103. [PMC free article: PMC5072953] [PubMed: 27741126]

6.

Liu L, Li F, Dong Z, Dong G, Xu J, Liu W, Wang X, Hai X, Yu K. Plasma fluoroacetic acid concentrations: Symptoms, hematological, and biochemical characteristics in patients with fluoroacetic acid poisoning in the emergency department. Hum Exp Toxicol. 2020 May;39(5):634-641. [PubMed: 31957492]

7.

Tong HF, Chan CY, Ng SW, Mak TW. Strychnine poisoning due to traditional Chinese medicine: a case series. F1000Res. 2021;10:924. [PMC free article: PMC8817065] [PubMed: 35169461]

8.

Doğan E, Güzel A, Ciftçi T, Aycan I, Celik F, Cetin B, Kavak GÖ. Zinc phosphide poisoning. Case Rep Crit Care. 2014;2014:589712. [PMC free article: PMC4101206] [PubMed: 25101186]

9.

Ravikanth R, Sandeep S, Philip B. Acute Yellow Phosphorus Poisoning Causing Fulminant Hepatic Failure with Parenchymal Hemorrhages and Contained Duodenal Perforation. Indian J Crit Care Med. 2017 Apr;21(4):238-242. [PMC free article: PMC5416795] [PubMed: 28515612]

10.

Balali-Mood M, Naseri K, Tahergorabi Z, Khazdair MR, Sadeghi M. Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic. Front Pharmacol. 2021;12:643972. [PMC free article: PMC8078867] [PubMed: 33927623]

11.

Ghose A, Sayeed AA, Hossain A, Rahman R, Faiz A, Haque G. Mass barium carbonate poisoning with fatal outcome, lessons learned: a case series. Cases J. 2009 Dec 16;2:9327. [PMC free article: PMC2804721] [PubMed: 20066057]

12.

Lauková M, Velíšková J, Velíšek L, Shakarjian MP. Tetramethylenedisulfotetramine neurotoxicity: What have we learned in the past 70 years? Neurobiol Dis. 2020 Jan;133:104491. [PMC free article: PMC6895414] [PubMed: 31176716]

13.

Waseem M, Perry C, Bomann S, Pai M, Gernsheimer J. Cholinergic crisis after rodenticide poisoning. West J Emerg Med. 2010 Dec;11(5):524-7. [PMC free article: PMC3027455] [PubMed: 21293782]

14.

Thomas HM, Simpson D, Prescott LF. The toxic effects of alpha-chloralose. Hum Toxicol. 1988 May;7(3):285-7. [PubMed: 3391628]

15.

Sverkeli LJ, Hayat F, Migaud ME, Ziegler M. Enzymatic and Chemical Syntheses of Vacor Analogs of Nicotinamide Riboside, NMN and NAD. Biomolecules. 2021 Jul 16;11(7) [PMC free article: PMC8301822] [PubMed: 34356669]

16.

LeWitt PA. The neurotoxicity of the rat poison vacor. A clinical study of 12 cases. N Engl J Med. 1980 Jan 10;302(2):73-7. [PubMed: 6243167]

17.

Koul PA, Ahmad SH, Ahmad F, Jan RA, Shah SU, Khan UH. Vitamin d toxicity in adults: a case series from an area with endemic hypovitaminosis d. Oman Med J. 2011 May;26(3):201-4. [PMC free article: PMC3191699] [PubMed: 22043417]

18.

Janoušek J, Pilařová V, Macáková K, Nomura A, Veiga-Matos J, Silva DDD, Remião F, Saso L, Malá-Ládová K, Malý J, Nováková L, Mladěnka P. Vitamin D: sources, physiological role, biokinetics, deficiency, therapeutic use, toxicity, and overview of analytical methods for detection of vitamin D and its metabolites. Crit Rev Clin Lab Sci. 2022 Dec;59(8):517-554. [PubMed: 35575431]

19.

Park J. Can we more efficiently save patients with vitamin K-dependent coagulopathy caused by superwarfarin intoxication? Korean J Intern Med. 2014 Jul;29(4):430-3. [PMC free article: PMC4101588] [PubMed: 25045289]

20.

Saponara S, Fusi F, Spiga O, Trezza A, Hopkins B, Brimble MA, Rennison D, Bova S. The Selective Rat Toxicant Norbormide Blocks K_ATP Channels in Smooth Muscle Cells But Not in Insulin-Secreting Cells. Front Pharmacol. 2019;10:598. [PMC free article: PMC6540933] [PubMed: 31191321]

21.

Coppock R. Advisory: Bromethalin rodenticide - No known antidote. Can Vet J. 2013 Jun;54(6):557-8. [PMC free article: PMC3659449] [PubMed: 24155445]

22.

Manganyi MC, Tlatsana GS, Mokoroane GT, Senna KP, Mohaswa JF, Ntsayagae K, Fri J, Ateba CN. Bulbous Plants Drimia: "A Thin Line between Poisonous and Healing Compounds" with Biological Activities. Pharmaceutics. 2021 Sep 01;13(9) [PMC free article: PMC8465487] [PubMed: 34575461]

23.

Tuncok Y, Kozan O, Cavdar C, Guven H, Fowler J. Urginea maritima (squill) toxicity. J Toxicol Clin Toxicol. 1995;33(1):83-6. [PubMed: 7837318]

24.

Curcić M, Dadasović J. [Suicide and attempted suicide with rodenticides from 1968 to 2000]. Med Pregl. 2001 May-Jun;54(5-6):256-60. [PubMed: 11759222]

25.

Babcock J, Hartman K, Pedersen A, Murphy M, Alving B. Rodenticide-induced coagulopathy in a young child. A case of Munchausen syndrome by proxy. Am J Pediatr Hematol Oncol. 1993 Feb;15(1):126-30. [PubMed: 8447555]

26.

Jimenez O, Cáceres H, Gimenez L, Soto L, Montenegro M, Rueda JAA. Thallium poisoning: a case report. J Yeungnam Med Sci. 2023 Jul;40(3):311-314. [PMC free article: PMC10390273] [PubMed: 36537175]

27.

Hardin J, Galust H, Bensel A, Bierly S, Seltzer J, Friedman N, Clark RF, Campbell C. Taking the bait: Strychnine poisoning. Am J Emerg Med. 2023 Dec;74:197.e5-197.e7. [PubMed: 37805370]

28.

Eizadi-Mood N, Momenzadeh M, Sadeghi M, Yaraghi A, Sabzghabaee AM, Alfred S. Toxicoepidemiology of Phosphide Poisoning in the Central Part of Iran. J Res Pharm Pract. 2023 Jan-Mar;12(1):21-28. [PMC free article: PMC10779690] [PubMed: 38213604]

29.

Gopalakrishnan S, Kandasamy S, Iyyadurai R. Rodenticide Poisoning: Critical Appraisal of Patients at a Tertiary Care Center. Indian J Crit Care Med. 2020 May;24(5):295-298. [PMC free article: PMC7358862] [PubMed: 32728318]

30.

Kumar A, Gangadharan H, Manju R, Prakash A, Arasan SS, Kumar S. A rare complication of Yellow Phosphorous poisoning. Trop Doct. 2022 Apr;52(2):346-348. [PubMed: 35098796]

31.

Zheng J, Zhang K, Liu Y, Wang Y. Fatal acute arsenic poisoning by external use of realgar: Case report and 30 years literature retrospective study in China. Forensic Sci Int. 2019 Jul;300:e24-e30. [PubMed: 31023496]

32.

Hardin J, Seltzer J, Suhandynata R, Spiegel B, Silver R, Thomas D, Galust H, Friedman N, Clark R, Momper J. Severe arsenic poisoning due to Ayurvedic supplements. Clin Case Rep. 2023 Jul;11(7):e7733. [PMC free article: PMC10363841] [PubMed: 37492071]

33.

Jamshidi N, Dhaliwal N, Hearn D, McCalman C, Wenzel R, Koutsogiannis Z, Roberts DM. Life-threatening barium carbonate poisoning managed with intravenous potassium, continuous veno-venous haemodialysis and endoscopic removal of retained ceramic glazes. Clin Toxicol (Phila). 2022 Aug;60(8):974-978. [PubMed: 35506754]

34.

Lenski M, Letrillart A, Gish A, Nisse P, Gaulier JM, Allorge D. Aldicarb-related suicide attempt cases in North of France (2012-2021). Toxicol Res (Camb). 2022 Jun;11(3):529-536. [PMC free article: PMC9244977] [PubMed: 35782643]

35.

Kumar S, Baggi TR, Zughaibi T. Forensic toxicological and analytical aspects of carbamate poisoning - A review. J Forensic Leg Med. 2022 Nov;92:102450. [PubMed: 36399917]

36.

Bergrath S, Castillo-Vargas JS, Koc NJ, Haake H, Graeven U. Suspected seizure-survival of a lethal dose of the rodenticide alpha-chloralose. Anaesthesist. 2019 Dec;68(12):843-847. [PubMed: 31701172]

37.

Roszkowski AP. The pharmacological properties of norbormide, a selective rat toxicant. J Pharmacol Exp Ther. 1965 Aug;149(2):288-99. [PubMed: 4953462]

38.

Pasquale-Styles MA, Sochaski MA, Dorman DC, Krell WS, Shah AK, Schmidt CJ. Fatal bromethalin poisoning. J Forensic Sci. 2006 Sep;51(5):1154-7. [PubMed: 17018099]

39.

Greene R, Meatherall R. Dermal exposure to strychnine. J Anal Toxicol. 2001 Jul-Aug;25(5):344-7. [PubMed: 11499889]

40.

Mumford JL, Wu K, Xia Y, Kwok R, Yang Z, Foster J, Sanders WE. Chronic arsenic exposure and cardiac repolarization abnormalities with QT interval prolongation in a population-based study. Environ Health Perspect. 2007 May;115(5):690-4. [PMC free article: PMC1867981] [PubMed: 17520054]

41.

Kuivenhoven M, Mason K. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jun 12, 2023. Arsenic Toxicity. [PubMed: 31082169]

42.

Wallbridge T, James S, Lee R, Khan A, Bradberry S, Elamin MEMO. Successful treatment of potentially lethal dose thallium sulfate poisoning with sequential use of Prussian blue and multiple-dose activated charcoal. Clin Toxicol (Phila). 2023 Mar;61(3):200-201. [PubMed: 36794304]

43.

Wang TT, Wen B, Yu XN, Ji ZG, Sun YY, Li Y, Zhu SL, Cao YL, Wang M, Jian XD, Wang T. Early diagnosis, treatment, and outcomes of five patients with acute thallium poisoning. World J Clin Cases. 2021 Jul 06;9(19):5082-5091. [PMC free article: PMC8283604] [PubMed: 34307559]

44.

Otter J, D'Orazio JL. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 7, 2023. Strychnine Toxicity. [PubMed: 29083795]

Disclosure: Bobbisue Isackson declares no relevant financial relationships with ineligible companies.

Disclosure: Lisandro Irizarry declares no relevant financial relationships with ineligible companies.