|Year : 2019 | Volume
| Issue : 4 | Page : 129-133
Rodenticide poisoning: Literature review and management
Kundavaram Paul Prabhakar Abhilash, Jonathan Arul Jeevan Jayakaran
Department of Emergency Medicine, Christian Medical College, Vellore, Tamil Nadu, India
|Date of Submission||28-Oct-2019|
|Date of Decision||13-Nov-2019|
|Date of Acceptance||25-Nov-2019|
|Date of Web Publication||12-Dec-2019|
Dr. Jonathan Arul Jeevan Jayakaran
Department of Emergency Medicine, Christian Medical College, Vellore - 632 004, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Rodenticide is a broad term, and there are a wide variety of such compounds depending on the geographical region and availability. These compounds differ in their chemical composition, mechanism of action, toxic doses, and lethal effects. Coumarins, aluminum phosphide, zinc phosphide, and yellow phosphorous are the most easily available and commonly used rodenticides for deliberate self-harm. Aluminum phosphide poisoning is rapidly fatal, whereas yellow phosphorous poisoning too is associated with a high mortality within 1–2 weeks of consumption.
Keywords: Coumarins, poisoning, rat killer, rodenticides, yellow phosphorous
|How to cite this article:|
Abhilash KP, Jayakaran JA. Rodenticide poisoning: Literature review and management. Curr Med Issues 2019;17:129-33
| Introduction|| |
Deliberate self-harm (DSH) is a problem that is increasing in prevalence with time. Since the ancient times to the postmodern era, people have deliberately tried and at many instances succeeded in taking their own life. The population is varied and not restricted to any socioeconomic class of people. Various methods of DSH are used across the world with rodenticides being one of the most common methods used in the Indian subcontinent.
“Rodenticide” is the name given to a group of pesticides that are used to kill rats. These are easily available and are very common in the society, largely due to the ease of access and availability. Although rodenticides are a common tool of DSH, this group of compounds has been greatly underreported as well as understudied. In a study done in Karnataka in South India, the incidence of rodenticide poisoning among all cases of acute poisonings was found to be 7.9%.
Rodenticide is a broad term, and there are a wide variety of such compounds depending on the geographical region and availability. These compounds differ in their chemical composition, mechanism of action, toxic doses, and lethal effects. As a result, the toxidrome produced by one rodenticide is largely different from that produced by another rodenticide. In addition, there is also a vast difference in the immediate and long-term outcomes based on the type of rodenticide consumed.
| Epidemiology|| |
In 2011, 12,886 cases of exposure to rodenticides were documented in the National Poison Data System of the American Association of Poison Control Centers.
The term “rodenticide” is a broad term that includes a wide variety of compounds. These vary depending on the geographical regions as well as the knowledge and availability of compounds in the various populations. The common compounds vary from powerful anticoagulants to phosphorus-based compounds, whereas rarer compounds such as hypercalcemia-inducing agents have also been reported. In a study done in the United States, Eisemann and Petersen had reported that there was a serial rise in the reported cases of rodenticide poisoning from 8705 in 1986 to as high as 20,300 in 1998, but the rate of poisoning still remained at 8 for every 100,000 individuals.
It was also noted that anticoagulants contributed to around 82%–89% of all rodenticide poisonings. Of these anticoagulants, second-generation anticoagulants, such as brodifacoum, contributed 83%–91% of all anticoagulant poisonings. With respect to other rodenticides, there were about 150 cases every year of poisoning due to zinc phosphide and strychnine.
There are no definite data from Europe describing the prevalence of the various rodenticide poisonings. Nevertheless, most studies with regard to rodenticides have been on anticoagulants. Berny et al. had studied the prevalence of anticoagulant rodenticide poisoning in France. Of the total number of poisonings, 8.96% were due to anticoagulant rodenticides, predominantly of the second generation rodenticides. The mortality rate was found to be 0.6%, mainly due to severe bleeding.
In the Far East, again the most common rodenticide used for self-poisoning is anticoagulants. Yu etal. reported a series of rodenticide poisonings in Taiwan. Of the twenty cases reported, 12 were due to bromadiolone and eight due to brodifacoum (both second-generation anticoagulants).
Poisoning due to hypercalcemia-inducing agents, such as cholecalciferol, has only been documented among animals and has not been reported as a mode of DSH.,
The western literature with regard to other rodenticides such as metal phosphides and phosphorus-based compounds is scarce except for the isolated case reports.,
There have also been case reports of strychnine poisoning, but no case series or studies have been published with regard to the same., There have also been isolated 28 reports of rarer rodenticide compounds like Tetramine which is an extremely lethal compound and has been banned worldwide but still available in parts of China.
The scenario India is quite different, as the most commonly reported rodenticide used for self-harm is predominantly of the metal phosphide and phosphorus group of compounds. It has also been seen that even within India, the rodenticides used for self-poisoning in the northern part of India vary from that used in the southern region.
In the northern states in India, the most commonly seen rodenticide poison used for self-harm is metal phosphides, of which aluminum phosphide is most prevalent. Based on a study conducted by Sharma et al., where they had observed the trends of poisoning in the northern states of Jammu and Kashmir and Chandigarh, it was found that between 1994 and 2000, 181 cases (54.35%) of metal phosphide consumption were reported, of which aluminum phosphide was the most common. The mortality in these cases was also significantly high. In another study from the All India Institute of Medical Sciences in New Delhi, aluminum phosphide was the most common rodenticide poisoning reported. Zaheer et al. had profiled cases of poisoning in a tertiary care hospital in North India and found that aluminum phosphide was most common (30.8%), followed by zinc phosphide (23.1%).
In South India, rat poisons did contribute to a significant proportion of all poisonings. In a study done in a tertiary care center in South India, it was found that rodenticides contributed to 11.33% of all cases of poisoning, but mortality among those cases was 33.3%. Yellow phosphorus is a rodenticide which is commonly seen in South India. It is highly toxic and lethal as it causes severe hepatic and renal dysfunction. In a study done in Salem, Tamil Nadu, 21 cases of poisoning due to yellow phosphorus were reported between 2010 and 2011. There have also been several isolated case reports of yellow phosphorus poisonings that have been reported, with most of these cases coming from South India. Suneetha et al. had retrospectively reported 56 cases of rodenticide poisonings at a tertiary care hospital in Mysore over a 1-year period from May 2014 to May 2015. Most of the cases were between the ages of 11 and 30, and that the incidence of these poisonings decreased with age. Zinc phosphide was the most common poison (18 cases, 32.14%). This was followed by 12 cases of aluminum phosphide (21.4%) and eight cases of yellow phosphorus (14.2%). The poison could not be identified in 16 patients (28.6%). This study had also reported significant mortality with aluminum phosphide (41.6%), followed by zinc phosphide (16.6%). Although no deaths were reported in cases who consumed yellow phosphorus, these patients were seen to have liver dysfunction (37.5%). Only two cases of poisoning due to bromadiolone were reported in the study. A study done at our center in Vellore, Tamil Nadu in 2014 showed that rodenticides comprised 4.4% of the modes of DSH.
It is therefore seen that rodenticide poisonings largely depend on the geographical region due the availability of certain compounds in certain regions and the understanding of the people in those regions.
| Classification of Rodenticides|| |
Rodenticides are a broad group of poisons with very different mechanisms of action, toxicity, and lethality. To get a comprehensive idea of the rodenticides, it is best to study each poison separately analyzing various mechanisms of action, organ involvement, toxicity, and lethal effects.
The toxic and lethal effects of rodenticide poisoning in humans are mainly by consumption of a large quantity in a single dose. This same potential of the poison that can kill a rat, when consumed by humans, has similar effects as well. If not lethal, they at the least have the potential to manifest their toxicity on various vital organs of the body. Since rodenticides have different mechanisms of action, a useful way of classifying these compounds is based on their toxicity profile.
They can be classified as:
Highly toxic rodenticides
The compounds that belong to this group are those with a single-dose LD50 lower than 50 mg/kg of body weight. Compounds included in this group are zinc phosphide, aluminum phosphide, yellow phosphorus, thallium, strychnine, arsenic, and sodium monofluoroacetate.
Moderately toxic rodenticides
The moderately toxic rodenticides were those compounds with a single-dose LD-50 between 50 and 500 mg/kg of the body weight. Compounds such as alpha-naphthylthiourea belong to this group. These compounds are not very commonly used in practice.
Low toxicity rodenticides
These are compounds with an LD50 ranging from 500 to 5000 mg/kg of the body weight. These include compounds such as norbormide, red squill, and anticoagulant type of rodenticides. These are commonly seen available in local markets.
There are also several other poisons which have been reported to have rodenticide property but are extremely rare in the community in this day and age. Compounds such as barium carbonate, bromethalin, chloralose, crimidine, endrin (organochlorine cyclodiene), fluoroacetamide, phosacetim, white phosphorus, pyrinuron, scilliroside, tetramethylenedisulfotetramine (tetramine), and Uragan D2., The following are the most common rodenticides seen in India with a brief description of clinical features and management.
| Anticoagulants (Warfarin and Related Compounds, Coumarins, and Indandiones)|| |
These compounds depress the hepatic synthesis of Vitamin K-dependent blood-clotting factors (II [prothrombin] and VII, IX, and X) that result in mucosal or internal bleeding.
The second-generation compounds, also called “super coumarins,” have a longer half-life and hence may require monitoring of the prothrombin time (PT) with international normalized ratio (INR) for many days. Some agents such as brodifacoum may not show an elevation of PT with INR until 48 h after ingestion.
- Prolonged INR with no bleeding:Administer injection. Vitamin K1 10 mg intravenous (IV) od or syrup Vitamin K1 10–50 mg orally, 2–4 times/day till INR normalizes. However, patients ingesting large doses of second-generation coumarins may require higher doses (100–400 mg oral) of Vitamin K1 and a longer duration of treatment (weeks to months)
- Prolonged INR with significant bleeding manifestations: injection Vitamin K1 and fresh frozen plasma as required.
| Phosphorous Compounds|| |
Aluminum and zinc phosphides
- Aluminum and zinc phosphides are highly effective insecticides and rodenticides and are easily available in the market
- They are commonly found in powder, pellet, or tablet forms
- Acute poisoning with these compounds may result from direct ingestion of the salts or indirectly from accidental inhalation of phosphine generated during their approved use.
- Both forms of poisoning are mediated by phosphine which has been thought to be toxic because it inhibits cytochrome c oxidase
- Mortality often occurs rapidly within the 1st day of severe metallic aluminum phosphide poisoning. Death typically results from cardiac arrhythmias or refractory shock and cardiac failure.,,
There is usually only a very short interval between the ingestion of phosphides and the appearance of systemic toxicity in case of aluminum phosphide toxicity, whereas there is a latent period of a few days in zinc phosphide toxicity. The following are the various organ system involvements due to consumption of these compounds:
- Cardiac: impaired myocardial contractility leading to circulatory collapse and shock
- Pulmonary: pulmonary edema, either cardiac or noncardiac
- Hepatic: hepatic necrosis and fulminant hepatic failure
- Hematological: disseminated intravascular coagulation
- Metabolic: severe metabolic acidosis.,,
- General supportive measures (IV fluids, inotropes, ventilation, and hemodialysis) are all that can be offered and many patients die despite intensive care
- Correct electrolyte abnormalities, especially hypomagnesemia as this may contribute to mortality
- N acetylcysteine (NAC) has been proposed as an antidote and may be given if the patient presents early (<12 h). The dose is as follows:
- 150 mg/kg in 200 ml of 5% dextrose over 15 min then
- 50 mg/kg in 500 ml of 5% dextrose over 4 h then
- 100 mg/kg in 1 L 5% dextrose over 16 h.
| Yellow Phosphorous|| |
Elemental phosphorous exists in two forms: red and white (yellow).
- The red form is used in matchstick production, is not absorbed, and has minimal toxicity
- Compounds of yellow phosphorus are commonly used as everyday rodenticides, fertilizers, and in firecrackers and are easily available in Tamil Nadu.
Phosphorous is readily absorbed through the gastrointestinal (GI) tract; leading to elevated levels of phosphorus in the kidney and liver within hours. It is commonly manufactured as RATOL: rat killer.
- Yellow phosphorous causes cardiac, hepatic, renal, and multiorgan failure similar to zinc phosphide and aluminum phosphide poisoning
- However, patients with yellow phosphorus intoxication pass through three stages:
- First stage: 24 h. Patient is either asymptomatic or has signs and symptoms of local GI irritation
- Second stage: 24–72 h. An asymptomatic period
- Third stage: >72 h. Features of cardiac, hepatic, renal, and multiorgan failure eventually resulting in death.
- Supportive measures are all that can be offered, and many patients die despite intensive care
- NAC may be given as an antidote if the patient presents early (<12 h)
- Liver transplantation, if possible, may be the only lifesaving option.
| Other Rare Rodenticides|| |
In addition to the rodenticides that are discussed above, there are other rodenticide compounds which are also used for self-harm and suicide but in a much rarer frequency. In this section, we will look at a few of those compounds in brief.
Thallium is a tasteless and odorless compound. It is a toxic compound that can be absorbed through the skin and can be extremely lethal. At present, no effective antidote against thallium. The other symptoms that manifest at lesser doses include loss of hair, nausea, vomiting, paresthesias, and abdominal pain. In certain cases, they can also have pulmonary edema or bronchopneumonia.,
Strychnine is a compound that affects the central nervous system. It causes recurrent episodes of painful motor seizures. It is absorbed at a very fast rate from the GI tract and other mucous membrane, but not through the skin. In addition to constitutional symptoms such as nausea and vomiting, these patients have also been reported to have blurring of vision and diaphoresis. Classically, these patients develop symmetrical spasms of the extensor muscles, and the consciousness of the patient is preserved during these episodes.,,,,,
A few case reports suggest that treatment with intravenous benzodiazepines (like diazepam) in a darkroom has shown improvement of the spasmic movements. In the event that these patients do not respond, the next line of management involves intubation, paralysis, and ventilation.
It is a white-colored compound which does not have any smell or taste, and it resembles cooking soda. The route of poisoning is oral consumption. It can also be inhaled or absorbed through breach in the skin as a result of open wounds.
The initial poisonous effects seen in human beings are an increased sense of apprehension and nausea. This can be followed by arrhythmias, convulsions, or coma. Death in these cases is due to ventricular arrhythmias such as tachycardia and fibrillations or a respiratory failure as a result of pneumonia or pulmonary edema.
| Conclusion|| |
In India, coumarins, aluminum phosphide, zinc phosphide, and yellow phosphorous are the most easily available and commonly used rodenticides for DSH. Each compound is different in its mechanism of action and clinical effects. Identifying the compound is of prime importance as it enables targeted treatment, resulting in better outcomes.
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| References|| |
Ramesha KN, Rao KB, Kumar GS. Pattern and outcome of acute poisoning cases in a tertiary care hospital in Karnataka, India. Indian J Crit Care Med 2009;13:152-5.
] [Full text]
Kishore PV, Palaian S, Prabhu M, Mishra P. Consumption of rodenticides by humans J Inst Med 2007;29:50-2.
Eisemann JD, Petersen BE. Human Poisonings and Rodenticides: Evaluation of Incidents Reported to the American Association of Poison Control Centers. USDA National Wildlife Research Center - Staff Publications. 2002. p. 481.
Berny P, Velardo J, Pulce C, D'amico A, Kammerer M, Lasseur R. Prevalence of anticoagulant rodenticide poisoning in humans and animals in France and substances involved. Clin Toxicol (Phila) 2010;48:935-41.
Yu HY, Lin JL, Fu JF, Lin JH, Liu SH, Weng CH, et al
. Outcomes of patients with rodenticide poisoning at a far east poison center. Springerplus 2013;2:505.
Moore FM, Kudisch M, Richter K, Faggella A. Hypercalcemia associated with rodenticide poisoning in three cats. J Am Vet Med Assoc 1988;193:1099-100.
Eason C, Wickstrom M, Henderson R, Milne L, Arthur D. Non-target and secondary poisoning risks associated with cholecalciferol. New Zealand Plant Protection Soc 2000;53:299-304.
Winek CL, Collom WD, Fusia EP. Yellow phosphorus ingestion--three fatal poisonings. Clin Toxicol 1973;6:541-5.
Simon FA, Pickering LK. Acute yellow phosphorus poisoning. Smoking stool syndrome. JAMA 1976;235:1343-4.
Perper JA. Fatal strychnine poisoning – A case report and review of the literature. J Forensic Sci 1985;30:1248-55.
Lindsey T, O'Hara J, Irvine R, Kerrigan S. Strychnine overdose following ingestion of gopher bait. J Anal Toxicol 2004;28:135-7.
Poon WT, Chan K, Lo MH, Yip KK, Lee T, Chan AY. A case of tetramine poisoning: A lethal rodenticide. Hong Kong Med J 2005;11:507-9.
Sharma BR, Harish D, Sharma V, Vij K. Poisoning in Northern India: Changing trends, causes and prevention thereof. Med Sci Law 2002;42:251-7.
Srivastava A, Peshin SS, Kaleekal T, Gupta SK. An epidemiological study of poisoning cases reported to the National Poisons Information Centre, All India Institute of Medical Sciences, New Delhi. Hum Exp Toxicol 2005;24:279-85.
Zaheer MS, Khan SA, Aslam M, Gupta V. Profile of poisoning cases at a North Indian tertiary care hospital. Health Popul Perspect Issues 2009;32:176-83.
Maharani B, Vijayakumar N. Profile of poisoning cases in a tertiary care hospital, Tamil Nadu, India. J Applied Pharma Sci 2013;3:91-4.
Balasubramanian K, Sethuraman VK, Balamurugesan K, Viswanathan S. A retrospective study of clinical profile and outcome of patients with rodenticide poisoning in a tertiary care hospital. Int J Adv Med 2019;6. [doi: 10.18203/2349-3933.ijam20190993].
Suneetha DK, Inbanathan J, Kannoth S, Reshma PK, Shashank MS. Profile of rat killer poisoning cases in a tertiary care hospital at Mysore. Int J Sci Stud 2016;3:264-7.
Jegaraj MK, Mitra S, Kumar S, Selva B, Pushparaj M, Yadav B, et al
. Profile of deliberate self-harm patients presenting to emergency department: A retrospective study. J Family Med Prim Care 2016;5:73-6.
] [Full text]
Proudfoot AT. Aluminium and zinc phosphide poisoning. Clin Toxicol (Phila) 2009;47:89-100.
Gupta S, Ahlawat SK. Aluminum phosphide poisoning – A review. J Toxicol Clin Toxicol 1995;33:19-24.
Stephenson JB. Zinc phosphide poisoning. Arch Environ Health Int J 1967;15:83-8.
Bhat S, Kenchetty KP. N-acetyl cysteine in the management of rodenticide consumption-life saving? J Clin Diagn Res 2015;9:OC10-3.
Cvjetko P, Cvjetko I, Pavlica M. Thallium toxicity in humans. Arh Hig Rada Toksikol 2010;61:111-9.
Jackson G, Ng SH, Diggle GE, Bourke IG. Strychnine poisoning treated successfully with diazepam. Br Med J 1971;3:519-20.
Herishanu Y, Landau H. Diazepam in the treatment of strychnine poisoning. Case report. Br J Anaesth 1972;44:747-8.
Teitelbaum DT, Ott JE. Acute strychnine intoxication. Clin Toxicol 1970;3:267-73.
Dasari S, Naha K. A rare case of strychnine poisoning by consumption of Strychnos nux-vomica
leaves. Asian Pac J Trop Biomed 2011;1:S303-4.
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