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Information About Rodenticides

Rodenticides, also known as "rat poisons," are mixtures used to get rid of rats. They are among the most dangerous substances frequently discovered in homes. Although historically heavy metals like arsenic were the first substances used to manage rat populations, anticoagulants are now the most widely used rodenticide. Every attempt should be made to identify the product when a clinician suspects rodenticide poisoning, including package information (such as brand name, chemical name, signal phrase, presence of skull or skulls on the label) and details (such as odor, look, and color). Depending on the type of rodenticide consumed, the clinical appearance differs.

Here is a quick summary of the pathophysiology and signs of common rodenticides:

 

Thallium

Thallium is a tasteless, odorless powder that can be inhaled or absorbed via the skin. The Krebs cycle and oxidative phosphorylation are disrupted, which reduces energy production. It displaces potassium in sodium-potassium-adenosine triphosphatase and the sulfhydryl or thiol group of mitochondrial membranes. Please refer to the Statpearls article on thallium poisoning for further details. [3]

·        Direct Exposure

 

·        Gastroenteritis acute (within 48 hours)

 

·        Seizures, peripheral neuropathy, and malfunction of the cranial nerves

 

·        Alopecia that spares the axilla and inner third of the brows

 

·        Hyperpigmentation

 

·        Constant Exposure

 

·        Ataxia, distal motor weakness, and tremor

 

·        Nystagmus with diplopia

 

·        Palsy of Cranial Nerve 7

 

·        Opacity of the eye lenses

Fluoroacetamide (Compound 1080), Sodium Monofluoroacetate (SMFA) 

Sodium monofluoroacetate (SMFA), sometimes known as fluoroacetamide (Compound 1080), is a tasteless and odorless white powder. To protect livestock from other species, SMFA-infused collars are utilized in the US. Coenzyme A (CoA) is changed into fluoroacetate CoA by fluoroacetamide and SMFA, which imitate acetate and irreversibly disrupt the Krebs cycle by causing citrate to build up. Together, they form a complex. [4] This inhibits cellular aerobic metabolism, fatty acid oxidation, gluconeogenesis, and the urea cycle.

From 30 to 20 hours after onset of symptoms:

 

·        Seizures

 

·        Hypocalcaemia

 

·        An aggravation of metabolic acidosis

 

·        Dysrhythmias

 

·        Shock that is resistant to resuscitation

 

·        Subsequent Complications

 

·        Kidney damage

 

·        Liver dysfunction

 

·        Atrophy of the brain or cerebellum

Strychnine

This substance is a powder that has no smell or color and turns bitter when dissolved in water. Pink tablets are frequently encountered. Due to competing inhibition of glycine receptors at the postsynaptic and motor neuron levels, strychnine poisoning manifests as uncontrollable muscular contraction. Please refer to the Statpearls article on strychnine poisoning for further details. [5]

10 to 20 minutes after the onset of symptoms :

·        Uncontrollable muscle spasms

 

·        Trismus

 

·        Sardonicus Risus

 

·        Opisthotonos

 

·        Rhabdomyolysis

 

·        Lactic acidemia

 

·        Hyperthermia

Zinc and Aluminum Phosphide

This substance releases phosphine gas, which has a rotting fish-like odor when it comes into contact with water. Iran and northern India have higher rates of poisoning. Although the toxin can potentially spread through inhalation and skin absorption, when it is consumed, gastric acid changes the substance into phosphine gas, which is then absorbed into the bloodstream from the gastrointestinal system. The toxin inhibits the cytochrome C oxidase system. [6]

 The 30-minute onset of symptoms :

·        acute gastritis

 

·        Cardiac irregularities

 

·        Pulmonary hemorrhage and edema

 

·        Breathing difficulties

 

·        Methemoglobinemia with intravascular hemolysis

 

·        Hepatotoxicity

 

·        Acidosis metabolic

 

·        respiratory alkalosis

 

·        Kidney failure

Elemental Phosphorus

When exposed to oxygen, this element may shine and have a subtle garlic smell. Red and white (yellow) phosphorus are the two colors that it can take. For matches, the former is used. In rodenticides, the latter is utilized. White phosphorus is extremely harmful and can harm both the local and global environment. When consumed, it directly damages tissue by producing phosphoric acid and phosphorus pentoxide in the area. Phosphorous also binds to calcium in the blood, causing severe hypocalcemia. [7]

• Acute Gastroenteritis

 

·        Burns to the skin or mucosa

 

·        Emesis or feces that are fluorescent (smoking stool)

 

·        Dysrhythmias

 

·        Hepatotoxicity

 

·        Kidney failure

Arsenic

The precise mechanism of action of the poisonous inorganic chemical arsenic is uncertain. Postulations include the inhibition of pyruvate dehydrogenase in the Krebs cycle, which results in decreased cell respiration and ATP depletion, and the production of sulfhydryl compounds, which results in significant vasodilation. The patient's breath may have a garlic smell if there has been sufficient consumption. Please refer to the StatPearls article on arsenic toxicity for further details. [8]

1 to 3 hours after symptoms start

·        nausea

 

·        Diarrhea with blood

 

·        A garlicky aftertaste

 

·        Hypotension

 

·        Excessive QT section

 

·        Delirium, convulsions, and coma

 

·        Renal harm

Barium Carbonate

Unlike its insoluble sibling, barium sulfate, which is used as a radiographic contrast medium, this chemical readily dissolves in water and is extremely poisonous. Hypokalemia is caused by the barium ion's inhibition of potassium transport out of cells. [9]

Symptoms:

·        Gastroenteritis

 

·        Hypertension

 

·        Cardiac irregularities

 

·        Breathing difficulties

 

·        Muscle atrophy

Tetramethylene Disulfotetramine (TETS, Tetramine)

This rodenticide, which is Chinese in origin, kills mice by permanently blocking the GABA receptor. [10]

·        Convulsions may begin 10 minutes to 13 hours after the first symptom.

 

·        Coma

 

·        Breathing difficulties

 

·        Arrhythmias

Aldicarb

This substance, which has Latin American roots, is also known as "tres pasitos," after the three little mouse movements required before the poison results in virtually immediate death. It produces a cholinergic toxidrome by acting as a strong cholinesterase inhibitor. [11]

Symptoms:

·        Excessive slobbering

 

·        Lacrimation

 

·        Urination

 

·        Diarrhoea

 

·        Digestive distress

 

·        Emetic

Alpha-chloralose:

This substance, which is European in origin, is utilized as a rodenticide as well as a veterinary anesthetic. Although the exact mechanism of action is unclear, it is similar to barbiturates in that it depresses the central nervous system. [12]

Symptoms:

·        Convulsions

 

·        Hypothermia

 

·        breathing depression

Pyriminil, Pyriminil, N-3-pyridylmethyl-N-p-nitrophenyl Urea, PNU

Pyriminil functions as a nicotinamide antagonist and hinders the production of NAD and NADH, which causes pancreatic beta cells to be abruptly destroyed within two hours. [13]

Symptoms:

·        breathing of Kussmaul

 

·        Hypotension

 

·        Encephalopathy

 

·        Lethargy

Cholecalciferol (Vitamin D3)

Cholecalciferol can induce serious symptoms through a hypercalcemic state, even though it requires a big amount to be poisonous. Hypercalcemia is ultimately brought on by vitamin D3's ability to mobilize calcium from the bones and increase intestinal calcium absorption. [14]

Symptoms:

·        Polyuria

 

·        Polydipsia

 

·        Vomiting

 

·        Kidney failure

 

·        Encephalopathy

Anticoagulants (Superwarfarin, Warfarin)

The anticoagulant rodenticides known as superwarfarins (brodifacoum, difenacoum, bromadiolone, and chlorophacinone) are chemically related to warfarin but lack the terminal methyl group. Superwarfarin is 100 times more potent than warfarin thanks to this group substitution. [15] Warfarin affects the clotting cascade components 2, 7, and 9 because it is a competitive inhibitor of the vitamin K epoxide reductase complex 2 (VKORC1). Please refer to the StatPearls article on warfarin toxicity for further details. [16]

Hematuria is one of the signs (earliest symptom):

 

·        Haemoptysis

 

·        Epistaxis

 

·        Backache

 

·        Quick bruising

 

·        Intracranial bleeding

Norbormide

•        This rat poison is essentially non-toxic to humans and works through extreme peripheral vasoconstriction that causes ischemia leading to organ death followed by animal expiration.

•        Symptoms may include a drop in blood pressure and/or temperature. [17]

 

Bromethalin

• Because it takes a large amount of intake to have a hazardous impact on people, it is rarely poisonous to them. Reduced ATP is the result of oxidative phosphorylation being decoupled by bromethalin. Because a lack of ATP results in an increase in fluid around neuron sheaths, it has a neurotoxic effect on both the central and peripheral nervous systems. [18]

• Delirium and altered mental status are possible symptoms that may appear within 4 hours to 7 days and are brought on by significant cerebral edema. based on a single report of a human case.

Red Squill (Urginea maritima)

Scillaren A and B, a glycoside, has convulsant and cardiotoxic effects. [20]

Symptoms:

·        Stomach ache

 

·        Vomiting

 

·        Seizures

 

·        Hyperkalaemia

 

·        Cardiac irregularities (resembles digitalis toxicity)

DIAGNOSIS

Classifying rodenticides according to their toxicity

Highly toxic: Median lethal dose (LD 50) ranging from 0 to 50 mg/kg body weight

 Moderately toxic: LD 50 ranging from 50 to 500 mg/kg

 Less toxic: LD 50 ≥ 500 mg/kg

The clinician may request the following tests if they suspect unidentified ingestion. Although non-specific, rodenticides are notable for related anomalies.

Hypoglycemia

·        •Zinc or aluminum phosphide

Hyperglycemia

·        Pyrimini

 Full Blood Count

·        Zinc phosphide for anemia

Fundamental Metabolic Panel

Hypocalcemia

·        White phosphorous, SMFA, and fluoroacetamide

Hypokalemia

·        Barium carbonate, zinc, or aluminum phosphide

Elevated blood urea nitrogen (BUN) or creatinine

·        Aluminium phosphide, thallium, arsenic, white phosphorous, zinc

Serum Phosphorous

·        •White phosphorous in serum: hyperphosphatemia

Panel for Hepatic Function

·        Thallium, arsenic, white phosphorous, zinc, or aluminum phosphide can all cause elevated liver enzymes.

 

 A coagulation profile with values for the prothrombin time, the international normalized ratio, and the partial thromboplastin time (PT, INR, PTT)

·        Anticoagulants

The enzyme creatinine phosphokinase (CPK)

·        Strychnine

 Blood gas analysis

·        Fluoroacetamide or SMFA for lactic acidosis

Troponin

·        Cardiotoxicity from aluminum phosphide and zinc

 Lipase

·        pyriminil, at an elevated level

Electrocardiography with 12 Leads (ECG)

·        QTc Prolongation: White phosphorous, SMFA, fluoroacetamide, arsenic.

 X-rays of the chest and abdomen

·        Radiopaque compounds include thallium, arsenic, and barium carbonate

TREATMENT

Supporting the airway, breathing, and circulation constitutes immediate management. The next step is to take off clothing and irrigate the skin with water if the patient is stable and if they are polluted. According to the American Academy of Toxicology, gastric lavage and activated charcoal are not recommended in cases of acute poisoning. [21] Data demonstrating a decline in morbidity and mortality are few. Call poison control right away for the most recent recommendations if the patient arrives within 30 to 60 minutes of consumption. Anti-emetics and rehydration may be beneficial for treating acute gastrointestinal effects to restore electrolyte balance. If someone is hyperthermic, as in the case of strychnine poisoning, start cooling techniques such as evaporative cooling. Anticholinergic drugs like atropine, glycopyrrolate, and others may be administered to treat cholinergic toxicity.

 

Specialized Medical Care

Hemodialysis, continuous renal replacement, or charcoal hemoperfusion are all forms of renal replacement therapy that are used to treat heavy metal toxicity from thallium, arsenic, or barium.

 

Benzodiazepines

 

·        Used to treat seizures and muscle spasms, particularly in strychnine poisoning[5].

 

anti-Lewisite British

 

·        Used to treat acute arsenic poisoning by chelation[8]

 

2,3-Dimercapto-1-propane sulfonate, also known as meso-2,3-dimercaptosuccinic acid (DMSA) (DMPS)

 

·        Used to treat chronic arsenic poisoning[8] via chelation

Either magnesium sulfate or sodium sulfate

·        It is a non-absorbable barium sulfate compound since it is specifically intended for acute barium carbonate ingestion[9].

Niacin (intravenous)

·        Used to restore NAD and NADH products for cellular energy metabolism in cases of criminal poisoning[13]

Mineralocorticoids

·        Used to treat orthostatic hypotension when pyriminil toxicity occurs.

 

Immune fab digoxin

Used to relieve the symptoms of red squill poisoning

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