rodenticide poisoning

Introduction

Introduction to rodenticide poisoning Commonly used rodenticides are zinc phosphide, enemy mice and warfarin. Rodenticides can be divided into four categories: organofluorines, zinc phosphides, tetramines and cyanides. Rodenticide poisoning is mainly seen in children who eat or suicide. Zinc phosphide is highly corrosive to the digestive tract, and the enemy mice and warfarin mainly affect the blood system. basic knowledge The proportion of sickness: 0.01% Susceptible people: no special people Mode of infection: non-infectious Complications: cerebral edema, pulmonary edema, renal failure, anemia

Cause

Rodenticide poisoning cause

Cause:

The disease is mainly caused by eating or suicide orally. Ingestion of rodenticides or baits is the most important way of poisoning children's rodenticides.

Pathogenesis

The anti-coagulant rodenticide poisoning mechanism interferes with the liver vitamin K, inhibits the blood coagulation factors II, VII, IX, X, affects the prothrombin synthesis, and prolongs the clotting time; the metabolites can damage the capillary wall. After 3 to 4 days after oral administration, symptoms appear and there is accumulation. Vitamin K1 is a special antidote.

Tetramine is a central nervous system excitatory rodenticide that does not require metabolism or toxic effects. Its mechanism of action may be the result of antagonizing -aminobutyric acid (GABA). GABA is a central nervous system inhibitor of spinal animals and has a strong and extensive inhibitory effect on the central nervous system. After the non-competitive inhibition of GABA by the tetramine, the central nervous system was overexcited and convulsed.

Organic fluorine-based rodenticides can be absorbed through the digestive tract and damaged skin and mucous membranes. The toxic mechanism is that fluoroacetamide enters the human body and then deamination is converted to fluoroacetic acid, and sodium fluoroacetate directly forms fluoroacetic acid. Fluoroacetic acid reacts with coenzyme A in intracellular mitochondria to form fluoroacetyl-CoA, which is then reacted with oxaloacetate to form fluorocitric acid. Because fluorine citric acid and citric acid are similar in chemical structure, they can not be affected by aconitase, but instead antagonize aconitase, so that citric acid can not be metabolized to produce aconitic acid, which leads to the interruption of the tricarboxylic acid cycle (called " Lethal metabolic synthesis"), hindered the metabolism of pyruvate, accumulation of fluorocitric acid, hindering the normal oxidative phosphorylation process, causing toxic damage mainly in the central nervous system and cardiovascular system.

Prevention

Rodenticide poisoning prevention

Children, especially younger children, lack the ability to distinguish between poisons. In addition, rodenticides are often mixed into fruits, biscuits and other foods for killing rats, and some poisons have attractive odors or tastes, such as lack of eye-catching signs. Promote the occurrence of poisoning. It is an effective prevention and treatment measure to put on the "skull" coat for the rodenticide, safely place the rodenticide, manage the education of children, and deeply bury the discarded rodenticide.

Try not to use yellow phosphorus as a raw material, and replace it with red phosphorus or other chemicals. Pay attention to safe production and enhance the storage of phosphorus and phosphorus compounds. Do not smoke and eat with hands contaminated with phosphorus and phosphorus compounds. Pay attention to oral hygiene. After contact with phosphorus, it is best to gargle with 5% sodium bicarbonate solution. When splashing into the eyes, rinse immediately with water or 2 to 5% sodium bicarbonate. Personnel engaged in phosphorus production should have regular physical examinations, including liver function tests and X-rays of the jaw. People with severe oral diseases, respiratory and liver and kidney diseases, blood diseases and metabolic endocrine diseases should not engage in phosphorus operations.

Complication

Rodenticide poisoning complications Complications cerebral edema pulmonary edema renal failure anemia

1. In severe cases, it can develop into a purulent fistula, leading to osteoporosis and necrosis of the mandible.

2. Neurological symptoms may have dizziness, insomnia, multiple dreams, and weakness.

3. Digestive system symptoms may have oral odor, nausea, anorexia, hepatomegaly, abnormal liver function, and anemia.

4. Brain edema, pulmonary edema, renal failure, liver damage.

Symptom

Rodenticide poisoning symptoms Common symptoms Gingival bleeding Booger nausea convulsion bleeding tendency sputum hemorrhagic shock

Symptoms of rodenticide poisoning: nausea, cyanosis, abdominal pain, and nasal discharge (also known as nosebleeds), which is one of the common clinical symptoms. It is caused by nasal lesions and can also be caused by systemic diseases. Occasionally, nasal bleeding due to nasal lesions passes through the nasal cavity. Outflow. Most of the nosebleeds are unilateral or bilateral; intermittent bleeding can also be repeated, and bleeding can continue; the amount of bleeding varies, the blood is only in the nose, the severe can cause hemorrhagic shock; repeated bleeding Can lead to anemia, most bleeding can be self-stop), blood in the stool, bleeding gums, convulsions, bleeding tendency.

1, enemy rats and warfarin poisoning: can appear nausea, vomiting, nosebleeds, purpura, hematemesis, blood in the stool, hemoptysis and so on.

2, zinc phosphide poisoning: can appear nausea, vomiting, hematemesis, shock, coma and so on.

Examine

Rodenticide poisoning check

Rodenticide poisoning inspection project:

Urine routine, blood routine, renal function test, liver function test, large biochemical test, blood pH (pH).

The biochemical tests mainly include liver function, kidney function, electrolytes, blood sugar, blood lipids, and myocardial enzymes. Changes in the concentration of certain metabolites in the blood reflect the metabolic or functional status of the body and are therefore closely related to clinical medicine.

Stomach contents check: The rodenticide was detected in the stomach contents.

Diagnosis

Diagnosis and identification of rodenticide poisoning

1. Interfering with metabolic rodenticides: the incubation period is about 3 to 4 hours. Oral nausea, vomiting, abdominal pain, anorexia and other gastrointestinal symptoms, followed by autonomic, central and peripheral nervous system dysfunction, such as orthostatic hypotension, limb pain, paresthesia, muscle weakness, visual impairment, mental Disorder, coma, convulsions, etc. In the early stage, there may be transient hypoglycemia, followed by diabetes, often accompanied by ketoacidosis. Electromyogram and EEG abnormalities.

2, zinc phosphide poisoning: generally more than 48 hours after eating, the first gastrointestinal symptoms, such as abdominal discomfort, nausea, vomiting, abdominal pain and diarrhea, sometimes the entire abdomen sustained pain, not easy to relieve; vomit is dark grey. Severe vomiting can be accompanied by bile and a small amount of bloody liquid, vomit and large smell of garlic. Gradually, irritability, decreased blood pressure, numbness and weakness in the limbs, and inactivity. Some patients have liver enlargement, jaundice, oliguria or hematuria. In severely poisoned patients, the neurological symptoms are obvious, and there may be tremors, convulsions, paralysis and coma. Most patients die due to respiratory paralysis.

3. Thiourea rodenticide: Gastrointestinal symptoms, mainly affecting pulmonary capillaries after absorption, causing increased permeability, causing pulmonary edema, pleural effusion and pulmonary hemorrhage, and causing liver and kidney damage, body temperature deviation Low, transient blood sugar rises. Pulmonary edema is the main cause of death. In acute poisoning, the main manifestations are mouth burning, nausea, vomiting, thirst, dizziness, lethargy, etc.; severe cases may have difficulty breathing, cyanosis, pulmonary edema, etc.; may also have convulsions, general paralysis, coma, shock, etc.; Later, there may be manifestations of hepatomegaly, jaundice, hematuria, and proteinuria.

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