Salicylic acid poisoning

Introduction to salicylic acid poisoning Salicylates commonly used in clinical practice include aspirin (acetic acid, acetylsalicylic acid), compound aspirin, sodium salicylate, sodium salicylate mixture, methyl salicylate (winter oil) and others. Salicylic acid-containing tinctures, ointments, etc., salicylic acid poisoning is mostly caused by excessive use of a large amount or long-term application, and it is more prone to accidental overdose accidents during infancy. External salicylic acid ointment or powder can be absorbed through the skin due to extensive damage to the skin. In patients with dehydration, liver, renal insufficiency, and low prothrombinemia, severe toxic reactions are more likely to occur. Salicylate can pass through the placental barrier, and pregnant women take too much, often causing fetal or neonatal poisoning. Poisoning symptoms can occur in children taking 2 to 4 times the amount of aspirin or sodium salicylate. The minimum lethal dose of aspirin is about 0.3-0.4 g/kg. The minimum lethal dose of sodium salicylate is about 0.15 g/kg, and the lethal dose of oral wintergreen oil in children is about 4 ml. basic knowledge The proportion of illness: 0.002% Susceptible people: good for children Mode of infection: non-infectious Complications: coma, shock, respiratory failure

Salicylic acid poisoning etiology

Cause:

Salicylic acid drugs are mainly acetylsalicylic acid and sodium salicylate. Salicylic acid itself is only irritating, and it is only used for external use, and has antifungal and keratinolytic effects. The most commonly used in this class of drugs is aspirin. After oral salicylate, it is quickly absorbed by the stomach and upper part of the small intestine. After being absorbed, salicylic acid is hydrolyzed into salicylic acid by esterases in gastric mucosa, plasma, red blood cells and liver. After 2 hours, the concentration of salicylic acid in plasma reached a peak. Salicylic acid is metabolized by the liver drug, and most of the metabolites are bound to glycine. A small part is combined with glucuronic acid and excreted from the kidney. However, the liver has limited ability to metabolize salicylic acid. When the body ingests too much salicylic acid, the binding reaction of salicylic acid with glycine and glucuronic acid is saturated, resulting in a sharp rise in the concentration of free salicylic acid in the blood. Poisoned.

Salicylate is mainly excreted by the kidneys. After oral administration, the rats with normal renal function can be seen in the urine in a few minutes. About half of the poisoning can be discharged in 24 hours. If the urine is alkaline (pH 7.5 or higher), the excretion is accelerated. In half, the blood salicylate can be reduced by half in 6 hours.

Pathophysiology:

1 High concentration of salicylate stimulates the respiratory center, and excessive exhalation occurs. As a result, a large amount of CO2 is excreted in exhalation, resulting in respiratory alkalosis (blood pH rise), which is more common in children over 5 years old. Aspirin is a weakly acidic substance that has a stimulating effect on the gastric mucosa. Long-term oral administration can induce gastrointestinal ulcer disease and chronic bleeding.

2 With the above-mentioned central pathophysiological changes, due to the presence of respiratory alkalosis, renal compensation occurs, resulting in a large discharge of sodium with urine; at the same time due to vomiting, loss of water, loss of sodium, and salicylate dehydrogenase Inhibition with aminotransferase, blocking the tricarboxylate cycle, causing disorder of carbohydrate metabolism, eventually leading to elevated blood ketones, resulting in metabolic acidosis. Especially in infancy, the pathophysiological process of the second stage develops very fast, making acidosis the main manifestation.

3 poisoning dose of salicylate can directly act on vascular smooth muscle, so that the surrounding blood vessels dilate, blood pressure drops; and can cause vasomotor center paralysis, leading to peripheral circulatory failure.

4 salicylate poisoning can cause kidney damage, severe tubular necrosis can occur, leading to acute renal failure. Long-term high-dose applications can cause changes in renal papilla, tubular necrosis, renal degeneration and atrophy.

5 general doses of aspirin can inhibit platelet aggregation and prolong bleeding time. Large doses (5g / day or more) or long-term use can also inhibit thrombin formation and prolong thrombin time. It can also be caused by the inhibition of bone marrow hematopoietic function, causing severe anemia and even a reduction in whole blood.

6 Aspirin can cause hepatitis, encephalopathy and allergic reactions. A small number of patients with allergic reactions may develop urticaria, angioedema, and anaphylactic shock.

Salicylic acid poisoning prevention

When applying this class of drugs, the dosage should be strictly controlled. For long-term use, attention should be paid to the changes of heart, blood, gastrointestinal tract, asthma, stomach and duodenal ulcer, nasal polyps, and before and after drinking; pregnant women, liver People with kidney disease, elderly and infirm, and those with a history of allergies to this class of drugs should be used with caution. Avoid use with dicoumarin, so as not to cause coagulopathy, leading to severe bleeding, can not avoid hypoglycemia reaction with metoclobutamide, combined with furosemide can reduce salicylic acid excretion, resulting in accumulation of poisoning, should be avoided.

Salicylic acid poisoning complications Complications, coma, respiratory failure

Severe poisoning, can occur stupor, can not speak, coma, shock, and finally complications such as circulation and respiratory failure, and even death.

Symptoms of salicylic acid poisoning Common symptoms Hairy coma, nausea, pale, high fever, protein, urine, respiratory failure, hallucinations, horror, complexion, flushing

1. Digestive system reaction: nausea, vomiting, abdominal pain, hematemesis, bloody stools.

2. Neurological symptoms: headache, dizziness, lethargy. Severe patients, especially infants and young children, may experience delirium, hallucinations, confusion, muscle tremors, and convulsions and coma.

3. Respiratory symptoms: deep breathing, respiratory alkalosis, manifestations of numbness, tingling, convulsions, chest tightness and bloating in the limbs; severe poisoning may occur pulmonary edema and respiratory failure. Children with allergies to salicylate can develop glottic edema and throat paralysis even with low doses of aspirin.

4. Circulatory system: vasodilation, flushing, cyanosis, purpura, nosebleeds, retinal hemorrhage. Salicylate can enter the neonate through the placenta, causing neonatal bleeding.

5. Urinary system: hematuria, proteinuria, uremia, etc.

6. Systemic symptoms: body temperature drops, sick children can have sweat, high fever, dehydration and so on.

7. Others: Poisoning can also have tinnitus, deafness, visual impairment, increased transaminase, jaundice, and other parts of bleeding. Allergic children can also have rash, epidermal necrosis and so on.

Salicylic acid poisoning

1 Qualitative test of ferric chloride: the gastric eluate or urine is boiled in a test tube, acid is added after cooling, and then a few drops of 5% to 10% ferric chloride solution are added, and the purple color turns purple-red, which proves that Salicylate.

2 Detection of salicylate level in blood: After taking salicylate for 30 minutes, the concentration can be determined. Mild poisoning is 2.16~2.88mmol/L (30-40mg/dl); moderate poisoning is 2.88~ 4.32mmol / L (40 ~ 60mg / dl), severe poisoning was 4.32mmol / L (60mg / dl) or more.

3 blood biochemical examination showed that CO2 binding capacity was greatly reduced, CO2 partial pressure and pH value decreased, and blood glucose decreased (may have a transient increase).

Diagnosis and identification of salicylic acid poisoning

Mainly differentiated from other antipyretic analgesic poisoning. Identification can be made by the patient's medication history and urine detection of the poison.

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