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Poisoning with acetylsalicylic acid
Last reviewed: 23.04.2024
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Poisoning with salicylates can cause vomiting, tinnitus, frustration, hyperthermia, respiratory alkalosis, metabolic acidosis and multiple organ failure. The diagnosis is based on clinical data and is confirmed by laboratory tests (the content of electrolytes in the blood, blood gases, the concentration of salicylates in the blood). Treatment includes activated charcoal, alkaline diuresis and hemodialysis.
Acute ingestion of more than 150 mg / kg of the drug can cause severe poisoning. Salicylate tablets can form bezoaras, prolonging absorption and poisoning. Chronic poisoning can occur several days after receiving high therapeutic doses, is often found, in some cases is not diagnosed, causes a more severe condition in comparison with an acute overdose. Chronic poisoning is more common in elderly patients.
The most concentrated and toxic form of salicylates is halutria oil (methyl salicylate, a component of some liniments and solutions used in perfumery), taking <5 ml of which can kill a child.
[Pathophysiology of poisoning with acetylsalicylic acid
Salicylates disrupt cellular respiration, rupturing the chain of oxidative phosphorylation. They stimulate the respiratory center of the medulla oblongata, causing primary respiratory alkalosis, which is often not recognized in young children. Simultaneously, and regardless of respiratory alkalosis, salicylates cause primary metabolic acidosis. Ultimately, when salicylates come out of the blood and penetrate the cells, where they affect the mitochondria, metabolic acidosis develops - the main disturbance of the acid-base equilibrium.
The poisoning with salicylates also leads to ketosis, fever, a decrease in glucose in the brain, despite the absence of systemic hypoglycemia. Dehydration develops as a result of fluid and electrolyte losses (K, Na) in the urine, as well as due to increased respiratory losses of the fluid.
Salicylates are weak acids and pass through the cell membranes relatively easily, so they are more toxic at a low blood pH. Dehydration, hyperthermia and continued use increase the toxicity of salicylates due to a greater distribution of the drug in the tissue. Salicylate excretion increases with increasing urine pH.
Symptoms of poisoning with acetylsalicylic acid
In acute overdose, early symptoms include nausea, vomiting, tinnitus and hyperventilation. Late symptoms include hyperactivity, fever, confusion and convulsions. Over time, rhabdomyolysis, acute renal and respiratory failure are possible. Hyperactivity can quickly change to lethargy; Hyperventilation (with respiratory alkalosis) is replaced by gipoventilation (mixed respiratory and metabolic acidosis) and respiratory failure.
In chronic overdose, the symptomatology is nonspecific and varies widely. There may be slight stun, changes in mental status, fever, hypoxia, non-cardiogenic pulmonary edema, dehydration, lactic acidosis and hypotension.
Diagnosis of poisoning with acetylsalicylic acid
Salicylate poisoning should be suspected in patients with a history of acute acute overdose or with repeated administration of therapeutic doses (especially in the presence of fever and dehydration), in patients with unexplained metabolic acidosis and in elderly patients with unexplained mental and fever disorders. If suspected of poisoning, it is necessary to determine the concentration of salicylates in the blood plasma (recruited at least several hours after administration), the pH of the urine, the blood gas composition, electrolytes, glucose, creatinine and urea.
When suspicion of rhabdomyolysis, it is also necessary to determine the blood CKK and the concentration of myoglobin in the urine.
Severe salicylate poisoning is suggested when the plasma concentration is significantly higher than the therapeutic range (10-20 mg / dL), especially within 6 hours after poisoning, when the absorption of the drug is almost complete, as well as with acidemia and changes in the blood gas composition characteristic of salicylate poisoning . Usually, in the first hours after taking the drug, the gas composition of the blood indicates respiratory alkalosis, later - on compensated metabolic acidosis or mixed metabolic acidosis / respiratory alkalosis. Ultimately, usually as the concentration of salicylates decreases, the main violation of the acid-base equilibrium becomes either subcompensated or decompensated metabolic acidosis. With the development of respiratory failure, the gas composition of the blood indicates mixed metabolic and respiratory acidosis, radiography shows diffuse infiltrates in the lungs. The concentration of blood plasma glucose can be within normal limits, increased or decreased. Repeated measurements of the concentration of salicylates can establish the fact that their absorption continues, and simultaneously with this study, the gas composition of the blood should be determined. Increase in CKK of blood serum and myoglobin of urine testifies to rhabdomyolysis.
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Treatment of poisoning with acetylsalicylic acid
Activated charcoal should be given as soon as possible and, with preserved peristalsis, repeat the intake every 4 hours until the appearance of charcoal in the stool.
After correction of electrolyte disorders and rehydration, alkaline diuresis can be used to increase urine pH (ideally> 8). Alkaline diuresis is indicated to patients with any symptoms of poisoning and should not be postponed until the salicylate concentration is determined. The method is safe and exponentially increases the excretion of salicylates. Since hypokalemia can interfere with alkaline diuresis, patients are given an infusion solution consisting of 1 liter of 5% glucose solution or 0.9% sodium chloride solution, 3 ampoules of NaHCO at 50 mEq, 40 mEq of KCI, at a rate exceeding the maintenance rate of intravenous infusions of 1 , 5-2 times. Monitor the concentration of K + plasma.
Drugs that increase the concentration of urinary acid in the urine (acetazolamide) should be avoided, as they aggravate metabolic acidosis and lower the pH of the blood. Avoid medications that depress the respiratory center, which can cause hypoventilation, respiratory alkalosis, and a decrease in blood pH.
Hyperthermia can be treated with physical means, such as external cooling. With cramps, benzodiazepines are used. In patients with rhabdomyolysis, alkaline diuresis can prevent kidney failure.
To accelerate the elimination of salicylates in patients with severe neurologic disorders, renal or respiratory failure and acidemia, despite other measures already taken, as well as with a very high concentration of salicylates in plasma [> 100 mg / dL (> 7.25 mmol / L) for acute overdose or> 60 mg / dl (> 4.35 mmol / L) for chronic] hemodialysis may be required.