تسمم الساليسيلات

Salicylate Toxicity

• Salicylates are available in various forms for ingestion (tablets, capsules, liquids) and topical application (creams, lotions).
• Salicylate poisoning is a common cause of poisoning in children and adolescents, often due to the readily available aspirin-containing pain relievers in households.
• The incidence of salicylate poisoning in children has decreased due to the use of child-resistant containers and the popularity of alternative pain relievers.
• Repackaging has reduced children's access to potentially lethal amounts of salicylates, and the association between salicylates and Reye's syndrome has also lessened their use.
• A toxic dose of aspirin is 150-300 mg/kg, with 500 mg/kg being potentially lethal.

Salicylate Poisoning - Background

• Willow bark, a source of salicylates, has been used for medicinal purposes since the 5th century BC.
• Salicylates were introduced as antipyretic, analgesic, and anti-inflammatory agents about 100 years ago.
• Despite a decline in use, salicylates are still used as prophylactic agents for migraine, colon cancer, and as antiplatelet agents.
• Over-the-counter (OTC) medications often combine salicylates with antihistamines and caffeine.

Sources of Salicylate Poisoning

• Aspirin overdose is a frequent cause.
• Topical application of products containing salicylates, such as Ben-Gay, salicylic acid (keratolytic), oil of wintergreen, or methyl salicylate, can lead to salicylate toxicity.
• One teaspoon of 98% methyl salicylate contains as much as 7000 mg of salicylate, equivalent to nearly 90 baby aspirin tablets and four times the potentially toxic dose for a 10 kg child.
• Salicylate toxicity has been reported with the topical use of salicylate-containing teething gels in infants.
• The increasing popularity of alternative medicines and herbal remedies in North America means that products containing salicylate may be encountered more frequently. Wintergreen oil, for example, is a topical pain reliever.

Salicylate Overdose - Risk Assessment

• A risk assessment table (not presented numerically) based on the quantity of salicylates ingested is provided.
• Ingestion of less than 0.125 kg/kg poses no danger, while quantities between 0.150 and 0.300 g/kg are moderate, and amounts of 0.300 to 0.500 g/kg are severe and prolonged risks. A quantity above 0.500 g/kg might be a potential lethal dose.

Mechanism of Toxicity - Metabolic Acidosis

• Inhibition of mitochondrial respiration prevents ATP formation, increasing pyruvate and lactic acid levels – leading to metabolic acidosis.
• Interference with the Krebs cycle enzymes promotes lipid metabolism and the accumulation of organic acids, further contributing to metabolic acidosis and ketogenesis.
• Inhibition of amino acid metabolism causes amino aciduria.

Mechanism of Toxicity - Respiratory Alkalosis

• Salicylates make the respiratory center more sensitive to pH and carbon dioxide partial pressure (Pco₂).
• This primarily occurs in the central nervous system (CNS) respiratory centers.
• Increased oxygen consumption and carbon dioxide production, along with elevated body temperature, lead to respiratory alkalosis.
• Hyperventilation, triggered by direct medulla stimulation, can occur early. This rapid breathing increases respiratory rate and can progress to coma and respiratory failure.

Mechanism of Toxicity - Hypoglycemia

• Salicylates cause insulin secretion, resulting in reduced glucose levels (hypoglycemia).
• Local irritation of the gastrointestinal tract (GIT) can cause emesis (vomiting) and upper gastrointestinal (GI) ulceration and bleeding - which can lead to severe dehydration
• Also, abdominal pain might be observed.
• Salicylates have a dose-dependent hepatotoxicity, leading to rare cases of hepatitis.

Mechanism of Toxicity - Water and Electrolyte Losses

• Increased metabolic rate caused by salicylate poisoning leads to pyrexia (fever), vomiting, and dehydration due to fluid loss.
• Compensation for respiratory alkalosis leads to increased renal excretion of bicarbonate, sodium, and potassium – potentially causing acidosis and hypokalemia (low potassium levels in the blood).
• Loss of bicarbonate reduces the buffering capacity, exacerbating the metabolic acidosis.

Mechanism of Toxicity - Coagulation Abnormalities

• Decreased thromboxane A2 synthesis impairs platelet activation and aggregation.
• In severe cases, the liver may fail to produce crucial clotting factors (factors 2, 7, 9, and 10), leading to prolonged prothrombin time.

Mechanism of Toxicity - Ototoxicity

• Vasoconstriction of the auditory microvasculature can cause tinnitus (ringing in the ears) or deafness.
• These symptoms are usually temporary in most cases.

Clinical Features

• Common initial manifestations (symptoms) of acute salicylate poisoning include tinnitus (ringing in the ears), impaired hearing, hyperventilation (rapid breathing), vomiting, dehydration, and hyperthermia (fever).

Lab Diagnostic Strategies

• A serum salicylate concentration should be measured 6 hours or more after ingestion.
• A second sample should be taken 2 hours later.
• Serial measurements are helpful to monitor continued absorption if the second measurement is higher than the first.
• Frequent monitoring of arterial pH is crucial to guide treatment, as acid-base balance can change rapidly.

Management

• Stabilization: Physical examination including vital signs (oxygen saturation, respiratory rate, temperature), and auscultation of the lungs are important to see signs of pulmonary edema.
• Decontamination: Multiple-dose activated charcoal (MDAC), gastric lavage, and whole bowel irrigation (WBI) may be considered for decontamination.
• Enhanced Elimination: Hemodialysis might be necessary if the patient develops pulmonary edema, vomiting, diarrhea, and fever.
• Antioxidant: Alkalinizing the urine (pH 7.5-8) through a constant infusion of sodium bicarbonate can help the body excrete the salicylates.
• Supportive Care: Intravenous fluids with dextrose should be administered to manage dehydration and electrolyte imbalances (including potassium). Careful monitoring of serum glucose is necessary to prevent hypoglycemia.

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