Salicylates remain one of the most widely used medications, and poisoning – both voluntary and accidental – is common. Aspirin is taken for its analgesic and antipyretic, or antiplatelet effects, but salicylates are also present in drugs in non-aspirin forms, such as methyl salicylate (oil of wintergreen) in liniments, and bismuth sub-salicylate in Pepto Bismol. Salicylates cause toxicity both through ingestion and dermal absorption. Aspirin poisoning is not easy to diagnose and is not always identified, especially in cases of chronic usage, when the symptoms may be atypical or misleading [1].

Salicylates impair the metabolism of all tissues through uncoupling oxidative phosphorylation and inhibiting the function of the Krebs cycle. In addition, drugs based on salicylate have organ-specific physiological responses like stimulation of the respiratory center.

In early stages, patients with acute poisoning most often present with nausea and vomiting because of gastrointestinal irritation and hyperventilation due to stimulation of respiration [3], and tinnitus [2], a characteristic although a non-specific sign of salicylate poisoning. Other signs are diaphoresis, hyperactivity, and tachycardia. Hyperventilation leads to respiratory alkalosis, but not typically in children. Once metabolic disturbances become prominent, the inhibition of aerobic respiration and activation of lipid breakdown lead to accumulation of lactic acid and ketone bodies, and consequently to aciduria and metabolic acidosis. Thus, a mixed acid-base disorder is generated. Late signs are fever, agitation, or conversely, lethargy, convulsions, and stupor. Patients in late stages may be mistakenly diagnosed as suffering from sepsis [4], having a heart attack [5], or being agitated.

Several organ systems are affected, and a variety of signs may be observed. Pulmonary edema is somewhat more frequent in chronic toxicity in the elderly population. Central nervous system (CNS) deterioration can also occur, especially in acidosis, which increases the proportion of uncharged salicylate molecules that are able to cross the blood-brain barrier. CNS toxicity can contribute to vomiting. In severe cases, the condition progresses to cerebral edema, seizures, coma, and death. The inhibition of prostaglandin and thromboxane synthesis is accompanied by increased bleeding times, gastrointestinal (GI) irritation, and, in chronic poisoning, GI bleeding.

Glucose metabolism is also disturbed, leading usually to hypoglycemia, and there is no correspondence between serum glucose levels and cerebrospinal fluid glucose content [6]. Thus, blood glucose levels may not adequately reflect mental responses of the patient. Other blood chemistry changes are dehydration, hypokalemia, and hypocalcemia.

Chronic toxicity may be difficult to recognize, especially in the elderly, because the symptoms are nonspecific (confusion, fever, dehydration and others), and because a confused patient may not remember having taken salicylates. Renal insufficiency exacerbates salicylate poisoning since most of the drug is eliminated by the kidneys [7].

The “Done nomogram” [8] was developed in 1960 for predicting salicylate toxicity after a single dose of ingestion [1]. Although successful in many cases, the premises used in its formulation restrict its general applicability [9], and it is not recommended for general use.

Serum salicylate levels do not always reflect the severity of poisoning. A general guide specifies 30 mg/dL above which symptoms usually appear, and 100 mg/dL above which the effects of poisoning may be fatal. Serial salicylate and arterial blood gas levels are more important for the better evaluation of the situation and for following acid-base alterations. A peak value may not be reached up to 4-6 hours after ingestion. Some salicylate tablets have a tendency to form a concretion in the stomach [10], in which case the serum concentrations will keep increasing for a longer time.

Levels of serum electrolytes, creatinine, blood urea nitrogen, and potassium (which may become very low if the patient is alkalinized), should be followed until salicylate concentrations start declining and anomalies are resolved. Urine pH should also be monitored. An abdominal radiograph or other imaging may be necessary if the formation of a concretion is suspected.

The treatment of salicylate poisoning aims to remove the excess salicylates from the body and manage symptoms. Activated charcoal may be administered to prevent further absorption if the ingestion was recent. Intravenous fluids are often used to correct dehydration and electrolyte imbalances. In severe cases, hemodialysis, a procedure that filters the blood, may be necessary to rapidly remove salicylates. Supportive care, including monitoring vital signs and providing oxygen, is also important.

The prognosis for salicylate poisoning largely depends on the amount ingested and the timeliness of treatment. With prompt and appropriate medical intervention, most patients recover fully. However, delayed treatment or severe poisoning can lead to complications such as kidney failure, respiratory distress, or neurological damage. Early recognition and treatment are critical for a favorable outcome.

Salicylate poisoning typically results from the ingestion of large quantities of salicylate-containing medications, such as aspirin. It can also occur from chronic use of these medications, especially in individuals with pre-existing health conditions. Accidental ingestion, particularly in children, and intentional overdose are common causes. Understanding the sources of salicylates is important for prevention and management.

Salicylate poisoning is a relatively common form of drug overdose, particularly in countries where aspirin is widely used. It affects individuals of all ages, but children and the elderly are at higher risk due to differences in metabolism and potential for accidental ingestion. The incidence of salicylate poisoning has decreased in some regions due to increased awareness and safer packaging of medications.

Salicylates affect the body by interfering with the normal function of cells and organs. They can disrupt the acid-base balance, leading to a condition called metabolic acidosis, where the blood becomes too acidic. Salicylates also stimulate the respiratory center in the brain, causing rapid breathing and further altering the body's acid-base status. These changes can affect multiple organ systems, leading to the symptoms observed in poisoning.

Preventing salicylate poisoning involves careful use and storage of medications. It is important to follow dosing instructions and avoid taking multiple salicylate-containing products simultaneously. Medications should be stored out of reach of children to prevent accidental ingestion. Educating patients about the risks of overdose and the importance of adhering to prescribed doses can also help reduce the incidence of poisoning.

Salicylate poisoning is a serious medical condition resulting from excessive intake of salicylates, commonly found in aspirin. It presents with a range of symptoms from mild to severe and requires prompt medical attention. Diagnosis involves clinical assessment and laboratory tests, while treatment focuses on removing the toxin and managing symptoms. With timely intervention, the prognosis is generally good, but prevention through education and safe medication practices is key.

If you suspect salicylate poisoning, it is important to seek medical attention immediately. Symptoms can range from mild, such as nausea and ringing in the ears, to severe, including confusion and difficulty breathing. Treatment is most effective when started early, so do not delay in contacting a healthcare provider. Always follow medication instructions carefully and keep medicines out of reach of children to prevent accidental ingestion.

1. O'Malley GF. Emergency department management of the salicylate-poisoned patient. Emerg Med Clin North Am. 2007 May;25(2):333-346.
2. Stolzberg D, Salvi RJ, Allman BL. Salicylate toxicity model of tinnitus. Front Syst Neurosci. 2012 Apr 20;6:28.
3. Proudfoot AT. Toxicity of salicylates. Am J Med. 1983 Nov 14;75(5A):99-103.
4. Chalasani N, Roman J, Jurado RL. Systemic inflammatory response syndrome caused by chronic salicylate intoxication. South Med J. 1996 May;89(5):479-482.
5. Paul BN. Salicylate poisoning in the elderly: diagnostic pitfalls. J Am Geriatr Soc. 1972 Aug;20(8):387-390.
6. Yip L, Dart RC, Gabow PA. Concepts and controversies in salicylate toxicity. Emerg Med Clin North Am. 1994 May;12(2):351-364.
7. Chin RL, Olson KR, Dempsey D. Salicylate toxicity from ingestion and continued dermal absorption. Cal J Emerg Med. 2007 Feb;8(1):23-25.
8. Done AK. Salicylate intoxication. Significance of measurements of salicylate in blood in cases of acute ingestion. Pediatrics. 1960 Nov;26:800-807.
9. Dugandzic RM, Tierney MG, Dickinson GE, et al. Evaluation of the validity of the Done nomogram in the management of acute salicylate intoxication. Ann Emerg Med. 1989 Nov;18(11):1186-1190.
10. Taylor JR, Streetman DS, Castle SS. Medication bezoars: a literature review and report of a case. Ann Pharmacother. 1998 Sep;32(9):940-946.