Approach
Salicylate poisoning is characterized by acid-base disturbances (particularly wide anion-gap metabolic acidosis; respiratory alkalosis is seen in 78% of adults; mixed disturbances are common), electrolyte abnormalities, and central nervous system (CNS) effects.[1][7] Lesser ingestions will result in tinnitus, nausea, and vomiting.[1] The diagnosis should be considered in any patient presenting with a history of unknown toxin ingestion or exposure, particularly in the presence of an unexplained acid-base disturbance.
Although considerable overlap exists between the signs and symptoms associated with acute versus chronic salicylism, the clinical presentation after chronic salicylate poisoning is often deemed as less severe and is either missed or recognition is delayed. Typically, the vulnerable population is the elderly patient consuming salicylates for a chronic condition such as one of the arthritides, or receiving prescriptions from more than one practitioner, leading to a risk of inadvertent dual prescribing.[1] Gastrointestinal symptoms are usually less prominent and CNS disturbances tend to dominate the clinical picture.[2] Patients present with a constellation of signs and symptoms similar to other conditions such as tinnitus, dementia, encephalopathy, alcoholic ketoacidosis, noncardiogenic pulmonary edema, cardiogenic shock, or sepsis.[1] Due to misdiagnosis, morbidity and mortality associated with chronic salicylism can be high.
History
The acute ingestion of 150 mg/kg or 6.5 g, whichever is less, of aspirin or aspirin equivalent warrants evaluation in a hospital emergency department due to the risk of salicylate poisoning. In addition, history of oil of wintergreen ingestion (98% methyl salicylate), especially more than a lick or taste by children <6 years old, or >4 mL by patients ages 6 years or older, carries a risk of salicylate poisoning.[2] One teaspoon of concentrated oil of wintergreen is approximately equivalent to 7 g of aspirin.[1][6]
A previous self-harm or suicide attempt among adolescents and adults may be suggestive; thus current suicidal overdose should be suspected. Children or their parents may give a history of accidental ingestion. Accidental, mostly chronic, ingestion is also of particular concern in older people (ages 70 years or older).[1] A full list of the patient's medications should be sought (prescribed and over-the-counter), with particular regard to the use of any salicylate-containing products (both topical and oral), and the amount and time of salicylate ingestion or exposure should be established. The presence of any medical conditions and coingestion of any additional potential toxins should be excluded (e.g., acetaminophen, drugs of abuse, and alcohol).
Patients may be asymptomatic in the initial stages after an acute ingestion or say they have tinnitus, nausea, vomiting, hematemesis, and epigastric pain. Impaired production of cellular energy and its release as heat may result in fever (hyperpyrexia may occur). A chief complaint of shortness of breath associated with a history of suspected poisoning should alert the physician to the possibility of an underlying metabolic acidosis and/or respiratory alkalosis.
CNS effects can occur and may be mild, moderate, or severe.[8] Mild symptoms include tinnitus, deafness, dizziness, and malaise, and are usually present in the early stages of acute ingestion.[1] Moderate and more severe symptoms usually occur at a later stage and include irritability, hallucinations, abnormal behavior, stupor, movement disorders, asterixis, confusion, seizures, coma, and symptoms of cerebral edema (e.g., headache).[1]
Physical exam
Metabolic acidosis and/or a respiratory alkalosis should be suspected in any patient presenting with dyspnea, tachypnea, or Kussmaul respirations (pattern of deep, labored breathing associated with severe metabolic acidosis).[1] Signs of volume depletion include poor skin turgor and dry mucous membranes. Profuse diaphoresis may mislead clinicians, and the state of dehydration in the salicylate poisoned patient may be missed.[1] Noncardiogenic pulmonary edema, as suggested by the presence of rales on auscultation plus low oxygen saturation in addition to dyspnea, can develop in both acute and chronic poisoning.[2] Mild CNS effects are usually established with history-taking, though tinnitus may complicate history-taking or be mistaken for alteration in mental status. Moderate and more severe CNS effects tend to occur at a later stage in the course of acute toxicity and are often prominent features of chronic poisoning. They include irritability, hallucinations, bizarre behavior, stupor, movement disorders, asterixis, confusion, seizures, coma, and signs of cerebral edema (e.g., presence of papilledema on fundoscopy).[1] The presence of a contact dermatitis may suggest cutaneous salicylate exposure.
Laboratory tests
Patients with salicylate poisoning present with respiratory alkalosis, metabolic acidosis, or both.[1] When metabolic acidosis is present, the anion gap is generally elevated. Baseline investigations should include serum electrolytes to evaluate for electrolyte abnormalities, as well as ABG to assess acid-base disturbance. The serum anion gap (SAG) can be calculated using the following formula: SAG = Na - Cl - HCO3. [ Anion Gap Opens in new window ] However, many toxicants and other disease states can cause wide-anion-gap metabolic acidosis, so a comprehensive workup should follow to identify the underlying cause. On the other hand, elevated salicylate levels can cause pseudonormalization of the anion gap on some lab analysis platforms, so a normal anion gap does not necessarily rule out salicylate poisoning.[9]
Further baseline tests should include measurement of serum urea nitrogen (BUN) and creatinine, serum ketones, and blood glucose levels. A serum salicylate level greater than the therapeutic range 10 to 20 mg/dL (0.72 to 1.45 mmol/L) increases index of suspicion for acute or chronic poisoning. A full workup for suspected poisoning or ingestion of analgesics should be performed as clinically indicated, and may include a screen for drugs of abuse, serum ethanol, and acetaminophen concentration if the history or physical exam are unclear. CBC, although nonspecific, may show an elevated WBC count. Serum LFTs are indicated because direct hepatotoxicity can occur and is usually reversible, but most patients develop an asymptomatic elevation of transaminases.[10][11] If the patient has active bleeding, prothrombin time (PT) and activated partial thromboplastin time (aPTT) should be measured to exclude coagulopathy.
Additional investigations
Patients with significant respiratory symptoms should have a chest x-ray and/or point of care ultrasound lung exam to exclude acute respiratory distress syndrome (ARDS) due to noncardiogenic pulmonary edema.[12] ARDS is an indication for urgent hemodialysis.[13] If the etiology is unclear, an echocardiogram may be considered to evaluate cardiac function and help differentiate ARDS from cardiogenic pulmonary edema.
[Figure caption and citation for the preceding image starts]: Chest x-ray image of bilateral infiltrates in a patient with ARDSFrom the personal collection of Dr Lorraine Ware; used with permission [Citation ends].
An ECG should be obtained in all cases of suspected salicylate poisoning. Sinus tachycardia is common, but a prolonged corrected QT interval is associated with severe ventricular dysrhythmias.[14] This is certainly an indication for alkalinization and may indicate a need for acute hemodialysis. Both monomorphic ventricular tachycardia and torsades de pointes have been reported in association with salicylate poisoning.[14]
A head CT scan is indicated for patients presenting with lateralizing signs, an evaluation for herniation, or to rule out a structural lesion of the CNS. For patients with known salicylism who have altered mental status, a CT scan of the head should not be pursued when it will cause a delay in the initiation of hemodialysis or if it would require sedation in a patient with tachypnea who is not already intubated.
An EEG may help to exclude an underlying seizure disorder.
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