Introduction
Acute or chronic poisoning with a salicylate, such as Aspirin, is referred to as salicylate poisoning, sometimes known as Aspirin poisoning. Ringing in the ears, nausea, abdominal pain, and rapid breathing are the typical symptoms. These may be mild initially, but higher doses may cause a fever. Seizure, low blood sugar, cardiac arrest, and brain or lung swelling are a few complications.
Although usually brought on by Aspirin, other potential reasons include bismuth sub-salicylate and oil of wintergreen. Excessive doses might be deliberate or accidental. The oil of wintergreen can be harmful in small amounts. Repeated blood tests that measure Aspirin levels and blood gases are typically used to make the diagnosis. Although a specific kind of graph has been developed to aid in the diagnosis, its use, in general, is not advised. Maximum blood levels can take up to 12 hours to reach in an overdose.
What Is the Etiology (Cause) Of Salicylate Toxicity?
Many over-the-counter medicines include salicylates. Due to their analgesic (pain-relieving), antipyretic (decreases elevated body temperature), and antithrombotic (reduces the risk of blood clots) qualities, they are frequently utilized. However, toxicity may result from prolonged ingestions that raise serum levels or sudden ingestions. In addition, salicylates can be combined with other drug classes, such as opioids, antihistamines, and anticholinergic drugs, to create formulations. This may make management more difficult.
What Is the Epidemiology of Salicylate Poisoning?
Thirty-nine people died in the United States from salicylate toxicity in 2011, which resulted in 30,000 cases. The fatality rate was less than 0.01 percent overall, but it rose to 15 percent for patients who experienced severe toxicity. The complications escalated when the diagnosis was not made at the time of the initial evaluation.
What Are the Physiological Processes Associated With Salicylate Poisoning?
Numerous metabolic diseases are brought on by salicylate intoxication. Hyperventilation and respiratory alkalosis are brought on by direct stimulation of the cerebral medulla. It separates oxidative phosphorylation in the mitochondria as it is broken down. Following that, lactate levels rise due to the increased anerobic metabolism. Metabolic acidosis is caused by lactic acid with a minor contribution from the salicylate metabolites. As a result of an effort to counteract metabolic acidosis, hyperventilation (deep and rapid breathing) worsens. The patient eventually becomes too exhausted to compensate by hyperventilating, and metabolic acidosis (buildup of acid levels in the body generally due to impairment in kidney functioning) takes over. End-organ damage and hemodynamic instability are the effects of this.
What Are the Signs and Symptoms of Salicylate Poisoning?
There are several critical pieces of information from the patient's history. These include the formulation, amount, and time of consumption. The latter is crucial because it could impact how quickly absorption occurs. Additionally, it is critical to determine whether any additional substances were consumed because doing so could make treatment more difficult and increase mortality. Lastly, decide if this was unintentional or intentional. It is advisable to have EMS (emergency medical services) workers, relatives, or close friends verify this information.
The symptoms of an acute salicylate overdose will appear within three to eight hours. The quantity consumed affects how severe the symptoms are. There is a high prevalence of nausea, vomiting, and nonspecific abdominal pain following modest ingestions (salicylate levels 40 to 80 mg/dL). Usually, tachypnea (rapid and shallow breathing) is present. Dizziness and headaches can also happen. But even at lower, non-toxic doses, this can happen.
Neurological symptoms in patients with mild salicylate poisoning (80 to 100 mg/dL) will be more severe. Confusion, slurred speech, and hallucinations are a few of them. In addition, orthostatic hypotension and tachycardia (heart rate over 100 beats per minute) are present, and tachypnea (abnormally rapid breathing) is more noticeable. These symptoms are typically observed 6 to 18 hours after intake.
The severe toxicity threshold for salicylate is 100 mg/dL, which happens 12 to 24 hours after intake. Edema (fluid buildup) in the brain and lungs results from damaged basement membranes. Patients may get seizures and become obtunded (dull). With approaching respiratory collapse, hypoventilation (breathing that is too slow) could take the place of hyperventilation. While not ideal for metabolic diseases, endotracheal intubation could be required to protect the airway. Acidosis and hypovolemia cause hypotension (drop in blood pressure). There could be cardiac dysrhythmias (irregular heartbeat). The most typical type is sinus tachycardia. Asystole is the most typical rhythm for cardiac arrest, which is another possibility.
Similar symptoms to acute poisoning, albeit at lower levels, will be experienced by patients with chronic salicylate toxicity. Pediatric patients will experience a quicker transition from minor signs to severe symptoms than adults.
How Can Salicylate Poisoning Be Treated?
Volume depletion occurs in patients with salicylate toxicity due to hyperventilation, fever, and increased metabolic activity. Therefore, we should use D5 (5-milligram Diazepam tablet) for fluid resuscitation and three amperes of sodium bicarbonate. Dextrose will cure hypoglycemia (glucose deficiency) in the central nervous system (CNS). The metabolic acidosis will be treated with sodium bicarbonate. If hypokalemia (lack of potassium in the bloodstream) is evident, potassium supplements may be given. The ideal hourly urine output is 2 to 3 mL/kg.
Patients who have had severe poisoning will eventually get exhausted and be unable to continue compensating for the metabolic acidosis through breathing. Even if it is not ideal, mechanical ventilation could be necessary. To stabilize the patient's pH until hyperventilation can be restarted on the ventilator, consider administering a bolus of 1 to 2 mEq/kg sodium bicarbonate at the time of intubation. The metabolic acidosis cannot be offset by mechanical ventilation either. After intubation, plans should be made for emergency hemodialysis (kidney dialysis). Following fluid resuscitation (treatment to replace the fluids lost from the body), patients may also have respiratory discomfort due to pulmonary edema.
Attempts should be undertaken to lower the serum salicylate levels after the initial stabilization. It has been demonstrated that activated charcoal reduces salicylate levels. However, no reduction in morbidity or mortality has been confirmed. Gastric cleansing may be an option if the patient has recently consumed enteric-coated Aspirin. These choices ought to be avoided if aspiration is a concern. Whole bowel irrigation has not demonstrated any advantages and may improve absorption.
Salicylate elimination will be boosted by serum alkalization and fluid resuscitation. This can also be achieved using hemodialysis. Severe acidosis or hypotension that persists despite fluid resuscitation, salicylate levels that are more than 100 mg/dL, mechanical breathing, or end-organ destruction are all indications of hemodialysis. Seizures, pulmonary edema, cerebral edema, and renal failure are typical indications of salicylate poisoning.
Benzodiazepines should be used to treat seizures. Given the possibility of CNS hypoglycemia, glucose should also be given. After a stroke, bicarbonate bolus is given if worsening of metabolic acidosis is expected.
If patients' salicylate levels are on the decline and there are no metabolic disturbances, they may be sent home with small ingestions and symptoms. However, patients with worsening serum pH and rising salicylate levels must be admitted to the intensive care unit for additional monitoring.
Conclusion
The morbidity and fatality rates of salicylate poisoning are substantial. One to two percent of individuals die from this medication. According to data from poison control centers, Aspirin, either alone or in combination with other drugs, is responsible for at least one-fourth of all medication-related deaths. The crucial aspect is that salicylate poisoning is curable with proper diagnosis and treatment. Some residual neurological deficits may last a few years for the survivors.
