Salicylate poisoning may be defined as an ability of salicylic acid or other salicylate containing drugs to reach an increased serum level in the blood stream, results from an overdose of aspirin or other drugs containing salicylates. The derivative of salicylic acid is used for pain relief, anti-inflammatory effects and to reduce fever, but if taken in high doses can have several dangerous adverse effects. The toxicity may be either single bolus in large doses or cumulative toxicity with repeated use over time mainly in children, elderly or in patients with kidney or liver disease. The effect of salicylate is mainly on the respiratory, CNS and metabolic systems. It results to hyperventilation owing to respiratory centre stimulation and results in respiratory alkalosis at initial phase. At the later stages of toxicity, the metabolic acidosis sets in because of accumulation of various organic acids. This can either destabilise the acid base balance, normal fluid and electrolyte concentrations, or the production of catabolic energy substrates. They include signs like nausea, vomiting, tinnitus, headache, dizziness, lethargy, and confusion and more complicated ones like seizures and multi-organ dysfunction.
Epidemiology
According to available data, in 2011 there were 30,000 reported cases of salicylate poisonings in the US with 39 fatalities. Altogether, the mortality was less than 0.01%; nonetheless, it reached 15% in individuals with severe toxicity. The complications increases if the diagnosis was not made on first assessment.
Anatomy
Pathophysiology
Stimulation of Neurons in the Brainstem Respiratory Centers:
salicylate poisoning directly affects the central respiratory chemoreceptors; medullary respiratory centre in the brain stem resulting into hyperventilation and respiratory alkalosis in the early stages. This causes increased COâ‚‚ excretion and initially lowers blood COâ‚‚ levels.
Metabolic Acidosis Uncoupling of Oxidative Phosphorylation:
It is established that salicylates inhibit the coupled oxidation phosphorylation and thus the energy generation through ATP and increases the generation of lactate. This results in lactic acidosis and plays a role in the development of the metabolic one as well.
There are other groups of toxic effects associated with salicylates. Salicylates stimulate lipolysis and increase levels of free fatty acids which are transformed into ketones that worsen metabolic acidosis.
Electrolyte and Acid-Base Imbalances:
It encompasses electrolyte and acid-base imbalance. In response to respiratory alkalosis, kidneys excrete bicarbonate, potassium and sodium, which may bring about hypokalemia as well as distort other electrolytes balances.
When acidosis increases due to lactate and ketoacidosis, compensation mechanisms can be overwhelmed and produce a condition that is a mixed respiratory alkalosis and metabolic acidosis.
CNS Effects:
Salicylates are lipid-soluble and can cross the blood-brain barrier, especially in high concentrations. This may breach the blood brain barrier and cause CNS toxicity particularly characterized by confusion, agitation, seizures and in the extreme by cerebral edema. Hyperthermia and Dehydration:
Since salicylates interfere with oxidative phosphorylation, their intake augments energy consumption and thermogenesis, relationship that cause hyperthermia.
Sweating intensifies dehydration and hyperventilation because both conditions are dehydrative.
Etiology
Acute Ingestion:
Intentional Overdose: Mostly in intentional self-harm cases where a huge, bulk quantity is taken at once.
Unintentional Overdose: May happen in cases when a person gave himself an overdose, for instance, with aspirin, using the wrong dosage or mixing several products containing salicylates.
Chronic Use:
Repeated Use of Salicylates:
Therapeutic dosages become toxic if used for a long time and more so to elderly patients who have weak kidneys and patients with liver diseases.
Topical Absorption:
Topical Preparations: Acidosis may result from overuse of salicylate-containing topical ointments such as creams containing methyl salicylate or wintergreen oil.
Pediatric Exposure: Children are most vulnerable because even traces of wintergreen oil are poisonous given the fact that it is absorbed through the skin or ingested.
Metabolic Factors:
Renal Impairment: End stage renal disease delays renal elimination of salicylate and increases their concentration in the body.
Hepatic Impairment: The liver plays a key role in metabolizing salicylates; liver dysfunction can impair detoxification and exacerbate toxicity.
Genetics
Prognostic Factors
Acid-Base Imbalance Metabolic Acidosis:
Raised levels of the above parameters are associated with more severe symptoms and negative prognosis, especially acidosis which becomes progressively worse during the disease.
Anion Gap:
Rising values for anion gap point towards the build-up of acidic metabolites and a poor outcome.
Electrolyte Abnormalities:
Hypokalemia: Seen frequently in salicylate poisoning and make the acid base status worse and the condition of the patient poor. Hypernatremia: May be a consequence of dehydration caused by losses of fluids and aggravates signs of the CNS pathology.
Clinical History
Age Group:
Children (especially under 12 years): Salicylates are far more easily absorbed by young children than by adults, and therefore young children are far more vulnerable to the poisonous effects of salicylates.
Even a small amount of aspirin can lead to toxicity in small children due to their lower body mass and developing metabolism. This is also true in this group because accidental ingestion is the leading cause.
Teenagers and Young Adults: This age group may experience toxicity from intentional overdose usually in suicide attempts. Aspirin is easier to obtain; therefore, teenagers can be at a higher risk of an overdose of the medication.
Physical Examination
Vital Signs
Tachypnea (Increased Respiratory Rate)
Tachycardia (Increased Heart Rate)
Hyperthermia (Elevated Body Temperature)
Hypotension
Neurological Signs
Confusion, Dizziness, Delirium
Tinnitus and Hearing Loss:
Altered Mental Status (Severe cases)
Respiratory System
Gastrointestinal Signs
Skin assessment
Age group
Associated comorbidity
Chronic Kidney Disease (CKD)
Liver Disease
Asthma
Metabolic Acidosis
Gastrointestinal Disorders
Associated activity
Acuity of presentation
Acute Salicylate Toxicity
Cause: It may be accidental or intentional, but it can occur just one or several times, for example, after an overdose.
Symptoms Onset: Rapid, within a few hours.
Early Symptoms:
Action: Nausea, vomiting, tinnitus, dizziness, hyperventilation owing to respiratory alkalosis.
Progression: At higher levels of toxicity, patients may present with metabolic acidosis manifesting confusion, agitation and lethargy, seizures and coma.
Severity: In its lethal form, acute toxicity can produce severe toxic effect within hours and thus necessitate immediate physiological treatment.
Chronic Salicylate Toxicity:
Cause: Because of the frequent use of supratherapeutic doses over time, seen in elderly or patients with renal disease taking aspirin for chronic disorders.
Symptoms Onset: Progressive, sometimes difficult to diagnose at first sight.
Symptoms: Undefined consisting of; tiredness, abnormality in balance, poor concentration, lack of water, varying blood pH, and respiratory alkalosis but no apparent hyperventilation.
Progression: If undetected early it may contribute to worsened metabolic acidosis, change in mental health status, acute end-organ dysfunction.
 Severity: It may take a longer time for the symptoms to develop, and if diagnosed as something else, it may be fatal.
Differential Diagnoses
Sepsis
Methanol or Ethylene Glycol Poisoning
Iron Toxicity
Lactic Acidosis
Caffeine toxicity
Hydrocarbon toxicity
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Decontamination (if recent ingestion):
Activated Charcoal: In case the patient arrives in the health facility within one to 2 hours of ingesting the substance, then activated charcoal may be given to help prevent further absorption of the salicylates.
Gastric Lavage: This may be considered for very large or life threatening overdosages; however, this is less used at present.
Correction of Acidosis:
Alkalinization of Urine: The management of severe salicylate poisoning is the augmentation of the renal clearance rate of salicylates by alkalinization of the urine.
This is through giving Sodium Bicarbonate (IV) to help alkalinise the urine (urinal pH of 7.5-8). This increases the ionization of salicylates preventing their reabsorption across the renal tubules.
Continuous IV Fluids: Other fluids contain IV fluids which are normal saline or lactated ringer’s solution to ensure the kidney is functioning properly.
Hemodialysis:
Indications for Hemodialysis: High toxicity when salicylic acid concentrations are higher than 100 mg/dL and more than 300 mg/dL in chronic use.
Failure to improve despite alkalinization and supportive care.
Severe acidosis (pH <7.2) that does not respond to treatment.
Renal failure: Salicylates are efficiently dialysed out and acid-base derangement is also ameliorated in patients on haemodialysis.
Other Supportive Measures:
Correcting Electrolyte Imbalances: Metabolic acidosis and hypokalemia are common with salicylate poisoning and should be treated.
Monitoring Acid-Base Balance: The specific adverse effects may encompass both respiratory alkalosis owing to stimulation of the respiratory centre and metabolic acidosis resulting from inhibition of oxidative phosphorylation by salicylates.
Glucose Administration: In cases where hypoglycemia develops (often in children), glucose should be administered.
Cooling: Salicylate toxicity will result to hyperthermia (elevated body temperature).
Cooling measures, like cooling blankets, air-conditioned rooms, and cool fluids, may help prevent complications related to overheating.
Hydration: The policy of temperature control and humidity are important for a body temperature regulation, and its influence on the kidneys.
Oxygenation and Ventilation Fresh Air
Avoiding Triggers: Patients may have respiratory problems resulting from metabolic acidosis or respiratory alkalosis.
Electrolyte Balance:
Nutrient-Rich Environment: There could be severe effects like salicylic poisoning that can cause electrolyte imbalance such as hypokalaemia or hypoglycemia, having easy access to IV fluids, and electrolyte solutions may support the recovery process.
Psychosocial Environment
Calm and Low-Stress Setting: Stress or nervousness may worsen the condition. A peaceful, slow and non-stressful, and less noisy place possibly with care givers or psychiatrists attending to the patient can be advantageous to the patient.
Monitoring: Continuous monitoring and a safe environment can help detect changes in mental status or physical health, which can worsen toxicity symptoms.
Use of activated Charcoal in treating salicylate toxicity
Activated charcoal
In cases where the toxicity is identified at the first few hours of ingestion of the substance, activated charcoal can be given to help absorb the salicylate in the stomach.
Use of Sodium bicarbonate in treating salicylate toxicity
It is administrated intravenously is given to alkalinize the urinary tract by requiring more of the Salicylates to be expelled through the kidneys.
Sodium bicarbonate assist in the correction of metabolic acid base imbalance since it contains bicarbonate ion that neutralise excess hydrogen ion in the human body.
For severe cases of poisoning or when other methods cannot lower salicylate levels they are recommended.
It is particularly useful when serum salicylate concentrations are elevated and the patient either has renal dysfunction or is receiving intravenous NSAIDs.
Haemodialysis should be most helpful in situations of life-threatening toxicity as in coma, seizures or hypotensive patients, or high serum salicylate concentrations, commonly greater than 100 mg/dL.
As initial assessments, check temperature, pulse, respiration and salicylate levels (blood levels).
Decontamination: If the ingestion was not very long time ago (within last 1-2 hours), activated charcoal could be given for decrease of absorption.
Hydration: For fluid overload, IV fluids to maintain blood pressure and the kidney function and to increase elimination of salicylate.
Phase 2: Toxicity Phase
Supportive Care: Oxygen therapy, ventilation support if necessary.
Alkalinization: This may be done by use of sodium bicarbonate to alkalinise the urine, thus increase the clearance of salicylates.
Monitoring: Regular checking of salicylate level, blood gases, and electrolyte, particularly potassium level.
Phase 3: Critical Phase (Severe Toxicity):
Hemodialysis: In severe cases (e.g., when salicylate levels are very high or there is renal failure), hemodialysis is used to remove salicylates from the blood rapidly.
Correcting metabolic disturbances: Managing acidosis, electrolyte imbalances, and dehydration.
Phase 4: Recovery Stage
Maintenance of Ongoing Hydration and correction of electrolytes continues until the patient stabilizes. Discharge planning: The patient can be discharged once salicylate levels become normal and the patient is stabilized.
Salicylate poisoning may be defined as an ability of salicylic acid or other salicylate containing drugs to reach an increased serum level in the blood stream, results from an overdose of aspirin or other drugs containing salicylates. The derivative of salicylic acid is used for pain relief, anti-inflammatory effects and to reduce fever, but if taken in high doses can have several dangerous adverse effects. The toxicity may be either single bolus in large doses or cumulative toxicity with repeated use over time mainly in children, elderly or in patients with kidney or liver disease. The effect of salicylate is mainly on the respiratory, CNS and metabolic systems. It results to hyperventilation owing to respiratory centre stimulation and results in respiratory alkalosis at initial phase. At the later stages of toxicity, the metabolic acidosis sets in because of accumulation of various organic acids. This can either destabilise the acid base balance, normal fluid and electrolyte concentrations, or the production of catabolic energy substrates. They include signs like nausea, vomiting, tinnitus, headache, dizziness, lethargy, and confusion and more complicated ones like seizures and multi-organ dysfunction.
According to available data, in 2011 there were 30,000 reported cases of salicylate poisonings in the US with 39 fatalities. Altogether, the mortality was less than 0.01%; nonetheless, it reached 15% in individuals with severe toxicity. The complications increases if the diagnosis was not made on first assessment.
Stimulation of Neurons in the Brainstem Respiratory Centers:
salicylate poisoning directly affects the central respiratory chemoreceptors; medullary respiratory centre in the brain stem resulting into hyperventilation and respiratory alkalosis in the early stages. This causes increased COâ‚‚ excretion and initially lowers blood COâ‚‚ levels.
Metabolic Acidosis Uncoupling of Oxidative Phosphorylation:
It is established that salicylates inhibit the coupled oxidation phosphorylation and thus the energy generation through ATP and increases the generation of lactate. This results in lactic acidosis and plays a role in the development of the metabolic one as well.
There are other groups of toxic effects associated with salicylates. Salicylates stimulate lipolysis and increase levels of free fatty acids which are transformed into ketones that worsen metabolic acidosis.
Electrolyte and Acid-Base Imbalances:
It encompasses electrolyte and acid-base imbalance. In response to respiratory alkalosis, kidneys excrete bicarbonate, potassium and sodium, which may bring about hypokalemia as well as distort other electrolytes balances.
When acidosis increases due to lactate and ketoacidosis, compensation mechanisms can be overwhelmed and produce a condition that is a mixed respiratory alkalosis and metabolic acidosis.
CNS Effects:
Salicylates are lipid-soluble and can cross the blood-brain barrier, especially in high concentrations. This may breach the blood brain barrier and cause CNS toxicity particularly characterized by confusion, agitation, seizures and in the extreme by cerebral edema. Hyperthermia and Dehydration:
Since salicylates interfere with oxidative phosphorylation, their intake augments energy consumption and thermogenesis, relationship that cause hyperthermia.
Sweating intensifies dehydration and hyperventilation because both conditions are dehydrative.
Acute Ingestion:
Intentional Overdose: Mostly in intentional self-harm cases where a huge, bulk quantity is taken at once.
Unintentional Overdose: May happen in cases when a person gave himself an overdose, for instance, with aspirin, using the wrong dosage or mixing several products containing salicylates.
Chronic Use:
Repeated Use of Salicylates:
Therapeutic dosages become toxic if used for a long time and more so to elderly patients who have weak kidneys and patients with liver diseases.
Topical Absorption:
Topical Preparations: Acidosis may result from overuse of salicylate-containing topical ointments such as creams containing methyl salicylate or wintergreen oil.
Pediatric Exposure: Children are most vulnerable because even traces of wintergreen oil are poisonous given the fact that it is absorbed through the skin or ingested.
Metabolic Factors:
Renal Impairment: End stage renal disease delays renal elimination of salicylate and increases their concentration in the body.
Hepatic Impairment: The liver plays a key role in metabolizing salicylates; liver dysfunction can impair detoxification and exacerbate toxicity.
Acid-Base Imbalance Metabolic Acidosis:
Raised levels of the above parameters are associated with more severe symptoms and negative prognosis, especially acidosis which becomes progressively worse during the disease.
Anion Gap:
Rising values for anion gap point towards the build-up of acidic metabolites and a poor outcome.
Electrolyte Abnormalities:
Hypokalemia: Seen frequently in salicylate poisoning and make the acid base status worse and the condition of the patient poor. Hypernatremia: May be a consequence of dehydration caused by losses of fluids and aggravates signs of the CNS pathology.
Age Group:
Children (especially under 12 years): Salicylates are far more easily absorbed by young children than by adults, and therefore young children are far more vulnerable to the poisonous effects of salicylates.
Even a small amount of aspirin can lead to toxicity in small children due to their lower body mass and developing metabolism. This is also true in this group because accidental ingestion is the leading cause.
Teenagers and Young Adults: This age group may experience toxicity from intentional overdose usually in suicide attempts. Aspirin is easier to obtain; therefore, teenagers can be at a higher risk of an overdose of the medication.
Vital Signs
Tachypnea (Increased Respiratory Rate)
Tachycardia (Increased Heart Rate)
Hyperthermia (Elevated Body Temperature)
Hypotension
Neurological Signs
Confusion, Dizziness, Delirium
Tinnitus and Hearing Loss:
Altered Mental Status (Severe cases)
Respiratory System
Gastrointestinal Signs
Skin assessment
Chronic Kidney Disease (CKD)
Liver Disease
Asthma
Metabolic Acidosis
Gastrointestinal Disorders
Acute Salicylate Toxicity
Cause: It may be accidental or intentional, but it can occur just one or several times, for example, after an overdose.
Symptoms Onset: Rapid, within a few hours.
Early Symptoms:
Action: Nausea, vomiting, tinnitus, dizziness, hyperventilation owing to respiratory alkalosis.
Progression: At higher levels of toxicity, patients may present with metabolic acidosis manifesting confusion, agitation and lethargy, seizures and coma.
Severity: In its lethal form, acute toxicity can produce severe toxic effect within hours and thus necessitate immediate physiological treatment.
Chronic Salicylate Toxicity:
Cause: Because of the frequent use of supratherapeutic doses over time, seen in elderly or patients with renal disease taking aspirin for chronic disorders.
Symptoms Onset: Progressive, sometimes difficult to diagnose at first sight.
Symptoms: Undefined consisting of; tiredness, abnormality in balance, poor concentration, lack of water, varying blood pH, and respiratory alkalosis but no apparent hyperventilation.
Progression: If undetected early it may contribute to worsened metabolic acidosis, change in mental health status, acute end-organ dysfunction.
 Severity: It may take a longer time for the symptoms to develop, and if diagnosed as something else, it may be fatal.
Sepsis
Methanol or Ethylene Glycol Poisoning
Iron Toxicity
Lactic Acidosis
Caffeine toxicity
Hydrocarbon toxicity
Decontamination (if recent ingestion):
Activated Charcoal: In case the patient arrives in the health facility within one to 2 hours of ingesting the substance, then activated charcoal may be given to help prevent further absorption of the salicylates.
Gastric Lavage: This may be considered for very large or life threatening overdosages; however, this is less used at present.
Correction of Acidosis:
Alkalinization of Urine: The management of severe salicylate poisoning is the augmentation of the renal clearance rate of salicylates by alkalinization of the urine.
This is through giving Sodium Bicarbonate (IV) to help alkalinise the urine (urinal pH of 7.5-8). This increases the ionization of salicylates preventing their reabsorption across the renal tubules.
Continuous IV Fluids: Other fluids contain IV fluids which are normal saline or lactated ringer’s solution to ensure the kidney is functioning properly.
Hemodialysis:
Indications for Hemodialysis: High toxicity when salicylic acid concentrations are higher than 100 mg/dL and more than 300 mg/dL in chronic use.
Failure to improve despite alkalinization and supportive care.
Severe acidosis (pH <7.2) that does not respond to treatment.
Renal failure: Salicylates are efficiently dialysed out and acid-base derangement is also ameliorated in patients on haemodialysis.
Other Supportive Measures:
Correcting Electrolyte Imbalances: Metabolic acidosis and hypokalemia are common with salicylate poisoning and should be treated.
Monitoring Acid-Base Balance: The specific adverse effects may encompass both respiratory alkalosis owing to stimulation of the respiratory centre and metabolic acidosis resulting from inhibition of oxidative phosphorylation by salicylates.
Glucose Administration: In cases where hypoglycemia develops (often in children), glucose should be administered.
Emergency Medicine
Temperature Regulation
Cooling: Salicylate toxicity will result to hyperthermia (elevated body temperature).
Cooling measures, like cooling blankets, air-conditioned rooms, and cool fluids, may help prevent complications related to overheating.
Hydration: The policy of temperature control and humidity are important for a body temperature regulation, and its influence on the kidneys.
Oxygenation and Ventilation Fresh Air
Avoiding Triggers: Patients may have respiratory problems resulting from metabolic acidosis or respiratory alkalosis.
Electrolyte Balance:
Nutrient-Rich Environment: There could be severe effects like salicylic poisoning that can cause electrolyte imbalance such as hypokalaemia or hypoglycemia, having easy access to IV fluids, and electrolyte solutions may support the recovery process.
Psychosocial Environment
Calm and Low-Stress Setting: Stress or nervousness may worsen the condition. A peaceful, slow and non-stressful, and less noisy place possibly with care givers or psychiatrists attending to the patient can be advantageous to the patient.
Monitoring: Continuous monitoring and a safe environment can help detect changes in mental status or physical health, which can worsen toxicity symptoms.
Emergency Medicine
Activated charcoal
In cases where the toxicity is identified at the first few hours of ingestion of the substance, activated charcoal can be given to help absorb the salicylate in the stomach.
Emergency Medicine
It is administrated intravenously is given to alkalinize the urinary tract by requiring more of the Salicylates to be expelled through the kidneys.
Sodium bicarbonate assist in the correction of metabolic acid base imbalance since it contains bicarbonate ion that neutralise excess hydrogen ion in the human body.
Emergency Medicine
Hemodialysis:
For severe cases of poisoning or when other methods cannot lower salicylate levels they are recommended.
It is particularly useful when serum salicylate concentrations are elevated and the patient either has renal dysfunction or is receiving intravenous NSAIDs.
Haemodialysis should be most helpful in situations of life-threatening toxicity as in coma, seizures or hypotensive patients, or high serum salicylate concentrations, commonly greater than 100 mg/dL.
Emergency Medicine
Phase 1:
Early Phase (Acute Exposure) Assessment:
As initial assessments, check temperature, pulse, respiration and salicylate levels (blood levels).
Decontamination: If the ingestion was not very long time ago (within last 1-2 hours), activated charcoal could be given for decrease of absorption.
Hydration: For fluid overload, IV fluids to maintain blood pressure and the kidney function and to increase elimination of salicylate.
Phase 2: Toxicity Phase
Supportive Care: Oxygen therapy, ventilation support if necessary.
Alkalinization: This may be done by use of sodium bicarbonate to alkalinise the urine, thus increase the clearance of salicylates.
Monitoring: Regular checking of salicylate level, blood gases, and electrolyte, particularly potassium level.
Phase 3: Critical Phase (Severe Toxicity):
Hemodialysis: In severe cases (e.g., when salicylate levels are very high or there is renal failure), hemodialysis is used to remove salicylates from the blood rapidly.
Correcting metabolic disturbances: Managing acidosis, electrolyte imbalances, and dehydration.
Phase 4: Recovery Stage
Maintenance of Ongoing Hydration and correction of electrolytes continues until the patient stabilizes. Discharge planning: The patient can be discharged once salicylate levels become normal and the patient is stabilized.
Salicylate poisoning may be defined as an ability of salicylic acid or other salicylate containing drugs to reach an increased serum level in the blood stream, results from an overdose of aspirin or other drugs containing salicylates. The derivative of salicylic acid is used for pain relief, anti-inflammatory effects and to reduce fever, but if taken in high doses can have several dangerous adverse effects. The toxicity may be either single bolus in large doses or cumulative toxicity with repeated use over time mainly in children, elderly or in patients with kidney or liver disease. The effect of salicylate is mainly on the respiratory, CNS and metabolic systems. It results to hyperventilation owing to respiratory centre stimulation and results in respiratory alkalosis at initial phase. At the later stages of toxicity, the metabolic acidosis sets in because of accumulation of various organic acids. This can either destabilise the acid base balance, normal fluid and electrolyte concentrations, or the production of catabolic energy substrates. They include signs like nausea, vomiting, tinnitus, headache, dizziness, lethargy, and confusion and more complicated ones like seizures and multi-organ dysfunction.
According to available data, in 2011 there were 30,000 reported cases of salicylate poisonings in the US with 39 fatalities. Altogether, the mortality was less than 0.01%; nonetheless, it reached 15% in individuals with severe toxicity. The complications increases if the diagnosis was not made on first assessment.
Stimulation of Neurons in the Brainstem Respiratory Centers:
salicylate poisoning directly affects the central respiratory chemoreceptors; medullary respiratory centre in the brain stem resulting into hyperventilation and respiratory alkalosis in the early stages. This causes increased COâ‚‚ excretion and initially lowers blood COâ‚‚ levels.
Metabolic Acidosis Uncoupling of Oxidative Phosphorylation:
It is established that salicylates inhibit the coupled oxidation phosphorylation and thus the energy generation through ATP and increases the generation of lactate. This results in lactic acidosis and plays a role in the development of the metabolic one as well.
There are other groups of toxic effects associated with salicylates. Salicylates stimulate lipolysis and increase levels of free fatty acids which are transformed into ketones that worsen metabolic acidosis.
Electrolyte and Acid-Base Imbalances:
It encompasses electrolyte and acid-base imbalance. In response to respiratory alkalosis, kidneys excrete bicarbonate, potassium and sodium, which may bring about hypokalemia as well as distort other electrolytes balances.
When acidosis increases due to lactate and ketoacidosis, compensation mechanisms can be overwhelmed and produce a condition that is a mixed respiratory alkalosis and metabolic acidosis.
CNS Effects:
Salicylates are lipid-soluble and can cross the blood-brain barrier, especially in high concentrations. This may breach the blood brain barrier and cause CNS toxicity particularly characterized by confusion, agitation, seizures and in the extreme by cerebral edema. Hyperthermia and Dehydration:
Since salicylates interfere with oxidative phosphorylation, their intake augments energy consumption and thermogenesis, relationship that cause hyperthermia.
Sweating intensifies dehydration and hyperventilation because both conditions are dehydrative.
Acute Ingestion:
Intentional Overdose: Mostly in intentional self-harm cases where a huge, bulk quantity is taken at once.
Unintentional Overdose: May happen in cases when a person gave himself an overdose, for instance, with aspirin, using the wrong dosage or mixing several products containing salicylates.
Chronic Use:
Repeated Use of Salicylates:
Therapeutic dosages become toxic if used for a long time and more so to elderly patients who have weak kidneys and patients with liver diseases.
Topical Absorption:
Topical Preparations: Acidosis may result from overuse of salicylate-containing topical ointments such as creams containing methyl salicylate or wintergreen oil.
Pediatric Exposure: Children are most vulnerable because even traces of wintergreen oil are poisonous given the fact that it is absorbed through the skin or ingested.
Metabolic Factors:
Renal Impairment: End stage renal disease delays renal elimination of salicylate and increases their concentration in the body.
Hepatic Impairment: The liver plays a key role in metabolizing salicylates; liver dysfunction can impair detoxification and exacerbate toxicity.
Acid-Base Imbalance Metabolic Acidosis:
Raised levels of the above parameters are associated with more severe symptoms and negative prognosis, especially acidosis which becomes progressively worse during the disease.
Anion Gap:
Rising values for anion gap point towards the build-up of acidic metabolites and a poor outcome.
Electrolyte Abnormalities:
Hypokalemia: Seen frequently in salicylate poisoning and make the acid base status worse and the condition of the patient poor. Hypernatremia: May be a consequence of dehydration caused by losses of fluids and aggravates signs of the CNS pathology.
Age Group:
Children (especially under 12 years): Salicylates are far more easily absorbed by young children than by adults, and therefore young children are far more vulnerable to the poisonous effects of salicylates.
Even a small amount of aspirin can lead to toxicity in small children due to their lower body mass and developing metabolism. This is also true in this group because accidental ingestion is the leading cause.
Teenagers and Young Adults: This age group may experience toxicity from intentional overdose usually in suicide attempts. Aspirin is easier to obtain; therefore, teenagers can be at a higher risk of an overdose of the medication.
Vital Signs
Tachypnea (Increased Respiratory Rate)
Tachycardia (Increased Heart Rate)
Hyperthermia (Elevated Body Temperature)
Hypotension
Neurological Signs
Confusion, Dizziness, Delirium
Tinnitus and Hearing Loss:
Altered Mental Status (Severe cases)
Respiratory System
Gastrointestinal Signs
Skin assessment
Chronic Kidney Disease (CKD)
Liver Disease
Asthma
Metabolic Acidosis
Gastrointestinal Disorders
Acute Salicylate Toxicity
Cause: It may be accidental or intentional, but it can occur just one or several times, for example, after an overdose.
Symptoms Onset: Rapid, within a few hours.
Early Symptoms:
Action: Nausea, vomiting, tinnitus, dizziness, hyperventilation owing to respiratory alkalosis.
Progression: At higher levels of toxicity, patients may present with metabolic acidosis manifesting confusion, agitation and lethargy, seizures and coma.
Severity: In its lethal form, acute toxicity can produce severe toxic effect within hours and thus necessitate immediate physiological treatment.
Chronic Salicylate Toxicity:
Cause: Because of the frequent use of supratherapeutic doses over time, seen in elderly or patients with renal disease taking aspirin for chronic disorders.
Symptoms Onset: Progressive, sometimes difficult to diagnose at first sight.
Symptoms: Undefined consisting of; tiredness, abnormality in balance, poor concentration, lack of water, varying blood pH, and respiratory alkalosis but no apparent hyperventilation.
Progression: If undetected early it may contribute to worsened metabolic acidosis, change in mental health status, acute end-organ dysfunction.
 Severity: It may take a longer time for the symptoms to develop, and if diagnosed as something else, it may be fatal.
Sepsis
Methanol or Ethylene Glycol Poisoning
Iron Toxicity
Lactic Acidosis
Caffeine toxicity
Hydrocarbon toxicity
Decontamination (if recent ingestion):
Activated Charcoal: In case the patient arrives in the health facility within one to 2 hours of ingesting the substance, then activated charcoal may be given to help prevent further absorption of the salicylates.
Gastric Lavage: This may be considered for very large or life threatening overdosages; however, this is less used at present.
Correction of Acidosis:
Alkalinization of Urine: The management of severe salicylate poisoning is the augmentation of the renal clearance rate of salicylates by alkalinization of the urine.
This is through giving Sodium Bicarbonate (IV) to help alkalinise the urine (urinal pH of 7.5-8). This increases the ionization of salicylates preventing their reabsorption across the renal tubules.
Continuous IV Fluids: Other fluids contain IV fluids which are normal saline or lactated ringer’s solution to ensure the kidney is functioning properly.
Hemodialysis:
Indications for Hemodialysis: High toxicity when salicylic acid concentrations are higher than 100 mg/dL and more than 300 mg/dL in chronic use.
Failure to improve despite alkalinization and supportive care.
Severe acidosis (pH <7.2) that does not respond to treatment.
Renal failure: Salicylates are efficiently dialysed out and acid-base derangement is also ameliorated in patients on haemodialysis.
Other Supportive Measures:
Correcting Electrolyte Imbalances: Metabolic acidosis and hypokalemia are common with salicylate poisoning and should be treated.
Monitoring Acid-Base Balance: The specific adverse effects may encompass both respiratory alkalosis owing to stimulation of the respiratory centre and metabolic acidosis resulting from inhibition of oxidative phosphorylation by salicylates.
Glucose Administration: In cases where hypoglycemia develops (often in children), glucose should be administered.
Emergency Medicine
Temperature Regulation
Cooling: Salicylate toxicity will result to hyperthermia (elevated body temperature).
Cooling measures, like cooling blankets, air-conditioned rooms, and cool fluids, may help prevent complications related to overheating.
Hydration: The policy of temperature control and humidity are important for a body temperature regulation, and its influence on the kidneys.
Oxygenation and Ventilation Fresh Air
Avoiding Triggers: Patients may have respiratory problems resulting from metabolic acidosis or respiratory alkalosis.
Electrolyte Balance:
Nutrient-Rich Environment: There could be severe effects like salicylic poisoning that can cause electrolyte imbalance such as hypokalaemia or hypoglycemia, having easy access to IV fluids, and electrolyte solutions may support the recovery process.
Psychosocial Environment
Calm and Low-Stress Setting: Stress or nervousness may worsen the condition. A peaceful, slow and non-stressful, and less noisy place possibly with care givers or psychiatrists attending to the patient can be advantageous to the patient.
Monitoring: Continuous monitoring and a safe environment can help detect changes in mental status or physical health, which can worsen toxicity symptoms.
Emergency Medicine
Activated charcoal
In cases where the toxicity is identified at the first few hours of ingestion of the substance, activated charcoal can be given to help absorb the salicylate in the stomach.
Emergency Medicine
It is administrated intravenously is given to alkalinize the urinary tract by requiring more of the Salicylates to be expelled through the kidneys.
Sodium bicarbonate assist in the correction of metabolic acid base imbalance since it contains bicarbonate ion that neutralise excess hydrogen ion in the human body.
Emergency Medicine
Hemodialysis:
For severe cases of poisoning or when other methods cannot lower salicylate levels they are recommended.
It is particularly useful when serum salicylate concentrations are elevated and the patient either has renal dysfunction or is receiving intravenous NSAIDs.
Haemodialysis should be most helpful in situations of life-threatening toxicity as in coma, seizures or hypotensive patients, or high serum salicylate concentrations, commonly greater than 100 mg/dL.
Emergency Medicine
Phase 1:
Early Phase (Acute Exposure) Assessment:
As initial assessments, check temperature, pulse, respiration and salicylate levels (blood levels).
Decontamination: If the ingestion was not very long time ago (within last 1-2 hours), activated charcoal could be given for decrease of absorption.
Hydration: For fluid overload, IV fluids to maintain blood pressure and the kidney function and to increase elimination of salicylate.
Phase 2: Toxicity Phase
Supportive Care: Oxygen therapy, ventilation support if necessary.
Alkalinization: This may be done by use of sodium bicarbonate to alkalinise the urine, thus increase the clearance of salicylates.
Monitoring: Regular checking of salicylate level, blood gases, and electrolyte, particularly potassium level.
Phase 3: Critical Phase (Severe Toxicity):
Hemodialysis: In severe cases (e.g., when salicylate levels are very high or there is renal failure), hemodialysis is used to remove salicylates from the blood rapidly.
Correcting metabolic disturbances: Managing acidosis, electrolyte imbalances, and dehydration.
Phase 4: Recovery Stage
Maintenance of Ongoing Hydration and correction of electrolytes continues until the patient stabilizes. Discharge planning: The patient can be discharged once salicylate levels become normal and the patient is stabilized.
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