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Salicylate Poisoning
Dr. VIVEK BENJAMIN
Salicylates
• Derivatives of Salicylic acid
• Acetyl Saliclic acid.
• Sodium Salicylate.
• Methyl Salicylate.
WILLOW TREE
SALICYLIC ACID AKA Orthohydroxy Benzoic
Acid
• Hoffman, a chemist at Bayer Company first synthesised acetyl salicylic
acid in the laboratory in 1897.
• ASPIRIN was coined in 1899.
Uses :
1. Sodium salicylate and acetyl salicylic acid:
a)Antipyretic
b)Analgesic
c) Antiplatelet
2. Para Amino Salicylic acid : A second line drug in treating Tuberculosis.
3. Bismuth Salicylate : Traveller’s Diarrhoea.
Uses :
4. New Derivatives :
a) Mesalamine (5 ASA) – Used in IBD.
b) Diflunisal - difluorophenyl derivative of salicylic acid more potent
than aspirin in the treatment of musculoskeletal sprains and
osteoarthritis.
c) Benorylate - ester of aspirin and paracetamol with less incidence of
gastric irritation and bleeding.
Uses :
5. Locally acting salicylates :
a) Salicylic acid is a keratolytic agent.
b) Methyl salicylate is also used as a flavouring agent for candy.
c) Homomenthyl salicylate (homosalate) is a sunscreen agent.
d) Trolamine salicylate cream is used in the management of
osteoarthritis
Toxicokinetics
• Salicylates are rapidly absorbed from the stomach and intact Skin.
• Salicylates distribute well into plasma, saliva, milk, and spinal,
peritoneal and synovial fluid and into body tissues including kidney,
liver, lung and heart.
• Metabolism occurs chiefly in the liver-
broken down into salicyluric acid, ether glucoronide, ester
glucoronide, and gentisic acid and Excreated In urine.
Pathophysiology of salicylate toxicity
1. CNS disturbance.
2. Metabolic disturbance.
3. Respiratory system disturbance.
4. CVS disturbance.
5. GIT disturbance.
6. Hematological disturbance.
7. Musculoskeletal
PATHOPHYSIOLOGY
A. CENTRAL NERVOUS SYSTEM
1) Increased central respiratory drive:Mechanism unclear.
Likely explanation may be the direct stimulation of medullary regulatory activity.
Hyperventilation predominates early in the course of salicylate toxicity resulting in
respiratory alkalosis,decreased ionized calcium, and compensatory renal excretion of
potassium, sodium, and bicarbonate.
2) Seizures and coma Etiology:
As glucose utilization increases, a decrease in brain glucose concentrations may occur
producing a relative CNS hypoglycemia despite normal blood glucose concentrations.
B. METABOLIC:
• Uncoupling of oxidative phosphorylation leads to a disruption in
cellular metabolism due to the interference of the Kreb’s cycle
and impaired carbohydrate and lipid metabolism.
• Substrates are metabolized but the energy produced is dissipated
as heat instead of being used to produce adenosine triphosphate
(ATP).
• The basal metabolic rate increases, placing increased demands on
the cardiorespiratory system.
• Excess lactic acid results from nonmitochondrial ATP production.
Disrupted cellular metabolism produces:
1. Increased oxygen consumption; compensatory increase in heart rate.
(tachycardia)
2. Increased CO2 production due to abnormal cellular respiration.
(hypercapnea)
3. Increased heat production (hyperthermia)
4. Patient’s commonly present with hyperglycemia but increased
glucose utilization, impaired glucose production, and eventually
reduced tissue glucose concentrations may lead to (hypoglycemia)
5. Increased production of organic acids (metabolic acidosis)
Respiratory system Disturbance
• Tachypnea & hyperpnea.
• Non cardiogenic pulmonary edema.
• Acute lung injury.
• Hypoxia.
CVS Disturbance
• Tachycardia
• Hypotension
• Dysrhythmias - Eg, ventricular tachycardia, ventricular fibrillation,
multiple premature ventricular contractions
• Asystole - With severe intoxication
• Electrocardiogram (ECG) abnormalities - Eg, U waves, flattened T
waves, QT prolongation; may reflect hypokalemia
GIT Disturbance
• Nausea & Vomiting.
• Abdominal pain.
• Bleeding.
• Intestinal perforation.
• Pancreatitis.
• Hepatitis.
• Pylorospasm, decreased GI tract motility, and bezoar formation can
occur with large doses.
Hematological Disturbance
• Hypoprothrombinemia
• Platelet dysfunction
• Inhibition of vitamin K–dependent enzymes
• Inhibition of thromboxane A2
Musculoskeletal Disturbance
• Rhabdomyolysis
Diagnosis
History :
• Amount
• Approximate time of ingestion
• Possibility of long-term ingestion
• Potential co-ingestants
• Presence of other medical conditions (eg, cardiac, renal diseases)
Physical examination:
• Vital signs.
• CVS
• Chest
• Abdomen
• CNS
Laboratory markers:
• Serum salicylate:
Low serum levels early after acute ingestion do not preclude toxicity .
Levels should be obtained every 2 hours until a decrease is noted on two
consecutive measurements.
• Acute ingestions of non–enteric-coated aspirin should result in peak serum
levels by 6 hours after ingestion. A delayed increase may be seen in patients
with a salicylate pharmacobezoar , patients who have ingested enteric-coated or
sustained-released products (due to delayed absorption), and patients with
worsening acidosis.
• Acute toxicity, levels ranging from 31 to 100 mg/dL
• Chronic toxicity, toxic levels may be as low as 30 to 40 mg/dL
Urinalysis:
• PH.
• ketones.
• Glucose.
• 10% ferric chloride test (100% sensitive, 71%specific)
Blood glucose:
• Hypoglycemia
• Normal
• Hyperglycemia
Urea & Electrolytes:
• Hypokalemia.
• Hyponatremia.
• Urea & Creatinine - Elevated.
• ABG
• CXR
• ECG
• Abdominal imaging:
- Suspicion of aspirin concretion & pharmacobezoar- US, CT,
Endoscopy.
• Hepatic, hematologic, and coagulation profiles - Obtain for patients
with clinical evidence of moderate to severe toxicity
.
Treatment
1. Fluid resuscitation :
Correction of dehydration with 0.9% sodium chloride or lactated Ringer
solution,
• 10 to 20 mL/kg/h over 1 to 2 hours until a good urine flow is
established of at least
2 to 3 mL/kg/h
2. GI decontamination:
Gastric lavage in the first hr (warmed NS 38C,protect airway) Activated
charcoal in the first 4 hr, 1-2g/kg (maximum 100g) Whole-bowel
irrigation (WBI) with polyethylene glycol{enteric coated or slow release
formulas, 2 L/h (20 mL/kg/h) until the rectal effluent is clear}
3. Urinary alkalinization with sodium bicarbonate: Moderate to severe
toxicity.
• 1 to 2 mEq/kg of sodium bicarbonate IV bolus, then infusion of DW5% with
100 to 150 mEq of sodium bicarbonate and 20 to 40 mEq of potassium
chloride in each liter at a rate of 1.5 to 2.5 mL/kg/h.Goal urine output is 2
to 3 mL/kg/h.
4. Hemodialysis:
• Management of patients with salicylate poisoning and a serum salicylate
level >100 mg/dL after acute ingestion or >40 mg/dL after chronic
ingestion, altered mental status, renal failure, pulmonary edema,
progressive clinical deterioration, refractory acidosis, or failure to respond
to more conservative therapy.
Prognosis
• The prognosis in patients with acute salicylate poisoning is very good:
the mortality rate is 1%, and the morbidity rate is 16% The prognosis
is worse in patients with chronic salicylate poisoning: the mortality
rate is 25%, and the morbidity rate is 30%
Refrences
1.The American Association of Poison Control Centers ,Chyka PA, Erdman AR, Christianson G,
et al. Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital
management . Clin Toxicol (Phila). 2007;45:95-131
2. The American Academy of Clinical Toxicology and the European Association of Poisons
Centres and Clinical Toxicologists ,Vale JA, Kulig K; American Academy of Clinical
Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position
paper: gastric lavage . J Toxicol Clin Toxicol. 2004;42:933-43 Position paper: whole bowel
irrigation . J Toxicol Clin Toxicol. 2004;42:843-54 Proudfoot AT, Krenzelok EP, Vale
JA. Position paper on urine alkalinization . J Toxicol Clin Toxicol. 2004;42:1-26
3.Supplement to Emergency Medicine Reports, January 17, 2011: “Aspirin Overdose.” Author:
Marc S. Lampell, MD, Associate Professor, Pediatric Emergency Medicine, University of
Rochester, NY.Emergency Medicine Reports’ “Rapid Access Guidelines.” Copyright © 2011
AHC Media, a division of Thompson Media Group LLC, Atlanta, GA. Editors: Sandra M.
Schneider, MD, FACEP, and J. Stephan Stapczynski, MD. Executive Editor: Russ Underwood.
Specialty Editor: Shelly Morrow Mark. F
Salicylate poisoning

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Salicylate poisoning

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  • 7. Salicylates • Derivatives of Salicylic acid • Acetyl Saliclic acid. • Sodium Salicylate. • Methyl Salicylate. WILLOW TREE
  • 8. SALICYLIC ACID AKA Orthohydroxy Benzoic Acid • Hoffman, a chemist at Bayer Company first synthesised acetyl salicylic acid in the laboratory in 1897. • ASPIRIN was coined in 1899.
  • 9. Uses : 1. Sodium salicylate and acetyl salicylic acid: a)Antipyretic b)Analgesic c) Antiplatelet 2. Para Amino Salicylic acid : A second line drug in treating Tuberculosis. 3. Bismuth Salicylate : Traveller’s Diarrhoea.
  • 10. Uses : 4. New Derivatives : a) Mesalamine (5 ASA) – Used in IBD. b) Diflunisal - difluorophenyl derivative of salicylic acid more potent than aspirin in the treatment of musculoskeletal sprains and osteoarthritis. c) Benorylate - ester of aspirin and paracetamol with less incidence of gastric irritation and bleeding.
  • 11. Uses : 5. Locally acting salicylates : a) Salicylic acid is a keratolytic agent. b) Methyl salicylate is also used as a flavouring agent for candy. c) Homomenthyl salicylate (homosalate) is a sunscreen agent. d) Trolamine salicylate cream is used in the management of osteoarthritis
  • 12. Toxicokinetics • Salicylates are rapidly absorbed from the stomach and intact Skin. • Salicylates distribute well into plasma, saliva, milk, and spinal, peritoneal and synovial fluid and into body tissues including kidney, liver, lung and heart. • Metabolism occurs chiefly in the liver- broken down into salicyluric acid, ether glucoronide, ester glucoronide, and gentisic acid and Excreated In urine.
  • 13. Pathophysiology of salicylate toxicity 1. CNS disturbance. 2. Metabolic disturbance. 3. Respiratory system disturbance. 4. CVS disturbance. 5. GIT disturbance. 6. Hematological disturbance. 7. Musculoskeletal
  • 14. PATHOPHYSIOLOGY A. CENTRAL NERVOUS SYSTEM 1) Increased central respiratory drive:Mechanism unclear. Likely explanation may be the direct stimulation of medullary regulatory activity. Hyperventilation predominates early in the course of salicylate toxicity resulting in respiratory alkalosis,decreased ionized calcium, and compensatory renal excretion of potassium, sodium, and bicarbonate. 2) Seizures and coma Etiology: As glucose utilization increases, a decrease in brain glucose concentrations may occur producing a relative CNS hypoglycemia despite normal blood glucose concentrations.
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  • 16. B. METABOLIC: • Uncoupling of oxidative phosphorylation leads to a disruption in cellular metabolism due to the interference of the Kreb’s cycle and impaired carbohydrate and lipid metabolism. • Substrates are metabolized but the energy produced is dissipated as heat instead of being used to produce adenosine triphosphate (ATP). • The basal metabolic rate increases, placing increased demands on the cardiorespiratory system. • Excess lactic acid results from nonmitochondrial ATP production.
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  • 19. Disrupted cellular metabolism produces: 1. Increased oxygen consumption; compensatory increase in heart rate. (tachycardia) 2. Increased CO2 production due to abnormal cellular respiration. (hypercapnea) 3. Increased heat production (hyperthermia) 4. Patient’s commonly present with hyperglycemia but increased glucose utilization, impaired glucose production, and eventually reduced tissue glucose concentrations may lead to (hypoglycemia) 5. Increased production of organic acids (metabolic acidosis)
  • 20. Respiratory system Disturbance • Tachypnea & hyperpnea. • Non cardiogenic pulmonary edema. • Acute lung injury. • Hypoxia.
  • 21. CVS Disturbance • Tachycardia • Hypotension • Dysrhythmias - Eg, ventricular tachycardia, ventricular fibrillation, multiple premature ventricular contractions • Asystole - With severe intoxication • Electrocardiogram (ECG) abnormalities - Eg, U waves, flattened T waves, QT prolongation; may reflect hypokalemia
  • 22. GIT Disturbance • Nausea & Vomiting. • Abdominal pain. • Bleeding. • Intestinal perforation. • Pancreatitis. • Hepatitis. • Pylorospasm, decreased GI tract motility, and bezoar formation can occur with large doses.
  • 23. Hematological Disturbance • Hypoprothrombinemia • Platelet dysfunction • Inhibition of vitamin K–dependent enzymes • Inhibition of thromboxane A2
  • 25. Diagnosis History : • Amount • Approximate time of ingestion • Possibility of long-term ingestion • Potential co-ingestants • Presence of other medical conditions (eg, cardiac, renal diseases) Physical examination: • Vital signs. • CVS • Chest • Abdomen • CNS
  • 26. Laboratory markers: • Serum salicylate: Low serum levels early after acute ingestion do not preclude toxicity . Levels should be obtained every 2 hours until a decrease is noted on two consecutive measurements. • Acute ingestions of non–enteric-coated aspirin should result in peak serum levels by 6 hours after ingestion. A delayed increase may be seen in patients with a salicylate pharmacobezoar , patients who have ingested enteric-coated or sustained-released products (due to delayed absorption), and patients with worsening acidosis. • Acute toxicity, levels ranging from 31 to 100 mg/dL • Chronic toxicity, toxic levels may be as low as 30 to 40 mg/dL
  • 27. Urinalysis: • PH. • ketones. • Glucose. • 10% ferric chloride test (100% sensitive, 71%specific) Blood glucose: • Hypoglycemia • Normal • Hyperglycemia Urea & Electrolytes: • Hypokalemia. • Hyponatremia. • Urea & Creatinine - Elevated.
  • 28. • ABG • CXR • ECG • Abdominal imaging: - Suspicion of aspirin concretion & pharmacobezoar- US, CT, Endoscopy. • Hepatic, hematologic, and coagulation profiles - Obtain for patients with clinical evidence of moderate to severe toxicity .
  • 29. Treatment 1. Fluid resuscitation : Correction of dehydration with 0.9% sodium chloride or lactated Ringer solution, • 10 to 20 mL/kg/h over 1 to 2 hours until a good urine flow is established of at least 2 to 3 mL/kg/h 2. GI decontamination: Gastric lavage in the first hr (warmed NS 38C,protect airway) Activated charcoal in the first 4 hr, 1-2g/kg (maximum 100g) Whole-bowel irrigation (WBI) with polyethylene glycol{enteric coated or slow release formulas, 2 L/h (20 mL/kg/h) until the rectal effluent is clear}
  • 30. 3. Urinary alkalinization with sodium bicarbonate: Moderate to severe toxicity. • 1 to 2 mEq/kg of sodium bicarbonate IV bolus, then infusion of DW5% with 100 to 150 mEq of sodium bicarbonate and 20 to 40 mEq of potassium chloride in each liter at a rate of 1.5 to 2.5 mL/kg/h.Goal urine output is 2 to 3 mL/kg/h. 4. Hemodialysis: • Management of patients with salicylate poisoning and a serum salicylate level >100 mg/dL after acute ingestion or >40 mg/dL after chronic ingestion, altered mental status, renal failure, pulmonary edema, progressive clinical deterioration, refractory acidosis, or failure to respond to more conservative therapy.
  • 31. Prognosis • The prognosis in patients with acute salicylate poisoning is very good: the mortality rate is 1%, and the morbidity rate is 16% The prognosis is worse in patients with chronic salicylate poisoning: the mortality rate is 25%, and the morbidity rate is 30%
  • 32. Refrences 1.The American Association of Poison Control Centers ,Chyka PA, Erdman AR, Christianson G, et al. Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital management . Clin Toxicol (Phila). 2007;45:95-131 2. The American Academy of Clinical Toxicology and the European Association of Poisons Centres and Clinical Toxicologists ,Vale JA, Kulig K; American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: gastric lavage . J Toxicol Clin Toxicol. 2004;42:933-43 Position paper: whole bowel irrigation . J Toxicol Clin Toxicol. 2004;42:843-54 Proudfoot AT, Krenzelok EP, Vale JA. Position paper on urine alkalinization . J Toxicol Clin Toxicol. 2004;42:1-26 3.Supplement to Emergency Medicine Reports, January 17, 2011: “Aspirin Overdose.” Author: Marc S. Lampell, MD, Associate Professor, Pediatric Emergency Medicine, University of Rochester, NY.Emergency Medicine Reports’ “Rapid Access Guidelines.” Copyright © 2011 AHC Media, a division of Thompson Media Group LLC, Atlanta, GA. Editors: Sandra M. Schneider, MD, FACEP, and J. Stephan Stapczynski, MD. Executive Editor: Russ Underwood. Specialty Editor: Shelly Morrow Mark. F