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Salicylate Poisoning: Signs, Symptoms, and Treatment, Slides of Pathophysiology

National Defense University (NDU)Pathophysiology

An in-depth analysis of salicylate poisoning, its causes, pathophysiology, and effects on various organ systems. It covers the acid-base status, respiratory system, glucose metabolism, fluid and electrolyte balance, central nervous system, gastrointestinal tract, hepatic effects, hematologic effects, musculoskeletal effects, clinical and laboratory manifestations, and medical care. It also includes information on lab studies and treatment principles.

Typology: Slides

2021/2022

Uploaded on 09/12/2022

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Salicylate (Aspirin) Ingestion
California Poison Control 1-800-876-4766
Background
1. The prevalence of aspirin-containing analgesic products makes
these agents, found in virtually every household, common sources
of both accidental and suicidal ingestion
2. Aspirin or aspirin-equivalent preparations (in milligrams):
a. Children’s aspirin (80-mg tablets with 36 tablets per bottle)
b. Adult aspirin (325-mg tablets)
c. Methyl salicylate (e.g., oil of wintergreen) (98% salicylate)
d. Pepto-Bismol (236 mg of nonaspirin salicylate per 15 mL)
Pathophysiology
1. Salicylates directly or indirectly affect most organ systems in the
body by uncoupling oxidative phosphorylation, inhibiting Krebs
cycle enzymes, and inhibiting amino acid synthesis
Acid-Base Status
1. Salicylates stimulate the respiratory center, leading to
hyperventilation and respiratory alkalosis
2. Salicylates also interfere with the Krebs cycle, limit production of
ATP, and increase lactate production, leading to ketosis and a wide
anion-gap metabolic acidosis
3. Adult patients who are acutely poisoned usually present with a
mixed respiratory alkalosis and metabolic acidosis
4. Respiratory alkalosis may be transient in children so that metabolic
acidosis may occur early in the course
5. Patients with mixed acid-base disturbances have been found to have
normal anion-gap metabolic acidosis; therefore, normal anion-gap
acidosis does not exclude salicylate
Respiratory System Effects
1. A salicylate level of 35 mg/dL or higher causes increases in both rate
(tachypnea) and depth (hyperpnea)
2. Salicylate poisoning may cause noncardiogenic pulmonary edema
3. Although the exact etiology is not known, hypoxia is considered a
major factor
Glucose Metabolism
1. Increased cellular metabolic activity due to uncoupling of oxidative
phosphorylation may produce clinical hypoglycemia, even though
the serum glucose levels are within reference range
2. As intracellular glucose is depleted, the salicylate may produce
discordance between levels of plasma and cerebrospinal fluid (CSF)
glucose
Fluid and Electrolyte Effects
1. Salicylate poisoning may result in dehydration because of increased
gastrointestinal tract losses (vomiting) and insensible fluid losses
(hyperpnea and hyperthermia)
2. All patients with serious poisoning are more than 5-10% dehydrated
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Salicylate (Aspirin) Ingestion

California Poison Control 1-800-876- Background

  1. The prevalence of aspirin-containing analgesic products makes these agents, found in virtually every household, common sources of both accidental and suicidal ingestion
  2. Aspirin or aspirin-equivalent preparations (in milligrams): a. Children’s aspirin (80-mg tablets with 36 tablets per bottle) b. Adult aspirin (325-mg tablets) c. Methyl salicylate (e.g., oil of wintergreen) (98% salicylate) d. Pepto-Bismol (236 mg of nonaspirin salicylate per 15 mL) Pathophysiology
  3. Salicylates directly or indirectly affect most organ systems in the body by uncoupling oxidative phosphorylation, inhibiting Krebs cycle enzymes, and inhibiting amino acid synthesis Acid-Base Status
  4. Salicylates stimulate the respiratory center, leading to hyperventilation and respiratory alkalosis
  5. Salicylates also interfere with the Krebs cycle, limit production of ATP, and increase lactate production, leading to ketosis and a wide anion-gap metabolic acidosis
  6. Adult patients who are acutely poisoned usually present with a mixed respiratory alkalosis and metabolic acidosis
  7. Respiratory alkalosis may be transient in children so that metabolic acidosis may occur early in the course
  8. Patients with mixed acid-base disturbances have been found to have normal anion-gap metabolic acidosis; therefore, normal anion-gap acidosis does not exclude salicylate Respiratory System Effects
  9. A salicylate level of 35 mg/dL or higher causes increases in both rate (tachypnea) and depth (hyperpnea)
  10. Salicylate poisoning may cause noncardiogenic pulmonary edema
  11. Although the exact etiology is not known, hypoxia is considered a major factor Glucose Metabolism
  12. Increased cellular metabolic activity due to uncoupling of oxidative phosphorylation may produce clinical hypoglycemia, even though the serum glucose levels are within reference range
  13. As intracellular glucose is depleted, the salicylate may produce discordance between levels of plasma and cerebrospinal fluid (CSF) glucose Fluid and Electrolyte Effects
  14. Salicylate poisoning may result in dehydration because of increased gastrointestinal tract losses (vomiting) and insensible fluid losses (hyperpnea and hyperthermia)
  15. All patients with serious poisoning are more than 5-10% dehydrated
  1. Renal clearance of salicylate is decreased by dehydration
  2. Hypokalemia and hypocalcemia can occur as a result of primary respiratory alkalosis Central Nervous System Effects
  3. Salicylates are neurotoxic, which is manifested as tinnitus, and ingestion can lead to hearing loss at doses of 20-45 mg/dL or higher
  4. CNS toxicity is related to the amount of drug bound to CNS tissue
  5. Other signs and symptoms include nausea, vomiting, hyperpnea, and lethargy, which can progress to disorientation, seizures, cerebral edema, hyperthermia, coma, and, eventually, death Gastrointestinal Tract Effects
  6. Nausea and vomiting are the most common effects
  7. Pylorospasm and decreased GI tract motility can occur with large doses Hepatic Effects
  8. Hepatitis can occur in children ingesting doses at or above 30. mg/dL
  9. Reye syndrome is another form of pediatric salicylate-induced hepatic disease characterized by nausea, vomiting, hypoglycemia, elevated levels of liver enzymes, fatty infiltration of liver, and coma Hematologic Effects
  10. Hypoprothrombinemia and platelet dysfunction are the most common effects
  11. Bleeding also may be promoted either by inhibition of vitamin K– dependent enzymes or by the formation of thromboxane A 2 Musculoskeletal effects
  12. Rhabdomyolysis can occur because of dissipation of heat and energy resulting from oxidative phosphorylation uncoupling
  13. Rhabdomyolysis- the destruction or degeneration of skeletal muscle tissue that is accompanied by the release of muscle cell contents (as myoglobin and potassium) into the bloodstream resulting in hypovolemia, hyperkalemia, and sometimes acute renal failure Clinical and Laboratory Manifestations
  14. Phase 1 a. Hyperventilation resulting from direct respiratory center stimulation, leading to respiratory alkalosis and compensatory alkaluria b. Both potassium and sodium bicarbonate are excreted in the urine c. May last as long as 12 hours
  15. Phase 2 a. Paradoxic aciduria in the presence of continued respiratory alkalosis occurs when sufficient potassium has been lost from the kidneys b. May begin within hours and may last 12-24 hours
  16. Phase 3

a. Serum electrolyte renal function studies (BUN and creatinine levels), Serum glucose levels, Serum acetaminophen levels, Liver function tests, Coagulation studies (prothrombin time and activated partial thromboplastin time), Urinalysis Medical Care

  1. California Poison Control 1-800-876-
  2. Principles of treatment include limiting absorption, enhancing elimination, correcting metabolic abnormalities, and providing supportive care
  3. No specific antidote is available for salicylates
  4. Gastrointestinal tract decontamination a. Initial treatment should include the use of oral activated charcoal, especially if the patient presents within 1 hour of ingestion b. Activated charcoal can limit further gut absorption by binding to the available salicylates c. Recommended initial dose of activated charcoal is 1-2 g/kg d. Some authorities may recommend performing gastric lavage in all symptomatic patients regardless of time of ingestion
  5. Urinary alkalization a. Renal excretion of salicylic acid depends on urinary pH b. Increasing the urine pH to 7.5 prevents reabsorption of salicylic acid from the urine c. Since acidosis facilitates transfer of salicylate into tissues, especially in the brain, it must be treated aggressively by raising blood pH higher than brain pH, thereby shifting the equilibrium from the tissues to the plasma d. Concomitant alkalinization of blood and urine keeps salicylates away from brain tissue and in the blood, in addition to enhancing urinary excretion e. When the urine pH increases to 8 from 5, renal clearance of salicylate increases 10-20 times f. Hypokalemia and dehydration limit the effectiveness of urine alkalization g. Urinary alkalization should be continued at least until serum salicylate levels decrease into the therapeutic range (< mg/dL)
  6. Hemodialysis a. Rapid salicylate elimination is required if the patient is very ill with salicylate poisoning, has a very high salicylate level (eg, >90-100 mg/dL after acute overdose or >40-50 mg/dL in long- term toxicity), has severe fluid or electrolyte disturbances, or is unable to eliminate the salicylate b. Although hemoperfusion has a slightly higher rate of drug clearance than hemodialysis, dialysis is recommended

because of its ability both to correct for fluid and electrolyte disorders and to remove salicylates c. Peritoneal dialysis is only 10-25% as efficient as hemoperfusion or hemodialysis and not even as efficient as renal excretion