Poisoning, Overdose and Antidotes

Central Nervous System and Metabolic Toxidromes: Opioids, Acetaminophen, and Salicylates

In the intensive care unit, rapid identification of classic toxidromes prevents catastrophic respiratory and metabolic decompensation. The classic opioid overdose toxidrome consists of central nervous system depression, miosis, and hypoventilation leading to respiratory acidosis. Naloxone is a competitive mu-opioid receptor antagonist that rapidly restores spontaneous ventilation in opioid toxicity. However, opioid effects may outlast naloxone, particularly after long-acting opioid ingestion or substantial exposure to potent synthetic opioids. The critical care nurse must reassess ventilation frequently and anticipate repeat doses or an infusion per provider orders. Titration requires caution; overly rapid or excessive titration of naloxone can trigger acute opioid withdrawal, severe hypertension, agitation, and noncardiogenic pulmonary edema.

Acetaminophen toxicity follows an insidious course where early intervention is lifesaving. In an overdose, saturation of the major clearance pathways increases NAPQI formation; NAPQI then depletes hepatic glutathione and accumulates when detoxification capacity is exceeded. For a single acute ingestion with a known time, the Rumack, Matthew nomogram estimates hepatotoxicity risk using a serum level obtained 4 to 24 hours after ingestion. N-acetylcysteine replenishes hepatic glutathione, enabling detoxification of NAPQI, and provides the greatest protection when started within eight hours of acetaminophen ingestion. When administering ordered intravenous N-acetylcysteine, the nurse must monitor closely for non-IgE-mediated anaphylactoid reactions, watching for flushing, urticaria, bronchospasm, and hypotension.

Salicylate poisoning presents a complex, multi-phase acid, base challenge. Salicylates directly stimulate the respiratory center, causing respiratory alkalosis, and simultaneously uncouple oxidative phosphorylation, causing a high anion gap metabolic acidosis. In adult patients, these two distinct disturbances frequently coexist. Early salicylate toxicity produces tinnitus, tachypnea, diaphoresis, nausea, and vomiting, whereas hyperthermia and altered mental status signal severe, life-threatening toxicity.

Management of salicylate toxicity centers on enhancing elimination and preventing tissue uptake. Intravenous sodium bicarbonate is used to alkalinize both serum and urine, which limits salicylate distribution into tissues and increases urinary elimination. During ordered therapy, the nurse monitors serum pH, potassium, and titrates toward a urine pH target of approximately 7.5 to 8.0. Crucially, hypokalemia impairs urine alkalinization; the nurse must monitor potassium closely and administer ordered replacement, accounting for kidney function. The nurse must promptly alert the provider and anticipate urgent hemodialysis for severe or worsening acidosis, kidney injury, pulmonary edema, neurologic deterioration, or markedly elevated or rising salicylate levels.