Toxicology nursing: overdose assessment, antidotes, and NCLEX review

Toxicology nursing requires rapid pattern recognition — identifying a toxidrome, initiating stabilization, and matching the antidote to the agent before lab confirmation is available. Whether the exposure is intentional or accidental, the nursing approach follows the same framework: secure the airway, recognize the toxidrome, call Poison Control, and administer the correct antidote at the correct time.

This article covers the full clinical scope: the four classic toxidromes, acetaminophen and opioid overdose protocols, TCA and salicylate poisoning, decontamination strategies, a complete antidote reference table, and 20 NCLEX high-yield scenarios. Pair it with the airway management reference and the critical lab values guide for complete overdose coverage.

Toxicology assessment framework

Primary survey: ABCDEs

Every overdose patient receives a primary survey first — before history, before triage questions, before anything else.

• Airway: Can the patient protect their own airway? Look for vomit, loss of gag reflex, snoring respirations. Be prepared for early intubation in patients with declining consciousness. See airway management nursing for rapid-sequence intubation (RSI) protocols.
• Breathing: Respiratory rate, depth, and oxygen saturation. Opioid toxicity causes hypopnea (slow, shallow breaths); salicylates cause hyperpnea (deep, rapid breaths); TCAs may cause both.
• Circulation: Heart rate and rhythm (monitor continuously), blood pressure, peripheral perfusion. Obtain 12-lead ECG promptly — QRS width and QT interval are life-saving data in overdose.
• Disability: Glasgow Coma Scale (GCS), pupil size and reactivity, blood glucose. Always check a point-of-care glucose — hypoglycemia mimics or complicates nearly every overdose.
• Exposure / Environment: Fully undress the patient. Look for track marks, transdermal patches (fentanyl patches are a common source of ongoing absorption — remove them with gloves), pills in pockets, skin findings (diaphoresis vs dry skin, color changes).

Toxicology history (SAMPLE + substance-specific)

When the patient is conscious or a bystander is available:

• Substance: what was taken? Name, formulation, and whether extended-release or immediate-release matters enormously
• Amount: estimated pills, milliliters, grams
• Time of ingestion: crucial for nomogram interpretation and decontamination timing
• Route: ingested, injected, inhaled, transdermal
• Intent: accidental vs intentional — affects psychiatric hold decisions and disposition
• Last known well: for altered-consciousness patients, when were they last seen normal?
• Co-ingestions: polypharmacy overdoses are the rule, not the exception in intentional overdoses
• Medical history / medications: renal or hepatic disease alters toxin clearance and antidote dosing

GCS and pupil exam

The GCS provides an objective, serial measure of CNS function. In overdose, the motor score is the most sensitive component — a patient with a motor score of ≤5 (abnormal flexion or worse) is at high risk for airway compromise.

Pupil findings are a rapid toxidrome clue:

• Miosis (constriction): opioids, cholinergics, clonidine, pontine hemorrhage
• Mydriasis (dilation): sympathomimetics, anticholinergics, serotonin syndrome
• Normal pupils with CNS depression: sedative-hypnotics, ethanol, carbon monoxide

A unilateral fixed and dilated pupil suggests herniation — rule out structural cause before attributing to toxin.

The four classic toxidromes

Sympathomimetic toxidrome

Mechanism: excessive catecholamine release or reuptake inhibition causing global adrenergic activation.

Signs: tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis, agitation, tremor, seizure in severe cases. Unlike anticholinergic toxidrome, the skin is wet (diaphoresis present).

Common agents: cocaine, methamphetamine, MDMA (ecstasy), amphetamines, pseudoephedrine, bath salts (synthetic cathinones).

Key nursing response:

• Benzodiazepines are the cornerstone treatment — they reduce agitation, control seizures, and blunt adrenergic surge
• Avoid beta-blockers: unopposed alpha-adrenergic stimulation after beta-blockade can cause severe hypertension and coronary vasospasm (cocaine toxicity)
• Active cooling for hyperthermia (evaporative cooling, ice packs to axillae/groin) — temperature >40°C risks rhabdomyolysis, seizure, and death
• Continuous cardiac monitoring — cocaine prolongs QT and has direct sodium-channel blocking effects
• Place in a low-stimulation environment; minimize noxious interventions that worsen agitation

Cholinergic toxidrome

Mechanism: excess acetylcholine at muscarinic and nicotinic receptors, typically from acetylcholinesterase inhibition.

Signs — two mnemonics:

SLUDGE (muscarinic): Salivation, Lacrimation, Urination, Defecation, GI upset (nausea/cramping), Emesis

DUMBELS (complete): Defecation/Diarrhea, Urination, Miosis, Bradycardia/Bronchospasm/Bronchorrhea, Emesis, Lacrimation, Salivation

Nicotinic signs (less prominent): muscle fasciculations, weakness, paralysis, hypertension and tachycardia initially (then bradycardia as muscarinic dominates)

Common agents: organophosphate pesticides (malathion, parathion), carbamates, nerve agents (sarin, VX), mushrooms (Clitocybe, Inocybe species), some eye drops.

Key nursing response:

• Don full PPE before any patient contact — organophosphates are dermally absorbed and have caused responder casualties
• Atropine is the priority antidote — blocks muscarinic effects. Give 2–4 mg IV every 5–10 minutes, titrating to drying of secretions (not heart rate — atropinization endpoint is dry secretions and clear lungs, not a specific heart rate number). Severe poisonings may require hundreds of milligrams over hours
• Pralidoxime (2-PAM) reactivates acetylcholinesterase before “aging” occurs (permanent enzyme inactivation). Must be given early — ideally within 24–48 hours of exposure. Give 1–2 g IV over 15–30 minutes then infusion
• Prepare for intubation — bronchospasm and bronchorrhea are the most life-threatening features

Anticholinergic toxidrome

Mechanism: muscarinic receptor blockade producing the opposite picture of cholinergic toxidrome — dry, hot, dilated, fast, confused.

Classic mnemonic:

• Dry as a bone — dry mouth, anhidrosis, dry skin
• Blind as a bat — mydriasis, loss of accommodation (blurred vision)
• Mad as a hatter — delirium, agitation, hallucinations (“picking at the air”)
• Hot as a hare — hyperthermia (lost ability to sweat)
• Red as a beet — flushed skin (cutaneous vasodilation)

Add: urinary retention, decreased bowel sounds (ileus), tachycardia.

Common agents: tricyclic antidepressants (TCAs), antihistamines (diphenhydramine, hydroxyzine), atropine, scopolamine, jimsonweed (Datura), antipsychotics (many), some anti-Parkinson drugs.

Key nursing response:

• Bladder scan and straight catheterization if urinary retention suspected
• Cooling measures for hyperthermia
• Benzodiazepines for agitation — avoid physical restraints (worsen hyperthermia and rhabdomyolysis)
• Physostigmine (cholinesterase inhibitor) can reverse anticholinergic delirium but is contraindicated in TCA overdose — can cause seizure and cardiac arrest. Use only if TCA has been ruled out and in consultation with Poison Control
• For TCA-induced anticholinergic plus cardiac toxicity, see TCA section below

Opioid toxidrome

Classic triad: altered consciousness (sedation to coma) + miosis (pinpoint pupils) + respiratory depression (rate <12, decreased tidal volume, oxygen desaturation)

Common agents: heroin, oxycodone, hydrocodone, morphine, fentanyl, methadone, buprenorphine, tramadol, antitussives (codeine, dextromethorphan at high doses).

Key nursing response:

• Naloxone administration (see opioid overdose section below)
• Position the patient in recovery position if not intubated — aspiration risk is high
• Bag-valve-mask ventilation if respiratory rate critically low before naloxone effect
• Monitor for re-narcotization after naloxone dose

For patients transitioning from acute toxicity to withdrawal, see opioid withdrawal nursing.

MUDPILES: anion gap metabolic acidosis in toxicology

When a toxicology patient has a metabolic acidosis with elevated anion gap (normal AG = 8–12 mEq/L; adjusted for albumin), use MUDPILES as the mnemonic to identify the culprit:

M — Methanol
U — Uremia
D — DKA (diabetic ketoacidosis)
P — Propylene glycol (found in IV lorazepam and other drug vehicles)
I — Isoniazid / Iron
L — Lactic acidosis (sepsis, cyanide, carbon monoxide, metformin)
E — Ethylene glycol
S — Salicylates

The osmol gap (measured osmolality minus calculated osmolality) expands MUDPILES context: an elevated osmol gap points to methanol, ethylene glycol, or isopropyl alcohol as unmeasured osmoles. Use this alongside the critical lab values reference when interpreting overdose ABGs and metabolic panels.

Acetaminophen overdose

Acetaminophen (APAP) is the most common pharmaceutical agent implicated in acute liver failure in the United States, responsible for approximately 56,000 emergency department visits and 500 deaths annually (NIH/NIDDK data). Its danger lies in the delay between ingestion and symptom onset — patients may feel well for 24–48 hours while hepatocellular destruction progresses silently.

Mechanism: NAPQI accumulation

Under normal conditions, acetaminophen is metabolized primarily via glucuronidation and sulfation (~90%). A small fraction (~5–10%) is oxidized by CYP2E1 to N-acetyl-p-benzoquinone imine (NAPQI), a highly reactive hepatotoxic intermediate. Normally, hepatic glutathione conjugates and detoxifies NAPQI rapidly. In overdose, glucuronidation and sulfation pathways saturate, shunting more APAP through CYP2E1. NAPQI accumulates faster than glutathione can neutralize it and begins covalently binding to hepatocyte proteins — causing centrilobular (zone 3) necrosis.

Glutathione stores are also depleted by malnutrition, chronic alcohol use, fasting, and HIV — conditions that lower the toxic threshold even at normal doses. See liver failure nursing for the downstream effects of acetaminophen-induced acute liver failure.

Four phases of acetaminophen toxicity

Rumack-Matthew nomogram

The Rumack-Matthew nomogram is a log-linear graph plotting serum acetaminophen concentration against time after ingestion. It identifies patients at risk for hepatotoxicity and guides the NAC treatment decision.

How to use it:

1. Obtain a serum APAP level at 4 hours post-ingestion (earlier levels may underestimate peak concentration)
2. Know the exact time of ingestion
3. Plot the level on the nomogram. If it falls above the “possible hepatic toxicity” line (150 μg/mL at 4 hours, 37.5 μg/mL at 12 hours), treat with NAC
4. For unknown ingestion time or staggered ingestion: treat empirically — the nomogram is not applicable

Important limitations:

• Valid only for single, acute ingestions with known timing
• Not applicable to chronic/repeated supratherapeutic ingestions
• NAC should be started based on clinical presentation in all unclear cases — the downside of unnecessary NAC treatment is minimal

N-acetylcysteine (NAC) therapy

NAC is the antidote for acetaminophen toxicity. It works by replenishing glutathione stores, providing alternate sulfate donors, and directly scavenging NAPQI. It is most effective when started within 8 hours of ingestion but provides benefit up to 24–36 hours and should be given even late if liver failure is established.

IV NAC protocol — 3-bag (21-hour) regimen (Acetadote):

Oral NAC protocol: 140 mg/kg loading dose followed by 70 mg/kg every 4 hours for 17 doses. IV preferred for altered mental status, vomiting, or fulminant hepatic failure.

Anaphylactoid reaction monitoring: The loading dose (Bag 1) carries the highest risk for anaphylactoid reactions — flushing, urticaria, bronchospasm, hypotension — occurring in 5–15% of patients. These are not true IgE-mediated anaphylaxis. Management: stop the infusion, give diphenhydramine ± albuterol for bronchospasm, then restart at a slower rate once symptoms resolve. True anaphylaxis requiring epinephrine is rare.

Lab monitoring during NAC therapy:

• AST, ALT, INR, bilirubin — baseline and every 12–24 hours
• BUN, creatinine (renal injury occurs in ~25% of cases with hepatotoxicity)
• Point-of-care glucose — hypoglycemia develops in Phase III
• Serum APAP level — confirm declining trend

Opioid overdose

Classic triad

Opioid overdose presents with three findings: altered consciousness (sedation, stupor, or coma), miosis (bilateral pinpoint pupils, typically <2 mm), and respiratory depression (rate <12/min, decreased tidal volume, hypoxia). Any two of the three should trigger treatment — waiting for all three delays critical intervention.

High-risk scenarios for nurses:

• Hospital inpatients receiving opioid analgesia — particularly post-surgical patients on PCA pumps, patients with untreated sleep apnea, or patients who have received multiple antiemetics that potentiate opioid CNS depression
• Patients found unresponsive in emergency department bathrooms (common pattern for fentanyl injection)
• Post-cardiac arrest patients where opioid overdose was the etiology

Naloxone administration

Naloxone (Narcan) is a competitive opioid receptor antagonist that rapidly reverses all three components of the opioid triad. It has no agonist effects and is safe to administer even when opioid toxicity is uncertain.

Dosing and routes:

Titration principle: The goal is adequate spontaneous respirations, not full wakefulness. Giving the minimum dose needed to restore breathing preserves some opioid analgesia (important in post-surgical or chronic pain patients) and reduces the risk of precipitating acute opioid withdrawal with its associated agitation, hypertension, pulmonary edema risk, and patient-care complications.

Fentanyl and extended-release opioids: Illicit fentanyl, carfentanil, and extended-release oral opioids (oxycodone ER, methadone) may require repeated naloxone doses or higher total doses. For patients with confirmed or suspected long-acting opioid ingestion, a naloxone infusion (two-thirds of the effective initial bolus dose per hour) is the standard approach to sustaining reversal.

Re-narcotization risk

Naloxone has a half-life of 60–90 minutes. Many opioids — particularly methadone (half-life 24–36 hours), fentanyl patches (sustained absorption), and extended-release formulations — far outlast a single naloxone dose. After initial reversal, the naloxone effect wanes while the opioid effect continues, producing re-narcotization: return of somnolence and respiratory depression hours after the patient appeared awake and well.

All patients receiving naloxone for opioid overdose require continuous monitoring for a minimum of 4–6 hours after the last naloxone dose. Patients on long-acting opioids may require 24-hour observation. Discharging a “reversed” patient too soon is one of the most consequential errors in overdose management.

Harm reduction: For substance use context and long-term nursing considerations, see substance use disorders nursing.

Salicylate overdose

Salicylate (aspirin/acetylsalicylic acid) overdose produces a distinctive metabolic picture that nurses must recognize rapidly, as it can be fatal if managed incorrectly.

Classic presentation

Early (mild-moderate): Tinnitus (high-pitched ringing — the single most characteristic symptom), nausea, vomiting, diaphoresis, hyperpnea (deep, rapid breathing). The hyperpnea is a direct effect of salicylate on the respiratory center in the medulla, producing a primary respiratory alkalosis.

As toxicity progresses: The primary respiratory alkalosis triggers a compensatory metabolic acidosis. With increasing salicylate levels, direct uncoupling of oxidative phosphorylation produces an independent high-anion-gap metabolic acidosis. The final picture is a mixed respiratory alkalosis and metabolic acidosis — a pattern highly specific to salicylate toxicity and a key NCLEX discriminator.

Severe toxicity signs: CNS manifestations (confusion, agitation, seizures, coma), hyperthermia (uncoupled oxidative phosphorylation generates heat), non-cardiogenic pulmonary edema, renal failure. Note: CNS depression in salicylate toxicity is ominous — it indicates the salicylate is crossing into the CNS and carries high mortality.

Severity grading and management

Urine alkalinization (alkaline diuresis):

• Sodium bicarbonate IV is the cornerstone of treatment for moderate-severe salicylate toxicity
• Mechanism: alkalinizing the urine (target urine pH 7.5–8.0) traps ionized salicylate in the tubular lumen, preventing reabsorption and enhancing renal elimination — ion trapping
• Also alkalinizes plasma, reducing CNS salicylate penetration (salicylic acid crosses membranes in unionized form)
• Target serum pH: 7.45–7.55. Monitor serum and urine pH closely
• Maintain adequate hydration and replace potassium — hypokalemia impairs alkalinization (the kidney preferentially reabsorbs potassium over hydrogen, competing with bicarbonate excretion)

Hemodialysis indications:

• Salicylate level >100 mg/dL (or >80 mg/dL with clinical deterioration)
• Renal failure preventing adequate clearance
• Altered mental status unresponsive to alkalinization
• Pulmonary edema
• Severe metabolic acidosis (pH <7.2)

Lab monitoring: serial salicylate levels (every 2 hours until peak confirmed and declining), ABGs for acid-base monitoring, serum glucose (salicylates can cause both hypo- and hyperglycemia), electrolytes, renal function. Coordinate with AKI nursing protocols if renal injury develops.

TCA (tricyclic antidepressant) overdose

TCA overdose is one of the most dangerous pharmaceutical overdoses because it combines anticholinergic toxicity with lethal cardiac and CNS effects from sodium-channel blockade. Even moderate ingestions can cause rapid deterioration.

Mechanism and presentation

TCAs block three receptor systems simultaneously:

1. Sodium channels (fast INa): slows Phase 0 depolarization → QRS widening, bundle branch block, ventricular arrhythmias
2. Muscarinic receptors: anticholinergic syndrome (see above)
3. Alpha-1 receptors: vasodilation, hypotension
4. GABA-A receptors (antagonism): seizure threshold lowered

Clinical findings:

• Anticholinergic syndrome (dry, hot, dilated, tachycardic, delirious)
• QRS ≥100 ms on 12-lead ECG: indicates sodium-channel toxicity and predicts high risk for ventricular tachycardia (VT), ventricular fibrillation (VF), and seizures
• QRS ≥160 ms: very high risk for VT/VF
• Terminal R wave in lead aVR (R/S ratio >0.7) — an additional ECG marker of TCA toxicity
• Hypotension (alpha-1 blockade + myocardial depression)
• Seizures — often brief initially but can progress to status

For the underlying ECG principles, see cardiac arrhythmias nursing.

Sodium bicarbonate treatment

Sodium bicarbonate is the antidote for TCA-induced cardiac toxicity:

• Dose: 1–2 mEq/kg IV bolus; repeat until QRS narrows (<100 ms) or pH 7.50–7.55 reached
• Mechanism: the sodium load overwhelms blocked sodium channels, restoring Phase 0 depolarization velocity; alkalemia also reduces TCA binding to sodium channels; alkalemia shifts protein-bound TCA to the bound form, reducing free drug

Infusion: After bolus response, continuous sodium bicarbonate infusion to maintain serum pH 7.45–7.55 until QRS normalizes.

Why physostigmine is contraindicated in TCA overdose: Physostigmine inhibits acetylcholinesterase — raising acetylcholine levels. This can trigger paradoxical bradycardia, asystole, and seizures in the presence of TCA sodium-channel blockade. In TCA overdose, the anticholinergic signs are managed supportively, not with physostigmine.

Lidocaine (not procainamide or quinidine, which also block sodium channels) is an acceptable adjunct for refractory ventricular arrhythmias.

Anticipate: TCA patients deteriorate rapidly and unpredictably. A patient who is awake and conversational at triage can seize and lose cardiac output within 30–60 minutes. Establish IV access, attach continuous cardiac monitoring, and prepare for intubation proactively. For ventilatory support in intubated TCA patients, see mechanical ventilation nursing.

Decontamination

Decontamination reduces ongoing toxin absorption when appropriate, but all decontamination decisions must weigh benefit against risk — particularly aspiration risk in patients with depressed consciousness.

Activated charcoal

Mechanism: Activated charcoal is a highly porous substance with an enormous surface area that adsorbs (binds to its surface) a wide range of drugs and chemicals in the GI tract, reducing absorption.

Indications:

• Oral ingestion of an adsorbed substance (see below)
• Patient presents within 1–2 hours of ingestion (small benefit after 2 hours for most agents)
• Airway is protected (patient fully conscious with intact gag reflex, or endotracheally intubated)

Contraindications:

• Altered level of consciousness without protected airway (highest risk for aspiration)
• Caustic ingestions (acids, alkalis — charcoal doesn’t adsorb these and can worsen esophageal injury)
• Hydrocarbon ingestions (gasoline, petroleum distillates — aspiration during vomiting causes hydrocarbon pneumonitis)
• Bowel obstruction or perforation (contraindication to any oral intervention)
• Substances not adsorbed by charcoal: PHAILS — Pesticides (some), Heavy metals, Alcohols, Iron, Lithium, Solvents (and cyanide)

Dose: 1 g/kg (typically 25–100 g) in a slurry; given via NGT if patient refuses or is unable to swallow reliably.

Multiple-dose activated charcoal (MDAC): Used for drugs with enterohepatic recirculation or sustained-release formulations — carbamazepine, dapsone, phenobarbital, quinine, theophylline. Standard dose every 4–6 hours.

Gastric lavage

Gastric lavage (stomach pumping) fell from routine use as evidence showed limited benefit beyond 1 hour and significant aspiration risk. It is still considered in rare scenarios: massive, life-threatening ingestion within 60 minutes, ingestion of agents that form bezoars (iron, lithium), or ingestion of agents with no other antidote and high lethality. Requires endotracheal intubation before placement if consciousness is depressed.

Whole bowel irrigation (WBI)

WBI — oral polyethylene glycol solution (GoLYTELY) via NGT at 1–2 L/hour until rectal effluent is clear — mechanically clears the gut. Indicated for:

• Sustained-release or enteric-coated tablets (diltiazem ER, metoprolol ER, opioid extended-release)
• Iron tablets (iron is not adsorbed by charcoal; iron tablets are radiopaque on abdominal X-ray)
• Lead (foreign body ingestion, paint chips)
• Body packers (drug smugglers with swallowed drug packets)

Contraindicated with bowel obstruction, perforation, or hemodynamic instability.

Antidotes quick-reference table

Poison Control: NPDS and the 1-800-222-1222 line

The National Poison Data System (NPDS) is operated by the American Association of Poison Control Centers (AAPCC). Poison Control Centers provide 24/7 expert toxicology consultation at no charge.

National Poison Control number: 1-800-222-1222 (US)

This line connects callers to their regional Poison Control Center and provides real-time guidance from toxicologists and pharmacists on antidote selection, dosing, observation requirements, and disposition decisions.

When to call:

• Any unknown ingestion where agent is uncertain
• Unusual toxidrome patterns or co-ingestions
• Guidance on antidote dosing or duration
• Disposition questions (safe for discharge vs. observation vs. ICU)
• Any pediatric ingestion — even small amounts of adult medications can be lethal in children

What to have ready when calling:

1. Patient age, weight, and current vital signs
2. Substance (name, formulation, strength, amount available/missing)
3. Estimated time of ingestion
4. Route of exposure
5. Current clinical status — symptoms, GCS, ECG findings
6. What treatment has already been given

Calling Poison Control is not an admission of uncertainty — it is best practice. Their guidance has been shown to reduce hospitalizations, antidote errors, and mortality.

Nursing diagnoses

1. Impaired gas exchange related to respiratory depression secondary to toxic substance Evidence: oxygen saturation <92%, respiratory rate <12/min, CO2 retention on ABG, opioid or sedative-hypnotic ingestion

2. Risk for aspiration related to altered consciousness and loss of protective airway reflexes Evidence: GCS <8, vomiting, known CNS-depressant ingestion

3. Decreased cardiac output related to dysrhythmia secondary to cardiotoxic agent Evidence: QRS ≥100 ms (TCA), hypotension, diminished peripheral pulses, ECG changes

4. Risk for self-directed violence related to intentional overdose Evidence: confirmed or suspected intentional ingestion — activate psychiatric consultation, institute appropriate precautions, and document per facility safety policy

Patient and family education

Safe medication storage

• Store all medications in their original child-resistant containers in a locked location
• Never store medications in accessible cabinets, bedside tables, or purses
• Keep all medications — including visitors’ medications — out of reach of children
• Even household and OTC medications cause serious overdoses in children: acetaminophen (Tylenol), iron supplements, eye drops (tetrahydrozoline — imidazoline toxicity), and antihistamines top pediatric ingestion lists

Safe disposal of unused medications

• Use a DEA-authorized medication take-back location (many pharmacies participate; find locations at DEA Diversion Control Division or Disposal Act database)
• If no take-back available: mix medications with coffee grounds or cat litter in a sealed bag; dispose in household trash (this is acceptable for most medications); do not flush (except for select controlled substances on the FDA flush list)
• Fentanyl patches: even used patches retain significant drug; fold sticky side together and dispose in take-back program or as above

Poison prevention at home

• Post Poison Control number (1-800-222-1222) on the refrigerator
• Know the difference between “safe amount” and “overdose” for common OTC medications — exceeding the acetaminophen daily limit (4 g in healthy adults; 2 g in elderly, alcohol users, or hepatic disease) is common and causes unintentional hepatotoxicity
• Child-resistant caps are not childproof — they slow access but do not prevent it; supervision and locked storage are necessary
• Carbon monoxide detectors on every floor; never use gas-powered generators indoors

20 NCLEX high-yield tips

20 NCLEX scenario questions

Clinical sources

This article draws on the following authoritative sources:

• NIH/NIDDK: acetaminophen-induced liver injury epidemiology and NAPQI mechanism
• AAPCC (American Association of Poison Control Centers): National Poison Data System annual report; 1-800-222-1222 guidance
• Rumack BH, Matthew H (1975): Acetaminophen poisoning and toxicity — original nomogram publication, Pediatrics 55(6):871–876
• Smilkstein MJ et al (1988): Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose, NEJM 319:1557–1562 (NAC protocol basis)
• Goldfrank’s Toxicologic Emergencies, 11th ed (2019): Standard reference for all toxidrome descriptions, antidote dosing, and decontamination protocols
• UpToDate (2024): Acetaminophen overdose in adults; opioid overdose; TCA poisoning; organophosphate poisoning
• American Heart Association: cardiac toxicity management in drug overdose
• FDA (2022): Safe drug disposal guidelines; FDA flush list
• ACMT (American College of Medical Toxicology): clinical practice guidelines, antidote use standards