History
• Timing, quantity of ingestion/exposure, access to household chemicals/other meds, coingestions, enteric-coated/extended-release substances
Physical Exam
• VS, pupils, skin, neuro findings (AMS, nystagmus, myoclonus, tremor), peristalsis, smell
Evaluation
• ECG, FSG, CBC, chemistries, LFT’s, UA, ABG, hCG, osmolar/anion gap
• Drug levels
• Exposures for which drug level is useful: APAP, salicylates, theophylline, lithium, digoxin, EtOH, carboxyhemoglobin, methemoglobin, iron, methanol, ethylene glycol, lead, mercury, arsenic, organophosphate, anticonvulsants
Treatment
Dermal Decontamination
• Irrigation w/ copious volumes of H2O (unless metallic Na, K, or phosphorus)
Ocular Decontamination
• Irrigation w/ copious volumes of H2O
Enhanced Elimination
• Urinary alkalinization w/ NaHCO3 (eg, salicylates, phenobarbital, formic acid)
• HD (eg, ethylene glycol, methanol, lithium, salicylates)
Disposition
• Admit for any significant ingestion/exposure; consider transfer for complex presentations & inadequate hospital resources
Pearl
• Hospital tox screens vary → learn your hospital’s screen to guide your practice
ANTICHOLINERGIC INGESTION
Definition
• Antagonists @ muscarinic cholinergic receptor → inhibit parasymp system
History
• Blurred vision, dry mouth, fever, AMS, flushing; “blind as a bat, dry as a bone, hot as a hare, mad as a hatter, red as a beet”
Differential
• Sympathomimetic OD, EtOH/benzo withdrawal, thyroid storm, sepsis/meningitis
Findings
• ↑ HR, ↑ temp, dilated pupils, dry MM/skin, ↓ bowel sounds, urinary retention, myotonic activity, choreoathetosis, confusion/delirium, szs
Evaluation
• ECG (≠ QTc Æ TCAs, neuroleptics); electrolytes; total CK (rhabdomyolysis); tox screen → r/o other ingestions; pulse ox; Tele
Treatment
• Supportive: IV hydration, external cooling
• Decontamination/elimination: Activated charcoal (1 dose, w/in 1–2 h), HD
• BZD (IV): For agitation, szs
• Physostigmine (IV): Reverses anticholinergic effects via acetylcholinesterase inhibition
• NOT for routine use due to risk of intractable szs, AV block, asystole
Disposition
• Admit; ICU for pts w/ cardiac instability or szs
Pearl
• Rarely fatal unless significant hyperthermia is present
PSYCHOPHARMACOLOGIC INGESTION
Selective Serotonin Reuptake Inhibitors and Serotonin Syndrome
Approach
• Spectrum for serotonin intoxication ranges from mild lethargy to serotonin syndrome
• Consider serotonin syndrome for anyone on meds w/ serotonin activity, esp ≥2 agents
• Greatest risk w/i min, h after starting new med or increasing dose of old med
Definition
• SSRI: Selective serotonin reuptake inhibitors; SRIs: Serotonin reuptake inhibitors (also activity on epinephrine, norepinephrine, dopamine)
History
• Akathisia, AMS, szs
Findings
• ↑ HR, ↑ temp, ↑ reflexes, diaphoresis, mydriasis, ↑ ↓ BP, tremor, clonus, neuromuscular rigidity, ataxia
Evaluation
• VS, CBC, chem 7, CK (rhabdo), ECG (↑ QRS, ↑ QTc, torsades), pulse ox, Tele
Treatment
Acute overdose
• Activated charcoal, admit for monitoring
Serotonin Syndrome
• Supportive: IV fluids, electrolyte correction, external cooling (may require sedation/paralysis for severe hypothermia)
• Benzos (IV): For agitation, rigidity, szs
• (Anecdotal evidence) Cyproheptadine (12 mg initially, 4 mg PO q1h), chlorpromazine 25–50 mg IV for severe sxs
Pearl
NEUROLEPTICS, NEUROLEPTIC MALIGNANT SYNDROME
Definition
• Characterized by D2 antagonism ± serotonin receptor antagonism
History
• Slurred speech, sedation, anticholinergic toxidrome, extrapyramidal sxs (dystonia, akathisia, parkinsonism, tardive dyskinesia)
• NMS: ↑ HR, rigidity, AMS, szs, autonomic instability, metabolic acidosis, rhabdomyolysis
Evaluation
• CBC, chem 20, CK (rhabdo), ECG (↑QTc, torsades), UA (myoglobin)
Treatment
• Dystonia/akathisia: Diphenhydramine, benztropine, BZD
• NMS: Cooling, IV fluids, benzos, nondepolarizing neuromuscular blockade, dantrolene, bromocriptine, amantadine
LITHIUM
History
• Acute tox: GI sxs initially; neurologic findings may develop later
• Chronic tox: Neurologic sxs
Evaluation
• VS, ECG, CBC, chem7, Ca, Mg, PO4, TSH, free T4, UA
• Lithium level: Not useful in acute ingestion (development of neurologic sx is better reflection of tox); in chronic tox, level >1.5 mEq is significant
• Assess for causes of decreased lithium clearance: Eg, dehydration, renal failure
Treatment
• IV fluids: Decreases tox & promotes Li excretion, NS bolus then ½ NS
• GI decontamination: Activated charcoal ineffective, whole bowel irrigation may be useful
• Sodium polystyrene sulfonate (Kayexalate), consider thiazides, indomethacin, or amiloride for nephrogenic DI
• BZD for szs (avoid phenytoin, which ↓ Li renal excretion)
• HD: For pts w/ severe neurologic sxs &/or clinical deterioration
Disposition
• Admit all pts w/ sustained release ingestions, lithium level >1.5 mEq, or new neurologic signs; lesser ingestions can be treated & observed 4–6 h → re√ level ± psychiatry eval
Pearl
• Li has narrow therapeutic window; consider Li tox in pts w/ ARF/↓ UOP
TRICYCLIC ANTIDEPRESSANTS
Approach
• Sxs of overdose almost always occur w/in 6 h of ingestion
Evaluation
• ECG, CBC, chem 7, Ca/Mg/PO4, CK, UA tox screen, pulse ox, Tele
Treatment
• Supportive: IV fluids
• GI decontamination/elimination: Activated charcoal ± gastric lavage, intralipid for clomipramine
• Sodium bicarbonate: 1–2 mEq/kg boluses titrated to pH 7.45–7.55
• Indications: QRS >100, new RAD, ↓ BP, &/or ventricular dysrhythmia
• BZD: For szs
• Lidocaine: For ventricular dysrhythmias refractory to NaHCO3, avoid procainamide or other type Ia or Ic antiarrhythmics
Disposition
• Admit all pts w/ e/o cardiotoxicity or sz; d/c pts w/o sxs at 6 h after ingestion
Pearl
• Antimuscarinic effects are absent in many cases of TCA overdose
ALCOHOLS
Definition
• Ingestions of toxic alcohols
Approach
• History
• Type of alcohol ingested, time of ingestion, coingestants
• PE: Monitor for airway protection, occult trauma (head injury)
• Labs: Bedside glucose test (may be all that’s needed), BAL (declines 20 mg/dL/h), anion gap, serum/urine tox screen (if coingestants suspected), osmolar gap for alcohols other than EtOH
• Osmol calc = 2 × Na + BUN/2.8 + glucose/18 + EtOH/4.6
• Osmol gap = Osmol measured − osmol calc
• Tx: Charcoal doesn’t bind alcohol, ± thiamine/folate
ETHANOL
History
• EtOH ingestion, found down, lethargy, nausea, vomiting, ± associated trauma, ± aspiration, gastritis
Physical Findings
• CNS, respiratory depression, slurred speech, ataxia, nystagmus
Evaluation
• Bedside glucose (hypoglycemia common in alcoholics), ± BAL (if ingestion uncertain), ± CBC/BMP/LFTs/lipase, ± ECG (if pulse if irregular), ± magnesium level
Treatment
• Maintain airway, serial exams, ± IVF/thiamine/folate (given but may not be necessary)
Disposition
• Ambulating w/o ataxia + speaking clearly → d/c
Pearls
• R/o head trauma, CNS infection, Wernicke encephalopathy, alcoholic ketoacidosis, hypoglycemia, alcohol withdrawal/DT, coingestions, SI/HI
• Known EtOH ingestion/intoxication in pt w/ h/o same does not require lab & can be observed until clinically sober
METHANOL
Definition
• Ingestion of methanol (peak levels 30–60 min, 24–30 h ½ life, hepatic metabolism)
History
• Drinking: Paint solvents/antifreeze/windshield-washing fluid/canned fuels/gasoline additives, shellac/copy machine fluid/home heating fuels
Physical Findings
• CNS depression, vomiting, papilledema/hyperemia, visual changes/loss, gastritis
Evaluation
• ↑ Methanol level, ↑ Osmol gap, ↑ anion gap (profound), chemistries, ABG
Treatment
• Based presumptive Dx if levels delayed, maintain airway
• Fomepizole: Loading dose (15 mg/kg in 100 mL D5W over 30 min) → maintenance (10 mg/kg q12h × 4 doses → 15 mg/kg q12 to methanol concentration <20/dL)
• Folate 50 mg IV q4h until resolution of acidemia (cofactor to convert formic acid → CO2 + H2O)
• Dialysis: Absolute indications → visual impairment + detectible methanol level or >50 mL/dL, osmol gap >10, ingestion >1 mg/kg, severe acidosis, renal failure
Disposition
• Admit
ETHYLENE GLYCOL
Definition
• Ingestion of ethylene glycol (peak levels 30–180 min, 3–7 h ½ life, 70% hepatic metabolism)
History
• Drinking: Antifreeze, coolants, paint, polishes, detergents, fire extinguishers
Physical Findings
• 3 phases: <12 h → ↓ CNS (like EtOH), gastritis; 12–24 h → ↑ HR/RR/BP/SOB; >12 h → ATN (oxylate crystal deposition)
Evaluation
• Ethylene glycol level, ↑ osmol gap, ↑ AG, calcium oxylate crystals in urine, beta-hydroxybutyrate (used to distinguish from alcoholic ketoacidosis)
Treatment
• Based presumptive Dx if levels delayed, maintain airway
• Fomepizole: Loading dose (15 mg/kg in 100 mL D5W over 30 min) → maintenance (10 mg/kg q12h × 4 doses → 15 mg/kg q12h to methanol concentration <20/dL)
• Folate/thiamine 100 mg IV q6h/pyridoxine 50 mg IV q6h until resolution of acidemia (cofactors in oxalic acid metabolism)
• HD: Severe acidosis (pH <7.25) + osmol gap >10, renal failure (Cr >1.2 mg/dL), ethylene glycol level >50 mg/dL, deterioration despite supportive care
Disposition
• Admit
Clinical Pearl
• Urine/gastric contents fluorescence w/ Woods lamp due to antifreeze additives (early)
ISOPROPYL ALCOHOL
Definition
• Ingestion of isopropyl alcohol (peak levels 30–180 min, 3–7 h ½ life, 80% hepatic metabolism, lethal dose 2–4 mL/kg)
History
• Drinking: Rubbing alcohol, paint thinner, solvents, skin/hair products, nail polish remover
Physical Findings
• Profound ↓ CNS (2–4 × EtOH), fruity odor on breath, respiratory depression, ↓ BP, gastritis
Evaluation
• Chemistries, UA, FSG, isopropyl level, nl AG, ↑ osmol gap, falsely ↑ Cr (from acetone)
Treatment
• Based presumptive Dx if levels delayed
• Supportive (rarely lethal)
• Dialysis: Refractory hypotension, levels >500 mg/dL
Disposition
• Admit
ALCOHOL WITHDRAWAL
Definition
• Abrupt cessation or significant reduction in alcohol intake (begins 6–24 h/peaks 48–72 h after last drink)
History
• Heavy alcohol use w/ cessation, insomnia, anorexia, nausea, vomiting, restlessness, diaphoresis, sz
Physical Findings
• Tremulousness, szs (25% of pts at 6–48 h), delirium, hallucinations (visual > auditory), autonomic hyperactivity (tachycardia, HTN, irritability, hyperreflexia), delirium tremens (rare/serious, 24 h–5 d after last drink): Tremor/autonomic hyperactivity/confusion/hallucinations/low-grade fever
Evaluation
• Bedside glucose testing, CBC, BMP, LFTs/coags (if liver Dysfxn suspected), BAL
Treatment
• Glucose (if hypoglycemic), thiamine, lorazepam 2 mg IV for sz, IV/IM/PO long-acting BZD (ie, lorazepam 1–4 mg IV q10–30min to sedation, diazepam 5 mg IV q5–10min to sedation, chlordiazepoxide), phenobarbital as 2nd-line
Disposition
• Admit for if requiring IV medication/DTs ± ICU
Clinical Pearls
• Rarely fatal (increased w/ aspiration due to sz) when treated appropriately
• May require very large doses of IV BZD to control/treat