Poisons and Vitamin Deficiencies
Julie J. Miller
Marcelo Matiello
Eyal Y. Kimchi
INITIAL MANAGEMENT & BASIC APPROACH FOR POISON INGESTION
Supportive care: Monitor airway, breathing, circulation, vitals. Obtain IV access.
Consider IV thiamine, glucose, naloxone for altered mental status, esp coma or sz.
Diagnosis often clinical (history ± exam), followed by lab confirmation (serum/urine).
Identify possible toxin/poison by si/sx (see below) & history: What? How much? When? Route of ingestion (e.g., oral, nasal, IV, rectal, etc.)? Obtain prescription records & bottles for pill counts. Consider over-the-counter meds, coingestions, local substance use patterns, & occupational exposures. Assess intention/suicidality.
Labs: electrolytes, anion gap, BUN, Cr, LFTs, NH3, CBC, PTT, PT/INR, serum/urine tox screen including acetaminophen & alcohol levels, Osm gap, lactate, CK, ABG.
Studies: EKG. CT/MRI if ? trauma or neurovascular complications/focal findings. EEG if ? sz. CXR for resp distress (aspiration, ARDS). Abdominal imaging if ? body packs.
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Poison control hotline (24/7): 1-800-222-1222, esp to consider antidotes.
Additional detox methods should be used selectively (early <1 h, or in severe cases): Activated charcoal (as effective as gastric lavage, fewer contraindications/complications), urinary alkalinization, hemodialysis, chelation
Additional management considerations
Agitation: antipsychotics, benzos if due to alcohol w/d or szs
Seizures: benzos
Dystonia: diphenhydramine or benztropine iv
Hyperthermia: cooling blankets, paralysis w/nondepol agents
If suspected attempted suicide, continuous suicide watch & psychiatry consult
STIMULANTS
Cocaine: Blocks presynaptic reuptake of monoamines (esp in ventral tegmental area, nucleus accumbens, prefrontal cortex) → euphoria, adrenergic stim; blocks voltagegated Na channels → local anesthesia, cardiac arrhyth.
Presentation (acute intox): Sympathomimetic syndrome; szs; stroke: Ischemic (vasospasm, intravascular thromb from ↑ platelet agg) & ICH (reperfusion or HTN). Mvmt d/os: dystonic reactions, buccolingual dyskinesia, choreoathetosis, akathisia.
Rx: Supportive measures; avoid β-blockers (coronary vasoconstriction, end-organ ischemia); szs: benzos best; VPA second line.
Withdrawal: Craving, depression (including suicidal ideation, psychomotor retardation), anhedonia, fatigue, ↑ sleep; ±musculoskel pain, tremor, invol mvmts.
Methamphetamine: Sympathomimetic. Causes release & prevents reuptake of monoamines. Long duration of action (20 h). Can lead to coma.
Sympathomimetic crisis: Syndrome as above → to CV collapse, stroke/ICH. MDMA is amphetamine derivative w/a similar si/sx; may → severe hypo-Na 2/2 SIADH & fatal szs.
Rx: Correct electrolytes (special attention to Na in case of MDMA). Severe HTN: BZ, nitroprusside, or phentolamine. Avoid β-blockers (including labetalol).
Phencyclidine (PCP): Dissociative anesthetic similar to ketamine (noncompetitive NMDA antagonist). Blocks reuptake of monoamines: sympathomimetic. Sigma receptor: Analgesia, sedation, anticholinergic.
Presentation: Violent/bizarre behavior, visual & auditory hallucinations, psychosis, sympathomimetic sx, vertical & horizontal nystagmus. High doses: Disorientation, agitation/violence, acidosis, szs, resp arrest, coma, rhabdomyolysis.
Rx: HTN: BZ, nitroprusside, phentolamine, labetalol. Gastric lavage for early si/sx or potentially lethal dose.
OPIOIDS
Heroin: Pure opioid agonist. Metabolized to active metabolites (including morphine).
Prescription opioid abuse: Oxycodone, hydrocodone, morphine. Regular use → tolerance, predisposes to w/d. Opiate receptors: Mu: analgesia, euphoria, respiratory depression, cough suppression, miosis, sweating, nausea, & vomiting. Kappa & Delta: analgesic.
Presentation: “Rush”: somnolence, calmed sensation, apathy, feeling of self-sufficiency. Anticholinergic effects: N/V, itching. Overdose → respiratory depression, coma, hypothermia, szs. Miotic pupils. Inhalation of heroin vapor can lead to cerebral leukoencephalopathy (coma, severe neurologic damage, death).
Dx: Urine drug screen often positive up to 3-4 days after last use.
Rx: Naloxone IV. Goal: Normal ventilation (not normal level of consciousness). Start 0.04 mg IV, titrate up 2 mg IV every few min until desired response (normalization of respiration or ↑ responsiveness). Repeat effective dose q2-3 min as needed, up to max total dose of 10 mg. If no resp after 5-10 mg, dx must be reconsidered (Vanden Hoek TL, et al. Circulation 2010;122:S829-S861). QRS prolongation: IV Na bicarb, bolus 1-2 mEq/kg. If complex narrows → bicarb infusion (mix 132 mEq of NaHCO3 in 1 L D5W, & infuse at 250 mL/h). QTc prolongation (>500 ms) or torsades de pointes. Correct low Ca, K, Mg.
Opioid Withdrawal: Can develop <6-8 wk w/chronic daily use. Early sxs: Fear of w/d → craving, anxiety, insomnia, yawning, rhinorrhea, lacrimation, salivation, stomach cramps, mydriasis, arthralgia, & myalgias. Up to 7-10 days: HTN, ↑ tremor, myoclonus, f/c, n/v/d, piloerection.
Rx: Oral, longer-acting opiate agonists (methadone, buprenorphine). Alpha-2-adrenergic agonists (clonidine). Possible addition of naltrexone. Loperamide: Abd sxs.
MARIJUANA AND CANNABIS
Contains psychoactive substance tetrahydrocannabinol (THC).
Presentation: Somnolence, euphoria, impaired concentration & short-term memory, tachycardia, conjunctival injection, dry mouth. May precipitate panic attack, paranoia, psychosis in pts w/pre-existing psychiatric dx. Dx: Urine drug screen. Rx: Reassurance, benzos & antipsychotics as need for acute psychiatric symptoms.
BARBITURATES
Physiology & metabolism: Potentiate effect of GABA at GABAA receptors by ↑ duration of chloride channel opening. Short-acting: Anesthetics. Intermediate action: Butalbital (Fioricet/Fiorinal), amobarbital (Amytal), pentobarbital (Nembutal), secobarbital (Seconal). Long-lasting: Phenobarb, primidone. Lethal doses: 6-10 g phenobarb, 2-3 g other barbs.
Presentation: Sedation pattern above
ALCOHOL INTOXICATION
General considerations
Tox screen should include EtOH, methanol, ethylene glycol, isopropyl alcohol, acetaminophen, salicylate (coingestion common). Osm gap: suspect other alcohols other than EtOH for Osm gap >10 after correcting for EtOH:
Osm gap = Osmol measured – Osmol calc
Osm measured = 2 × Na + BUN/2.8 + glucose/18 + ethanol/4.6
Thiamine 100 mg + folate 1 mg + MVI 1 amp to 1 L of D5NS + 3 g MgSO4. Expect ↓ of blood alcohol level (BAL) of 20 mg/dL/h w/EtOH.
Ethanol
Most commonly abused drug. Stimulates GABA-A Rs, suppresses NMDA Rs. Peak serum levels: 30-90 min after ingestion w/empty stomach. Chronic use → (1) downregulation of GABA receptors → tolerance; (2) up-regulation of glutamate receptors (to maintain normal state of arousal). Abrupt discontinuation → imbalance (less GABAergic, more glutamatergic effects). Metabolism by alcohol dehydrogenase follows zero-order kinetics.
Presentation/syndromes:
Acute intoxication: Somnolence, slurred speech, nystagmus, disinhibited behavior, ataxia. Severe intoxication → lethargy, coma. Hypoglycemia → focal deficits, szs, coma.
Wernicke encephalopathy: Encephalopathy, oculomotor dysfxn, nystagmus, ataxia.
Korsakoff syndrome: Wernicke + selective amnesia + confabulation.
Marchiafava-Bignami: Dementia, spasticity, dysarthria, gait instability. Onset: Acute, subacute, chronic. 2/2 demyelination/necrosis of corpus callosum, WM.
Cerebellar degeneration: Gait impairment, arm tremors, dysarthria, diplopia, blurred vision.
Cerebral atrophy: Ventricular enlargement w/cognitive dysfxn.
Neuromuscular issues: Peripheral neuropathy, acute/chronic myopathy.
Methanol
Oxidized by alcohol & aldehyde dehydrogenase → formate, formaldehyde. Peak serum concentrations w/in 1-2 h (delayed if EtOH coingestion). Pyridoxine & thiamine partially involved metabolite elimination. Zero-order kinetics.
Presentation: Intake of paint solvents, antifreeze, windshield fluid, canned fuel (sterno), gasoline additives, shellac, copy machine fluid, home heating fuels (usually by alcoholic or child). Blurred vision (“snowstorm-like”), blind. ↓ LOC, vomiting, abd pain.
Diagnosis: Typical si/sx + anion gap metabolic acidosis (serum bicarb typically <10 mEq/L). Funduscopy: Hyperemia, papilledema. Check methanol level, Osm gap, ABG.
Management:
Fomepizole (inhibitor of alcohol dehydrogenase): Loading dose 15 mg/kg in 100 mL D5W over 30 min → 10 mg/kg q12h × 48 h → 15 mg/kg q12h until methanol concentration <20 mg/dL (EtOH used in past but IV form often not available & has erratic pharmacokinetics [NEJM 2001;344:424]).
Folate 50 mg IV q4h or 2 mg/kg IV q6h (cofactor degrading toxic metabolites).
Hyperventilation: If pt is intubated, hyperventilating to PCO2 <30 reduces acidemia.
Sodium bicarbonate: For serum pH < 7.3; start 1-2 mEq/kg IV × 1; maintenance infusion: 133 mEq of sodium bicarbonate in 1 L of D5W.
Hemodialysis: For pH < 7.3, methanol >16 mmol/L, visual impairment, renal failure.
Ethylene glycol
Oxidized by alcohol & aldehyde dehydrogenase → glycolic acid & oxalate. Peak serum concentrations in 1-2 h (delayed if EtOH coingestion). First-order kinetics.
Presentation: Ingestion of antifreeze, paint, polish, coolant, detergent, fire extinguisher foam. Three phases: 0.5-12 h neurologic: Transient inebriation, euphoria (like EtOH effects), n/v, then lethargy, nystagmus, ataxia, ophthalmoplegia, myoclonic
jerks. If severe: Coma, hypotonia, sz. 12-24 h cardiopulmonary: ↑ HR, RR, BP, arrhythmias, pulm edema. Multiorgan failure → death (2/2 severe AG metab acidosis). 24-72 h renal: Oliguria, flank pain, ATN, ARF (2/2 oxalate crystal deposition).
jerks. If severe: Coma, hypotonia, sz. 12-24 h cardiopulmonary: ↑ HR, RR, BP, arrhythmias, pulm edema. Multiorgan failure → death (2/2 severe AG metab acidosis). 24-72 h renal: Oliguria, flank pain, ATN, ARF (2/2 oxalate crystal deposition).
Dx: UA for calcium oxalate crystals. Ethylene glycol level, Osm gap.
Rx: Similar to methanol poisoning. IVF at 250-500 mL/h IV to enhance renal clearance & limit renal oxalates deposition. Fomepizole: Same as for methanol. Thiamine & pyridoxine 100 mg IV/IM qd (cofactors for metabolite elimination).
Isopropyl alcohol
Metabolized to acetone. Peak concentration ˜4 h.
Presentation: Ingestion of rubbing alcohol, solvents, paint thinner, hair spray, skin cleansers. Same as ethanol, but more severe. Fruity breath (acetone). Hemorrhagic gastritis, shock.
Dx: Serum isopropanol level. Does not produce anion gap. Acetone → falsely ↑ Cr.
Rx: Dialysis for refract hypotension or level >400 mg/dL.
ETHANOL WITHDRAWAL
Presentation: Discontinuation/significant ↓ in EtOH intake. Insomnia, anorexia, n/v, tremors, anxiety, hallucinations, palpitations; autonomic hyperactivity (tachycardia, HTN, hyperreflexia, irritability, sweating, low-grade fever). Onset ˜6 h after last use. Resolves over 24-48 h. Szs: GTCs w/in 6-48 h (most 12-18 h), ˜25% pts. SE rare. Halluc: Mostly visual; onset first 12-24 h; resolve over 24-48 h. DTs in 1/3 cases if w/d untreated after 2-4 days. Risk factors: Chronic drinking, previous DTs, concurrent illness, >30 yo, w/d sx despite high EtOH levels, >2 days b/n last drink & onset of w/d. Disorientation, agitation, sweating, tachycardia, HTN, halluc (usually visual). Mort: 5%, 2/2 arrhyth or underlying conditions.
ED Rx: Thiamine 100 mg IV BEFORE glucose 1 amp IV. Sz 2/2 EtOH w/d (no other cause identified): Lorazepam 2 mg IV significantly reduces risk of more szs.
In-house Rx: Thiamine 100 mg IV qd indefinitely (consider higher doses for Wernicke). MVI & folate 1 mg (thiamine, folate, MVI together as “banana bag”). BZ: For agitation & sz prevention. Goal: Pt calm but alert. Long-acting benzos preferred, e.g., diazepam (Valium) or chlordiazepoxide (Librium). Lorazepam (Ativan) or oxazepam (Serax) (shorter acting) useful in pts w/cirrhosis. If no response to escalating doses of BZs, consider intubation, phenobarbital or propofol. Do not treat psychotic sx w/phenothiazines or butyrophenones (may precip sz).
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