Emergency Medicine Residency Program
Take Home Points –Toxicology
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|Beta-Blocker Toxicity |Calcium-Channel-Blocker Toxicity |
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|Background – blocks beta receptors (1 & 2, selectivity depending on agent)|Background – 3 drug sub-classess; Verapamil most common cause of |
|resulting in decreased cAMP and blunting of catecholamine effects, some |death; decreases myocardial/smooth muscle contractility and pacing |
|agents are lipophilic |impulse generation, leads to myocardial depression and peripheral |
| |vasodilation |
|Symptoms/Signs – bradycardia, hypotension, cardiogenic shock; Propranolol | |
|widens QRS (Na-Ch blocking) and altered mentation/seizures/coma (crosses |Symptoms/Signs – bradycardia (sinus, AV block; Verapamil =most), |
|blood brain barrier), Sotalol prolongs QT/torsades/PVCs/VT/VF (K-Ch |hypotension, AMS/seizures/coma during stages of shock and massive |
|blocking); non-selective can affect respiratory/Bronchospasm, |ingestions (typically no neuro sx when not in shock) |
|potential/uncommonly Hypoglycemia (blocks gluconeogenesis/glycogenolysis),| |
|Hyperkalemia |Diagnosis – consider over BB if normal mentation/ Hyperglycemia |
| |(inhibits insulin release)/ Hypokalemia, tends to be more severe than |
|Diagnosis – clinical; clues=AMS / HypoGluc/HyperK/bronchosp |BB Toxicity |
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|Treatment – A: be weary of RSI drugs that can worsen myocardial |Treatment – A: early airway protection for aspiration |
|depression; “antidote” = Glucagon (see below when indicated) (bypasses B |precaution/avoiding crash intubation; “antidote” = High Dose Insulin |
|receptors to increase myocardial contractility), bolus 3-10mg with repeat |works by myocardial carbohydrate utilization (1U/kg bolus, 0.5-1U/kg |
|15min post, 1-5mg/h drip if effective, no max |drip), add Amp D50 and D10W drip if glucose 120 = Na Bicarb; Contractility = Glucagon / High Dose |C: similar to approach to BB Toxicity; CaCl 1g IV over 5min (x3 if |
|Insulin/Adrenergics (Epi/NE)/Ca/ECMO; Bradyc = |Gluconate; repeat q10-20min, drip 2-6g/h if needed) |
|Glucagon/Adrenergics/Pacing; Decreased SVR = Vasopressors/IABP/ECMO |D: AC if within 1 hour, M-AC if extended, WBI if extended; G-lavage |
|D: AC if within 1 hour (longer if extended release); consider WBI for |not recommended routinely |
|large; G lavage not recommended |E: Lipid Emulsion – see BB Toxicity |
|E: Lipid Emulsion - acts as sink or fatty acid energy supply, most | |
|effective for Propranolol/Carvedolol (lipophilic agents), 20% @ 1.5ml/kg |Dispo: extended release need monitoring 12-24 hours; standard release |
|bolus over 1min (can repeat) then 0.25ml/kg/min (may increase to 0.5ml), |asymptomatic and stable VS can be d/c or psyc after 6 hours |
|can give bolus dose during cardiac arrest | |
|Dispo: ICU if cardiovascular; sustained needs admit; regular release 6 | |
|hours asymptomatic can be d/c or psyc | |
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|Digoxin Toxicity |
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|Background – cardiac glycoside found in plants (foxglove, oleander, red squill, lily of the valley) helpful for patients with CHF and atrial |
|fibrillation; high vol distribution/protein binding, renal elimination; Na-K-ATPase inhibitor leads to increased intracellular Na/Ca & |
|extracellular K resulting in increased contractility and increased vagal tone resulting in decreased HR; increases vascular tone (though CHF |
|patients can have vasodilation/decreased tone); toxicity can be Acute (intentional OD) or Chronic (drug interactions, renal dysfunction even at |
|therapeutic levels) |
| |
|Symptoms/Signs – Acute: N/V/Abd pain, HA/dizzy/confusion/coma, brady/SVT with AV block, HyperK (severity correlates more with K levels than |
|digoxin levels); Chronic: N/V/D/Abd pain, fatigue/weakness/confusion/delirium/Yellow-Green halo, almost any ventricular/supraventricular |
|dysrhythmia, normal/decreased/increased K/ Hypomagnesia |
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|Diagnosis – Levels Therapeutic 0.5-2.0, Toxic >2.5 at 6hrs; EKG Changes: @ therapeutic =long PR, QT shortening, scooped ST segment, Tw |
|flat/inversion, increased U-w height; @toxicity = (almost any dysrhythmia except rapid atrial) PVCs (#1), bidirectional V-tach (pathognomonic), |
|“regular A-fib”, AV block |
| |
|Treatment – A: “antidote”= Digifab Indications – K >5 (or 6), Ventric dyshrhth, severe bradycardia, Acute if dosage >10mg adult (4mg child) or |
|level >10, Chronic if >4; Dosing – Acute 1 Vial for each 0.5mg ingested (give half, repeat if no response 1-2 hours after) or 10 Vials if unknown|
|over 30min; or #of Vials=TBL (total body load=dose ingested x0.8); or #of Vials = (dig level x Wt)/100; Chronic give ½ dose; Cardiac Arrest 20 |
|Vials IV bolus push |
|C: Bradydysrhthmias = Atropine 0.5-1mg (temporizing)/TC Pacing (temporizing)/Digifab; Cardiac Arrest = CPR with Digifab (50% survival!); |
|Ventricular Dysrhthmias = Mg (treats HypoMg) / Phenytoin (increases AV conduction) / Lidocaine (decreases ventric automaticity); Hyperk = Digifab|
|(Ca controversial, other agents for temporaizing); HypoK = treat if chronic but not acute |
|D: AC if early in acute ingestion; G-lavage not recommended E: Forced diuresis/HD/Hemoperfusion not helpful |
|Dispo: asymptomatic patients observe until decrease serial levels and K normal; symptomatic toxicity needs monitored setting; patients who |
|receive digi-fab should be ICU at least 6-12 hours (potential delayed toxicity) |
References:
Tintinalli 8e Chapters 194 (Beta-blockers), 195 (Calcium Channel Blockers), 193 (Digitalis Glycosides)
One Pill Can Kill
Previously discussed:
TCA
CCB
BB
Salicylates
Sulfonylureas
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|Camphor |Clonidine |Opiates |
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|Background – ingredient in topical liniments |Background – treatment for ADHD/nasal |Background – affects mu, K, delta receptors; mu |
|(Vick’s Vapo-Rub, Ben Gay, Tiger Balm), induces |decongestant, central acting alpha-2 |activation causes respiratory depression and |
|hyperemia and warmth, used as |antihypertensive resulting in decreased |analgesia |
|analgesics/antipruritic/antittusive |adrenergic tone; oral or transdermal forms; | |
| | |Symptoms/Signs – CNS depression, miosis, |
|Symptoms/Signs – GI distress, sensation warmth, |Symptoms/Signs – opioid toxidrome with decreased|respiratory depression (#1 cause of pediatric death|
|CNS hyperactivity (excitement, restless, |LOC, miosis, bradycardia, hypotension, |– hypoxia, pulm edema, aspiration pneumonitis) |
|delirium, seizures) then depression; death from |respiratory depression, hypotonia | |
|respiratory depression or status epilepticus | |Treatment – Naloxone (onset |disturbances; supportive care, dextrose, |
|Symptoms/Signs – Biphasic Toxicity: initial |Glycolic Acid, Oxalic Acid, Ca Oxlate; |epinephrine, diazepam, airway management |
|antimuscarinic 2-3 hrs post ingestion then |Isopropanol -> Acetone) | |
|delayed opioid symptoms; fatal coma and | |Dextropropoxyphene – antitussive opioid, opiate |
|respiratory depression can be delayed |Symptoms/Signs – Methanol sx delayed 8-24 hours |toxidrome but can cause ventricular tachycardia |
| |and includes CNS depression, coma, hyperpnea, |(local anesthetic effects, Na Ch blocker); |
| |visual symptoms (blurred/double/hazy vision aka |supportive care |
|Treatment – similar to other opiates; symptoms |“snowstorm”, dilated pupils); EG period of | |
|may be delayed |inebriation 4-8 hours then metabolic acidosis, | |
| |renal toxicity/ATN, profound hypoCa (EKG |Theophylline –vomiting, agitation, seizures, SVT, |
| |changes, tetany), and CN deficts (opthalmoplegia|vomiting, hypotension, tachycardia; supportive |
|Dispo: all need admission to monitored setting |facial weakness, hearing loss, dysarthria, |care, IVF, ionotropes, benzodiazepines, |
|for at least 24 hours |dysphagia) |anti-emetics, GI decontamination |
| | | |
| |Diagnosis – High AG and OG Metabolic Acidosis |Amphetamines, Ecstasy – agitation, confusion, |
| |for Methanol and EG, normal AG and high OG for |hypertension, hyperthermia; treat with |
| |Isopropanol; serum Methanol and EG levels not |benzodiazepines for agitation, supportive care |
| |readily available but can confirm later; Urine |otherwise |
| |Fluorescein and Ca Oxalates | |
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| | | |
| |Treatment – Supportive care initially; | |
| |Fomepizole (inhibits alcohol dehydrogenase, | |
| |alternative IV Ethanol); NaBicarb for | |
| |acidosis/decreasing visual problems/increases | |
| |elimination of glycolic acid; HD if toxic levels| |
| |>25/significant Metabolic Acidosis/Renal | |
| |Impariment, Supplemental Folate for Methanol, | |
| |Thiamine/Pyridoxine for EG | |
| | | |
| |Dispo: typically admit all patients with | |
| |exposure | |
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