Toxicology

History Must Include

• Time, route, duration, and circumstances of exposure

• Name and amount of each substance involved

• Onset, nature, and severity of symptoms

• First aid measures already taken

• Medical/psychiatric history and occupation

Physical Exam Focus

• Vitals, cardiopulmonary system, neurologic status

• Eyes: nystagmus, pupil size, reactivity

• Skin: burns, color, warmth, moisture, puncture marks

• Abdomen: bowel sounds, bladder size

• Neuromuscular: dyskinesia, fasciculations, rigidity, tremors

Stimulated State

• Sympathomimetic/anticholinergic

  • Increased HR

  • Increased BP

  • Increased temperature

  • Mydriasis

Depressed State

• Opioids, sedatives, cholinergics

  • Decreased HR

  • Decreased BP

  • Miosis

Discordant State

• Asphyxiants, CNS syndromes, AGMA inducers → mixed findings

Drugs that have Normal Response

Qualitative Screening

• Urine drug screen → confirms/rules out suspected poisoning

• Obtain baseline ECG for any suspected cardiac toxin

• Rapid qualitative tests for drugs of abuse may screen but not diagnose → most useful when

  • Unexplained coma

  • Seizures

  • Cardiac instability

  • Metabolic or respiratory acidosis

Quantitative Serum Levels

Guide clinical management for specific agents

• APAP

• Alcohols

• Anti-convulsants

• Barbiturates

• Digoxin

• Heavy metals

• Iron and lithium

• Salicylates

Antidote Trial

• Resolution of altered mental status/abnormal vitals within minutes of IV antidote is virtually diagnostic (dextrose, naloxone, flumazenil)

Leading Overall Cause of Death from Poisoning

CO

Most Common Pharmaceutical Agent Implicated in Fatal Poisoning

Acetaminophen

Pre-Toxic Phase

• Before onset of poisoning

• Decontamination is highest priority: assume the maximal potential toxicity

  • Most effective phase for decontamination

Toxic Phase

• Onset → peak effect

• Resuscitation is priority

  • IV access

  • O2 saturation

  • Cardiac monitoring

• Consider decontamination, but less effective

• Consider elimination enhancement

Resolution

• Continued supportive care until clinical, lab, and ECG abnormalities resolve

• Some agents may rebound from tissues

  • Things stored in fat

Airway and Breathing

• Consider intubation for CNS depression or seizures (aspiration protection)

• Mechanical ventilation for respiratory depression

• ECMO for critically ill patients refractory to resuscitation

Hemodynamics and Rhythm

• Hypotension unresponsive to fluids → vasopressors (epinephrine, NE)

• SVT with instability → treat based on causative agents

• Seizures/hyperthermia → benzodiazepines or barbiturates

  • Phenytoin contraindicated in toxicologic seizures

• Ventricular arrhythmias from TCAs → sodium bicarbonate

  • Anti-arrhythmics contraindicated in TCA dysrhythmia

• Psychosis → haloperidol or ziprasidone

Activated Charcoal Mechanism and Efficacy

• Absorbs ingested poisons within the gut lumen → charcoal-toxin complex evacuated in stool

• Efficacy by time of administration

  • Within 5 minutes → 73% reduction in absorption

  • Within 30 minutes → 51% reduction

  • Within 60 minutes → 36% reduction

Activated Charcoal Not Effective For

• Mineral acids

• Alkalis

• Highly dissociated salts

• Corrosive agents → obscures endoscopy

• Altered airway → aspiration risk

Multiple Dose Activated Charcoal (MDAC)

• Repetitive oral dosing every 2-4 hours enhances elimination of already absorbed substances

• Approaches efficacy of hemodialysis for:

  • Phenobarbital

  • Theophylline

  • Carbamazepine

  • Dapsone

  • Quinine

• Contraindications

  • Ileus

  • Bowel obstruction

  • Hemodynamic instability

  • Cathartics

Gastric Lavage

• Used for life threatening poisons not treatable with other methods (colchicine)

• Patient position → Trendelenburg, left lateral decubitus

  • Put a bunch of fluid in and then flush it out

• Efficacy

  • 52% decrease in absorption within 5 minutes

  • 16% decrease in absorption within 60 minutes

  • Not done often because it loses efficacy so quickly

• Contraindications

  • Corrosives or petroleum distillates → risk for perforation/aspiration

  • Compromised/unprotected airway

  • Combative patients or those who refuse

Whole Bowel Irrigation

• Ideal for: objects

  • Foreign bodies

  • Drug packets

  • Agents poorly absorbed by charcoal (heavy metals)

• Use PEG electrolyte solution at 2L/hr PO or NG until rectal effluent is clear

• Patient must be sitting upright

• Contraindications

  • Bowel obstruction

  • Ileus

  • Hemodynamic instability

  • Compromised airway (aspiration risk): could potentially do for someone who is intubated

Syrup of IPECAC

• No longer has role in poisoning management

• Can cause electrolyte/cardiac toxicity

Urinary Alkalization

• Goal

  • Urine pH > 7.5

  • Urine output 3-6 mL/kg/hr

• Use IV NaHCO3

  • Ion trapping prevents renal reabsorption of acidic poisons (salicylates)

• Contraindications

  • CHF

  • Renal failure

  • Cerebral edema

• Monitor

  • Acid-base

  • Fluids

  • Electrolytes

Extracorporeal Removal

• Most useful for:

  • Low molecular weight

  • High water solubility

  • Low protein binding

  • Small Vd

• Indications

  • Carbamazepine

  • EG

  • Isopropyl alcohol

  • Lithium

  • Methanol

  • Theophylline

  • Salicylates

  • Valproate

• Use when:

  • Deterioration despite aggressive supportive care

  • Dangerous blood levels

  • Renal failure

Other Techniques to Enhance Poison Elimination

• Chelation

  • For elimination of heavy metals (deferoxamine, DMSA, BAL, EDTA)

• Hyperbaric oxygenation

  • Can help to remove CO: consider for CO levels > 25%, LOC, pregnancy

• Dilution

  • Only used after corrosive ingestion (acid/alkali)

  • 5 mL/kg water/milk

  • Do not use for other toxins → may increase absorption

Indications, Contraindications, and Complications of GI Decontamination Procedures

Fundamentals of Poisoning Management

Common Toxidrome’s

Anticholinergic Common Agents

• Four A’s

  • Antihistamines

  • Antipsychotics

  • Antidepressants

  • Antiparkinsonian drugs

• Atropine

• Benztropine

• Scopolamine

• TCAs

• Datura (Jimson weed)

Anticholinergic S/S

• Dry, warm, flushed skin

• Fever

• Dry mouth

• Decreased bowel sounds, ileus

• Urinary retention

• Sinus tachycardia

• Mydriasis/blurred vision

• Delirium, restlessness, hallucinations → coma, psychosis, seizures

Mad as a hatter, dry as a bone, red as a beet, blind as a bat, hot as a hare, seizing like a squirrel

Anticholinergic Treatment

• Benzodiazepines → first line for agitation

  • Physostigmine if benzodiazepines ineffective → inhibits acetylcholinesterase and more ACh competes for blocked receptors

• Cooling measures

Cholinergic Agents and Mechanism

• Agents

  • Organophosphates (malathion, diazinon)

  • Carbamates

  • Nerve agents

  • Some mushrooms

• Absorbed via inhalation, gut, skin, mucous membranes: inhibits cholinesterase → excess ACh at muscarinic and nicotinic receptors

Cholinergic S/S

SLUDGE

• Salivation

• Lacrimation

• Urination

• Defecation

• GI distress

• Emesis

Killer B’s

• Bradycardia

• Bronchorrhea

• Bronchospasm

Cholinergic Treatment

• Decontamination: brush dry chemical before irrigation

• Airway management

• Activated charcoal

• IV fluids

• Atropine and 2-PAM (pralidoxime)

  • Atropine

    • Excellent BBB penetration

    • Dries secretions

    • Does not reverse paralysis

  • 2-PAM

    • Reactivates AChE → reverses respiratory muscle paralysis

    • Poor BBB penetration

  • Both are needed → each covers what the other cannot

Sympathomimetic Agents

• Cocaine

• Amphetamines

• MDMA

• Methamphetmaine

• Ephedrine

• Pseudoephedrine

Sympathomimetic S/S

• Anxiety

• Agitation

• Paranoia

• Diaphoresis

• Hyper-reflexia

• Mydriasis

• Piloerection

• Distinguished from anticholinergics by:

  • Hyperactive bowel sounds and diaphoresis

• Complications

  • HTN

  • Tachycardia

  • ICH

  • MI

  • Aortic dissection

  • Rhabdomyolysis

Sympathomimetic Treatment

• Supportive measures: sedation with benzodiazepines, cooling

• NO BB: unopposed alpha → HTN crisis

• Cocaine ACLS modification

  • Increase epinephrine interval to 15-10 minutes

  • Avoid high dose epinephrine

  • Consider withholding in refractory V-fib

Sympathomimetic Clinical Pearl

• Cocaine prevents NE re-uptake → giving exogenous epinephrine may worsen catecholamine excess

• In cocaine overdose with V-fib, consider catecholamine excess as the cause before giving more epinephrine

TCA Mechanisms of Toxicity

• Antihistamine → CNS sedation/coma

• Antimuscarinic → anticholinergic syndrome (dry, tachycardic, confused)

• Alpha adrenergic blockade → orthostatic hypotension

• Na+ channel blockade

  • Widened QTS

  • Conduction delays

  • Contractility decreased

• K+ channel blockade → QT prolongation

• GABA antagonism → seizures

• Serotonin uptake inhibition → serotonin syndrome

TCA EKG Changes

• Sinus tachycardia

• Rightward axis

• Prolonged PR and QT

• Widened QRS → worsens as toxicity increases

• Terminal R wave (right bundle affected > left bundle)

TCA Treatment

• Sodium bicarbonate

  • 1-2 mEq/kg bolus → drip

  • Use if:

    • QRS > 100 ms

    • Rightward axis > 120 degrees

    • Hypotension

• Benzodiazepines for seizures

• Charcoal if alert

• Dialysis ineffective due to large Vd

• Antiarrhythmics contraindicated → can worsen dysrhythmias

MAOIs

• Inhibits MAO → increase storage/release of epinephrine, NE, dopamine, serotonin, and tyramine

• Tyramine reaction

  • Occurs when taking MAOIs with aged cheese, preserved meats, chianti wine, fava beans)

  • Causes severe HTN crisis

  • Treat tyramine crisis with phentolamine (alpha blocker) or nitroprusside

SSRIs

• S/S

  • GI side effects (most common)

  • Sedation

  • Tremor

  • Tachycardia

  • QT prolongation and seizures → rare

• Treatment

  • Supportive

  • NaHCO3 if QT prolonged

Serotonin Syndrome

• Life threatening increase in serotonergic CNS activity from drug interactions, therapeutic use, or intentional OD

• Classic triad

  • Altered mental status

  • Autonomic hyperactivity

  • Neuromuscular abnormalities (clonus, hyper-reflexia, lower extremity rigidity)

• Treatment

  • Benzodiazepines for sedation

  • Cyproheptadine (serotonin antagonist) → more definitive

Serotonin Syndrome vs Anticholinergic Toxicity vs Malignant Hyperthermia

Atypical Antipsychotic Overdose

• Less extrapyramidal effect than typicals

• S/S

  • Sedation

  • Seizures

  • Temperature instability

  • Hypotension

  • Tachycardia

  • QT prolongation

  • Watch for NMS even at therapeutic doses

• Treatment

  • Supportive

  • NaHCO3 if QT prolonged

  • Magnesium if TdP

NMS Diagnosis

• Fever

• Altered mental status

• Leukocytosis

• Tremors

• Elevated CPK

• Rigidity (lead pipe)

Caused by dopamine receptor blockade or rapid withdrawal of dopaminergic medications

NMS Treatment

• Stop the offending agent

• Cooling

• IV fluids

• NaHCO3 infusion

• Dantrolene

  • Stops calcium leak from sarcoplasmic reticulum → controls hyperthermia and rigidity

• Bromocriptine

  • Dopamine agonist to restore dopaminergic tone

Acetaminophen Toxicity Mechanism of Toxicity

• Small doses → glucuronidation and sulfation

• High doses → CYP450 saturates → NAPQI accumulates → depletes glutathione → covalent binding to hepatocytes → necrosis

• Main organ injured → liver (may be fatal and could require transplant)

Acetaminophen 4 Stages of Toxicity

• Stage 1 (0-24 hours) → N/V, weakness, fatigue

• Stage 2 (24-48 hours) → elevated LFTs, RUQ pain, decreased urine output

• Stage 3 (72-96 hours) → liver function disruption, peak toxicity

• Stage 4 (4-14 days) → recovery or progressive liver failure

Acetaminophen Toxicity Treatment

• Within 1 hour of ingestion and airway intact → activated charcoal

• 4 hour serum APAP level → Rumack-Matthew nomogram to assess hepatotoxicity risk

• NAC (IV preferred)

  • Replenishes glutathione

  • Nearly 100% hepatoprotective if given within 8 hours

  • Monitor APAP levels and LFTs throughout

NSAIDs

• More problematic in normal use than in overdose

  • Ibuprofen < 100 mg/kg usually benign

  • Ibuprofen > 400 mg/kg very toxic

• S/S

  • Acute (within 4-6 hours) → visual changes, HA, seizures

  • Hypotension

  • Bradycardia

  • Anion gap acidosis

  • GI upset

  • Hyperkalemia, hypocalcemia, hypomagnesemia

  • Patient with borderline renal function → acute renal failure

• Treatment

  • Activated charcoal and supportive care

Salicylates

• Primary toxicity → uncouples oxidative phosphorylation

• S/S

  • Early: respiratory alkalosis (from direct CNS stimulation)

  • Later: metabolic acidosis and respiratory alkalosis

  • Tinnitus

  • Hyperthermia

  • N/V

  • Altered mental status

  • Seizures

• Treatment

  • Urinary alkalization (NaHCO3) → ion trapping in urine

  • If altered mental status, renal failure, serum level > 100 mg/dL → hemodialysis

  • Avoid acetazolamide → worsens acidemia

Digitalis Mechanism Presentation

• Inhibits Na+/K+/ATPase → increase intracellular calcium → increases vagal tone and have bradydysarrhythmias

• Narrow therapeutic to toxic margin

Digitalis S/S

• Bradycardia

• AV block

• Frequent PVCs

• Multifocal V-tach

• Junctional escape

• Yellow green halos

• Dizziness and weakness

• Flu-like symptoms

• Toxic hyperkalemia

Digitalis Treatment

• If < 2 hours after ingestion → charcoal

• Severe bradycardia → atropine and pacing

• Ventricular arrhythmia → phenytoin

• Definitive treatment → digoxin specific FAB fragments

  • Sheep derived anti-digoxin antibodies bind free digoxin

Digitalis Key Points

• Do not aggressively treat hyperkalemia in digitalis toxicity → Digibind will correct it as Na+/K+ pumps are restored

• Slow diffusion and high Vd mean blood level may appear near normal in chronic toxicity

• Acutely high levels may not appear very toxic initially → monitor closely

BB Overdose Presentation

• Negative inotropy → hypotension

• Negative chronotropy → bradycardia

• Bronchospasm

• Hypoglycemia

• QRS widening

• CNS: sedation, coma, seizures, psychosis

• Sustained release → may delay symptoms 4h+ (toxic time bomb)

BB Overdose Treatment

• Activated charcoal within 1-2 hours of ingestion

• Trial of atropine (may not work)

• Normal saline bolus and IV calcium (increase inotropy)

• High dose insulin (100-120 units per hour) and glucose

  • Overcomes BB interference with insulin → glucose to myocytes

• Glucagon

  • Increase cAMP → increase intracellular calcium → improved contractility

  • Pre-medicate with anti-emetics (high dose glucagon causes severe N/V)

• Lipid emulsion therapy

  • Lipid sink for highly lipophilic BBs (propranolol)

• Catecholamines → epinephrine most effective

• Pacing if refractory (do not need long term therapy because drug will eventually be eliminated)

CCB Overdose Presentation

• Most deadly cardiac drug → most cardiovascular drug deaths in U.S

• Verapamil and diltiazem → bradycardia, hypotension, AV block

  • More of the heart affects in addition to hypotension

• Amlodipine → vasodilation, reflex tachycardia

  • Does not really work on the heart and more on the vasculature

• All can cause:

  • Complete heart block

  • Cardiovascular collapse

  • Hyperglycemia and acidosis (blockade of pancreatic insulin release)

  • Pulmonary edema

  • Altered mental status

• Onset delayed up to 12 hours with SR formulations

CCB Overdose Treatment

• Mainstay → calcium

• High dose insulin and glucose

• Trial of atropine and 0.9% NS

• Glucagon

• Adrenergics (epinephrine)

• Whole bowel irrigation for sustained release formulation

• < 2 hours → charcoal

• Gastric lavage considered within 1 hour given high toxicity

• Pacing if refractory (do not need long term therapy because drug will eventually be eliminated)

Diuretics Overdose

• Thiazides and loop diuretics in overdose can cause:

  • Hypotension

  • Hyponatremia, hypokalemia, hypocalcemia

  • Metabolic acidosis

  • Mechanism of excreting too much fluid

• Treatment

  • 0.9% NS and electrolyte replacement

  • Pressors if fluid unresponsive for acute hypotensive phase (NE)

  • Do frequent labs

  • Most diuretics last around 12 hours → very self limiting

ACE-I Overdose

• S/S

  • Hypotension

  • Hyperkalemia

• Treatment

  • Largely supportive

  • 0.9% NS

  • Pressors if needed

  • Monitor kidney function long term because the can be nephrotoxic

Cyanide Poisoning Mechanism and Sources

• Inhibits cytochrome c oxidase → cells cannot use O₂ → anaerobic metabolism → lactic acidosis

• Sources:

  • Combustion of wool/rubber/silk

  • Industrial use

  • Apricot/cherry pits

  • Jewelry manufacturing

Cyanide Poisoning S/S

• Headache

• HTN

• Tachycardia

• Seizures

• Coma

• Bitter almond odor

• Pulmonary edema

Cyanide Poisoning Treatment

• Supportive care + 100% O₂

• Three antidote strategies:

  • Direct cyanide binding — hydroxocobalamin (cyanokit) is 1st line

    • High dose vitamin B12

    • Directly binds cyanide → forms cyanocobalamin → renally excreted

    • May cause transient reddish discoloration of skin, plasma, urine, and mucous membranes — expected and not harmful

    • Preferred over nitrite/thiosulfate in victims with concomitant CO poisoning (avoids methemoglobin formation)

  • Methemoglobin induction

    • Amyl/sodium nitrite (ferric Fe³⁺ binds cyanide)

  • Sulfur donors

    • Sodium thiosulfate (rhodanese → thiocyanate)

CO Poisoning Exposure

• Leading overall cause of death from poisoning

• Poorly ventilated heating systems, confined spaces

• Inhaled colorless, odorless gas

• Think: groups of people with similar complaints

CO Poisoning S/S

• CO has 240× greater affinity for Hgb than O₂ and drastically outcompetes oxygen

• Early:

  • Headache

  • N/V

  • Poor concentration

  • Tachypnea

• Progressive: confusion, lethargy, coma

• Late: cherry-red skin (unreliable finding)

CO Poisoning Diagnosis

• ABG/VBG co-oximetry

  • SpO₂ unreliable → falsely normal

    • Pulse oximetry measures the percentage of hemoglobin that is bound to something: can’t differentiate between oxygen and CO

CO Poisoning Treatment

• High-flow, high-concentration O₂

  • Reduces CO half-life from from around ~5 hours (room air) to ~1 hour

• Hyperbaric O₂ therapy:

  • Indications

    • CO level >25%

    • Loss of consciousness

    • Neurologic signs

    • Pregnancy (due to complications that can arise)

  • High levels and pressure of oxygen to decrease the half life and eliminate it quicker

Caustic Substance Ingestion Acids vs Alkalis

• Acids → coagulation necrosis with significant injury at exposure sites

• Alkalis → liquefaction necrosis and allows for tissue transforms to viscous liquid with more wide spread tissue damage

• Both can damage mouth, esophagus, and GI tract

  • Industrial >> household strength

  • Strong acids may be worse than strong alkalis for GI injury

Caustic Substance Ingestion S/S

• Facial burns

• Oral/throat pain

• Dysphagia, odynophagia

• Drooling, dysphonia (damage around vocal cords), hoarseness, stridor (can cause angioedema and localized swelling)

• Abdominal pain, N/V

• Respiratory distress

• Most symptoms from local effects caused by caustic ingestion

Caustic Substance Ingestion Treatment

• Safety first

  • PPE

  • ABCs because high risk for hoarseness, stridor, dysphonia, and significant local edema → at risk for losing airway

  • Dilution with water/milk → only thing that we can use dilution for

  • Caustic skin/eye → copious irrigation

  • Early endoscopy

  • Surgical intervention if needed → if they have significant damage and a perforation, need OR for intervention

• NO activated charcoal (obscures endoscopy)

• NO NG tube (tissue damage risk: may risk creating a perforation)

• NO neutralization

• Steroids to prevent stricture:

  • Significant esophageal or tracheal damage and heals → can form strictures

  • Controversial and likely unhelpful

Hydrocarbon Poisoning Presentation

• Gasoline, kerosene, lighter fluid

  • May be ingested, inhaled, or dermally absorbed (large amount on skin for prolonged period of time)

• Pulmonary:

  • Wheezing

  • Dyspnea

  • Hypoxia

  • Pneumonitis

• CNS:

  • Headache

  • Dizziness

  • Slurred speech

  • Ataxia

  • Coma

  • Cardiac dysrhythmias

• Peripheral:

  • Foot/wrist drop

  • Numbness and tingling

Hydrocarbon Poisoning Treatment

• Personal safety + PPE first

• Support and ABCs

• Decontaminate patient

• Nothing by mouth — NO activated charcoal

• NEVER induce vomiting — lethal aspiration risk

• Aspiration causes severe lung damage — be prepared to manage airway aggressively

Iron Toxicity Presentation

• Most ODs in young children → initially asymptomatic but acute cases can be fatal

• Moderate toxicity: 20–60 mg/kg elemental iron

• Iron toxic to GI tract → GI upset within 6 hours is nearly universal with toxic dose

• Five stages of toxicity

  • GI → apparent recovery → systemic toxicity → hepatic failure → GI scarring

Iron Toxicity Diagnosis

• X-ray abdomen → may visualize iron tablets

  • Negative plain film does not rule out ingestion

Iron Toxicity Treatment

• Antiemetics

• IV fluids

• Deferoxamine

  • Binds iron → vin rosé urine when active (stop when urine color clears)

  • Oral for mild toxicity

  • IV for severe/systemic

• Charcoal NOT effective for iron

• Gastric lavage <1 hour if toxic ingestion

• Whole bowel irrigation can limit absorption

Ethanol Toxicity S/S

• Slurred speech

• Nystagmus

• Disinhibition, CNS depression, poor coordination

• Peripheral vasodilation → ↓BP, ↑HR

• Level 400–500 mg/dL: fatal respiratory depression (especially for non-drinkers)

  • Chronic alcoholics may tolerate surprisingly high levels and have no symptoms

• Is the most common cause of osmolar gap:

  • Osmolality = (2×Na+) + (glucose/18) + (BUN/2.8) + (EtOH/4.6)

Ethanol Toxicity Treatment and Work Up

• Supportive

• D5NS is fluid of choice

  • Young patients have risk of hypoglycemia

• Ethanol does NOT bind to charcoal

• Evaluate for co-ingestions, trauma, and infection

  • Subdural hematoma

  • Aspiration pneumonia

  • C-spine injury

  • Thrombocytopenia

• Elimination rate:

  • Non-drinkers: 15–20 mg/dL/hr

  • Alcoholics: 25–35 mg/dL/hr (withdrawal symptoms quicker)

Isopropyl Alcohol

• Rubbing alcohol: 2× potent and 4× longer than ethanol

• Metabolized to acetone — fruity/ketone breath without ↑glucose

• Causes osmolar gap but NO anion gap acidosis

• GI: hemorrhagic gastritis

• Treatment:

  • Supportive

  • IV fluids

  • PPI

  • Hemodialysis for very large amounts

Methanol

• Windshield washer fluid, sterno, moonshine

• ADH → formaldehyde → formic acid → inhibit mitochondria

• Toxicity develops over 12–30 hours (latent period)

  • 'Snowstorm vision', optic neuritis, blindness

  • TIME = EYES

• Treatment:

  • Correct acidosis

  • Fomepizole or ethanol to compete for ADH

  • Hemodialysis

  • Folate

Ethylene Glycol

• Antifreeze: lethal dose ~2 mL/kg

• ADH → glycolic acid + calcium oxalate

• Stages

  • Stage 1 (<12 hours): CNS depression, seizures

  • Stage 2 (12–24 hours): cardiac toxicity, hypocalcemia

  • Stage 3 (24–72 hours): acute renal failure, ATN

  • TIME = KIDNEYS

• Treatment:

  • Calcium gluconate

  • Fomepizole or ethanol for ADH

  • Hemodialysis

  • Pyridoxine + thiamine

Antidote Pairs

Potential Interventions in Toxin Induced Cardiac Arrest