Toxicology Flashcards
General assessment
Hx of ingestion/inhalation should try to be obtained -Time -Amount -Pill bottles found Physical exam -CC/symptom may suggest the dx Toxicology lab assessment -Platelets, CMP, drug screen, EtOH level Look for anything on children's clothes
Gastrointestinal decontamination
Emesis: little evidence of help
Indications for gastric lavage
Within 1 hr of ingestion Ingested substance not bound by activated charcoal No effective antidote Symptomatic -Intubate -Lavage -Cathartic Make sure airway is secure before you do this!
CIs for gastric lavage
Caustic agents
Glass
Sharp objects
Procedure for gastric lavage
Large NG tubes
-28-40 French adults
-16-20 French for children
Left Lateral decubitus position
Intubate/secure airway if needed
200-300 mL saline injected then aspirated
First 100 mL sent for toxicology evaluation
LUQ massage to help with breaking up material
Continue until fluid is clear and at least 2 L used
Indications for activated charcoal
Presents 1-2 hrs after ingestion
Ingestion of large amount that will bind to charcoal
CIs for activated charcoal
Oral antidote is available Poor absorption (iron, lithium, heavy metals, alcohols) > 2 hrs since ingestion EGD planned/needed 1g/kg is dose with 30 gm max
Polyethylene glycol (PEG) dose
1-2 L/hr via NG/OG tube
Indications for polyethylene glycol
Removal of drug packets (body stuffers)
Large ingestion of sustained-release drug
Potential toxic ingestion that can’t be treat with activated charcoal (lithium, lead, iron)
CIs for polyethylene glycol
Infants
Pts receiving oral antidotes
Dynamic ileus, severe diarrhea, obstruction
Abdominal trauma/recent abdominal surgery
What can be done to enhance elimination?
Multiple-dose activated charcoal (MDAC) -Repeat dose every 2-4 hrs -Disrupts the enterohepatic circulation Urinary alkalinizations Hemodialysis -Alkaline diuresis: ionizes weak acids preventing renal reabsorption --Barbiturates, salicylates, lithium --1-2 amps NaHCO3 followed by gtt -Dialysis --Ethylene glycol, methanol, Paraquat
Presentation of benzodiazepines
Mild-moderate intoxication, based on what they took, how often they take it. Lethargy Slurred speech Drowsiness Ataxia Nystagmus Coma Severe intoxication: coma, resp depression Hypotension IV overdose has 2% mortality rate
Dx of benzodiazepine toxicity
UDs Except Klonopin (gas chromatography)
Tx of benzodiazepine toxicity
Supportive (airway, BP support)
Flumazenil, GI decontamination efforts
-Don’t use Flumazenil if pt on chronic Benzos. Can cause withdrawal.
Activated charcoal if <1 hr and no significant CNS depression
Examples of sympathomimetics
Ritalin Adderall Ephedrine Cocaine Methamphetamines
Mechanism of sympathomimetics
Increased release of epi, NE from alpha, beta adrenergic receptors, decreased enzymatic breakdown/reuptake
Clinical presentation of sympathomimetic toxicity
Toxidrome: Agitation Tachycardia HTN Large pupils Diaphoretic
Dx of sympathomimetic toxicity
Clinical presentation (hx and PE)
ECG (establish rhythm and r/o ischemia)
UDS
Tx of sympathomimetic toxicity
Supportive care (active/passive cooling measures), IV hydration
Benzodiazepines: for sedation, hyperthermia, muscular rigidity
Sodium bicarb: for wide complex dysrhythmias
Avoid BBs
-Unopposed alpha receptors, will make BP worse
Mechanism of phencyclidine (PCP)
Sigma receptor stimulation leads to dysphoria
Antagonism of glutamate activity at NMDA receptor leads to sedation
Clinical presentation of PCP toxicity
Distortion of time, space and somatic sensation are hallmark signs
Delusions, hostility, bizarre/violent behavior
Dx of PCP toxicity
Hypoglycemia Elevated creatinine kinase AST ALT UDS sometimes -Depends on facility on whether or not it gets tested
Tx of PCP toxicity
Reassurance/calming pt
Benzodiazepines
Comatose: intubate
Mechanism of acetaminophen, including how an overdose occurs
Metabolized in liver
90% conjugated with glucuronide or sulfate to nontoxic metabolites.
5% oxidized by CYP-450 to NAPQI
Glucuronide can bind to NAPQI forming nontoxic metabolite but in overdoses the stores of glucuronide become depleted
The free NAPQI binds to cellular proteins causing hepatic injury
Phase 1 of acetaminophen toxicity
12-24 hrs
N/V
Anorexia
Diaphoresis and pallor
Phase 2 of acetaminophen toxicity
Complete return to nl well-being
24 hrs-4 days
Increase in AST, ALT, INR and other liver enzymes
RUQ pain
Phase 3 of acetaminophen toxicity
3-5 days Symtomatic from hepatic injury Anorexia Nausea Malaise Abd pain
Phase 4 of acetaminophen toxicity
Recovery 5 days- 2 weeks
Regeneration of liver
AST/ALT return to baseline
What tool should be used whether to give an antidote for acetaminophen toxicity?
Rumack Matthew nomogram
Activated charcoal and acetaminophen
Avidly binds to charcoal
Even up to 8 hrs has shown some benefit
Tx for acetaminophen toxicity
N-acetylcysteine
140 mg/kg loading dose
70 mg/kg q4h x 17 doses
Special considerations for acetaminophen toxicity
Emesis after N-acetylcysteine: Zofran
Pregnancy: consult toxicologist
Chronic EtOH: Treat below nomogram line
Child: use nomogram
TCAs
Associated with life-threatening CNS and cardiovascular toxicity
Chronic pain
Migraine prophylaxis
Enuresis
SSRIs
More commonly used
Less toxicity
MAOIs
Uncommon
Clinical presentation of TCA toxicity
Anticholinergic: Confusion Anxiety Delirium Hallucinations Hyperactive DTRs Seizures/coma Time from ingestion to seizure can be very short QRS duration >0.10 sec has poor outcome- need EKG
Sodium channel blockade in TCAs
Causes hypotension with QRS widening >100 msec
ECG findings in TCA toxicity
Right axis deviation
PR, QRS, QT intervals become prolonged
-QRS >160 msec associated with increased risk wide complex dysrhythmia
Tx of TCA toxicity
Aggressive
Fluids, GI contamination (lavage if <2 hrs)
Alkalinization pH 7.45-7.55
-RAD, QRS >100 msec, dysrhythmia
Symptomatic bradycardia
-Alkalinization, isoproterenol, pacemaker
-NO atropine
-VTach
–Alkalinization, Lidocaine
Hypotension
-Alkalinization, IV fluids, vasopressors (levophed)
Alcohols
Ethanol -MC poison seen in the ED Methanol Ethylene glycol Isopropyl alcohol
Clinical presentation and dx of ethanol toxicity
CNS depressant, ataxia, dysarthria, visual impairment, nystagmus
Hx and PE
Serum levels available in ED
Tx of ethanol toxicity
ABCs Other injuries Thiamine, glucose Fluids? Time!
Methanol
Pain thinner, wood alcohol, windshield wiper fluid
-Accidental ingestion and suicide
Metabolized by ADH to formic acid
-FA accumulation causes anion gap metabolic acidosis, retinal toxicity
Clinical presentation of methanol toxicity
Similar to ethanol (HA, intoxication, CNS depression)
More pronounced drowsiness
Visual changes: looking through a snow field
-Progresses to blindness
Dx of methanol toxicity
Anion gap metabolic acidosis with high osmolar gap
Tx of methanol toxicity
Antidote: Fomepizole or ethanol
-Blocks ADH preventing formic acid production
Folate: improves metabolism of formic acid
Urinary alkalinization: improve renal clearance of FA
Consider hemodialysis with severe acidosis, visual changes
Ethylene glycol
Antifreeze -Colorless, odorless, sweet taste Metabolized to oxalic acid by ADH Oxalic acid accumulation causes anion gap metabolic acidosis and direct renal toxicity 100 mL can be fatal
Ethylene glycol toxicity dx
Anion gap metabolic acidosis with osmolar gap and acute renal failure
Calcium oxalate crystals in UA
Clinical presentation of ethylene glycol toxicity
N/V Ataxia Nystagmus then to: Tachypnea and cyanosis, pulmonary edema Then to: renal failure
Tx of ethylene glycol toxicity
Antidote: Fomepizole or ethanol
-Complete for ADH and prevent formic acid production
Thiamine and Pyridoxine (Vit B6)
-May help convert oxalic acid to nontoxic metabolites
Isopropyl alcohol
Rubbing alcohol
Metabolized directly to acetone by ADH
Clinical presentation of isopropyl alcohol toxicity
CNS depression and severe hemorrhagic gastritis
Hypotension, hypothermia
Death by respiratory arrest
Dx of isopropyl alcohol toxicity
Serum measurements
Suspect in an intoxicated pt with low/neg EtOH levels
Osmolar gap but no anion gap metabolic acidosis
Tx of isopropyl alcohol toxicity
Airway/ventilatory support
Fluid resuscitation, vasopressors
Clinical presentation of iron toxicity
5 phases
1: Abd pain, N/V, gastritis, bloody diarrhea (0-6 hrs)
2: Latent phase (6-24 hrs)
3: Systemic toxicity:
- Metabolic acidosis (lactate), hepatic/renal necrosis and failure
4: Fulminant hepatic failure (2-5 days)
5: Delayed sequelae
Dx of iron toxicity
Radiographic imaging
-Not always seen
Iron/TIBC not useful due to time (4 hrs)
ABG for acidosis
Tx of iron toxicity
Admit
Fluids
Deferoxamine- antidote
No GI sx within the first 6 hrs means NO toxicity!
Whole bowel irrigation if seen on abd X-ray
Activated charcoal will not help. Does not bind.
Lead toxicity
Usually pediatric cases from chronic exposure, not acute ingestion
Think paint chips from old homes
Clinical presentation of lead toxicity
N/V
Abd pain
Neuropathies
Stupor
Dx of lead toxicity
Anemia
Red cell stippling on smear
Densities on long bone radiographs
Tx of lead toxicity
Remove pt from source
Dimercaprol
Calcium disodium edetate (EDTA)
Indication for chelation tx: lead level >70 micrograms/dL or presence of sx
Sx/exam of opiate toxicity
CNS depression Resp depression Pinpoint pupil Bradycardia Hypotension Hypothermia
Dx of opiate toxicity
Clinical
Hx and PE
UDS
Tx of opiate toxicity
Supportive
Naloxone (Narcan)
-Possible SE of neurogenic pulmonary edema: very difficult to correct
Withdrawal sx of opiates
Nausea Vomiting Diarrhea Abd pain Insomnia Asthenia
Anticholinergics
Antipsychotics Scopolamine GI anti-spasmotics: Immodium Muscle relaxers Antihistamines Jimsonweed Deadly nightshade (Atropa belladonna)
Mechanism of anticholinergics
Competitive antagonism of acetylcholine at muscarinic and CNS cholinergic receptors
Sx/exam of anticholinergic toxicity
Agitation, delirium, hallucinations, coma, sz Hyperthermia, dry/warm skin Mydriasis and blurred vision Tachycardia Urinary retention
Dx of anticholinergic toxicity
Clinical dx based on hx and physical
EKG to screen for TCA toxicity
Similar to sympathomimetic
Tx of anticholinergic toxicity
Supportive care: cooling IV fluids Benzodiazepines for seizures/agitation Antidote: physostigmine -Only if tachycardia/agitation are not controlled
Examples of cholinergics
Donepezil Pyridostigmine (MG) Edrophonium Organophosphates Pilocarpine (glaucoma)
Mechanism of cholinergics
Inhibition of enzyme acetylcholinesterase leading to excess acetylcholine at muscarinic/nicotinic receptors
Sx of cholinergic toxicity
Salivation Lacrimation Urination Defecation GI upset Emesis "Killer bees" -Bronchospasm -Bradycardia -Bronchorrhea AMS, seizures
Dx of cholinergic toxicity
Hx and PE
EKG to screen for blocks/dysrhythmias
RBC cholinesterase levels
Tx of cholinergic toxicity
Supportive Atropine (high doses) -Hemodynamically unstable bradycardia -Excessive secretions Benzodiazepines for seizures/agitation Antidotes: -Atropin -Pralidoxime (2-PAM) for organophosphate poisoning
