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Flashcards in topic 25 Deck (29):

What are 4 steps to the general approach to a toxic patient?

• Vital Signs
– The A,B,C’s – “Treat the patient, not the poison”

• Consider decontamination

• Is there an antidote?

• Can the toxin be removed?


What are 4 things that should be considered in the differential diagnosis of a person in a toxic coma?

• Differential diagnosis of a patient in coma:

– Vital signs
– Patient odor
– Physical exam and history
– Consider along with toxic causes other possibilities:

• Metabolic

• Infectious (e.g. meningitis, encephalitis)

• Structural (e.g., tumor, hemorrhage, and edema)

• Vascular (e.g., arteritis)

• Psychiatric causes of brain dysfunction


What are 7 components of the physical exam that will help diagnose a toxic patient?

• Physical Exam

– patient odor

– skin, hair, nails

– pupil changes

– clues in respiratory exam

– clues in cardiovascular exam

– clues in gastrointestinal exam

– Specific “toxidromes”


What are some skin, hair and nail findings that are possible results of poisoning? What could cause them?

• Skin color (cyanosis) – Consider methemoglobinemia
• Nitrates
• Aniline dyes
• Phenazopyridine (Pyridium®)
• Benzocaine – Nail changes

Nail Changes
• white transverse growth arrest bands (Mee’s
lines) seen with heavy metals such as arsenic or

Hair changes
Toxic Allopecia
• Differential Diagnosis: – Alopecia totalis – Thallium (~2 wks) – Radiation


What are possible pupil changes and what could cause them?

• Miosis (small pupils)
– Opiates
– Clonidine
– Nicotine
– Cholinergic excess (e.g. organophosphate insecticides - must know for boards)

• Mydriasis (dilated pupils)
– Sympathomimetics
– Cocaine
– Amphetamines
– Anticholinergics
– Antihistamines


What are some clues that can be found in the respiratory exam? What could they be caused by?

• Tachypnea (fast respiratory rate)
– Toxins that produce acid metabolites
• ethylene glycol, methanol
– Toxins that uncouple oxidative phosphorylation
• cyanide, carbon monoxide, hydrogen sulfide, salicylates
– Toxins that result in hypoxemia
• CO, methemoglobin formers
– Toxins that stimulate the patient
• Sympathomimetics, cocaine, PCP

• Bradypnea (slow breathing)
– Opiates (may have apnea = absent breathing)
– Many other toxins that suppress respirations

• Pulmonary edema
– Many toxins (e.g. heroin, salicylates)

• Hypoxia (consider differential)


What are 4 common antidotes for a toxic patient? What are some possible downsides to using an antidote?

• While determining etiology of coma consider
the Basic Four Antidotes:
– Oxygen
– Naloxone
– Thiamine
– Dextrose

• Can be downsides to using antidotes
– e.g., arrhythmias & pulmonary edema after
naloxone administration in opiate addicts
– e.g., excessive Methgb after sodium nitrite


What is the antidote for methemoglobinemia? How does it work? When is improvement normally seen? When is it less effective?

• Methylene Blue for methemoglobinemia, which forms when the iron within hemoglobin is oxidized from the 2+ to the 3+ state. It does not carry oxygen.

• Methylene blue is itself an oxidizing agent, which is first converted in vivo to leukomethylene blue, and this reduced form is then able to reduce the hemoglobin back to the oxygen-carrying 2+ state.

• Symptomatic improvement usually occurs within
30 minutes. – A 2nd dose of methylene blue may be required in very severe cases or if there is evidence of ongoing methemoglobin formation.

• Less effective or ineffective in the presence of
glucose-6-phosphate dehydrogenase deficiency since its antidotal action is dependent on nicotinamide-adenine dinucleotide phosphate(NADP+). Exchange transfusion may be necessary in this case.


What are five important questions for the toxic patient history?

– Specific chemical or generic/brand drug name
– If unknown, what meds are available in home?
– Estimate of ingested dose & dosage strength
– Pharmaceutical formulation
• tablet, enteric coated, sustained release
• liquid vs. granules vs. solid
– What drugs are available
• “Medicine Cabinet Manifest”
• Grandparent’s medications


What is a general principle for the clues found in CVS exam? Which drug can cause a wide variety of arrythmias in overdose?

• Effects of toxins and drugs on the cardiovascular
system are complex

• Digoxin is an example of a drug that can cause a
wide variety of arrhythmias in overdose (atrial and ventricular).


Which drugs can cause arrythmias? How do they do it? What might they lead to?

– Prolonged QRS and/or prolonged QT
• e.g., Tricyclic antidepressants
– Poison the sodium channel (widens the QRS)
– Poison the potassium channel (prolongs QTc)
– May lead to tachyarrhythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF)


Which drugs can cause tachycardia?

• Tachycardia (fast heart rate) – Amphetamines and other stimulants – Antihistamines – Anticholinergic drugs (antimuscarinic) – Caffeine

– Cocaine

– Cyclic antidepressants

– Synthroid® (levothyroxine)
– Withdrawal from sedative/hypnotics/alcohol


Which drugs can cause bradycardia?

• Bradycardia (slow heart rate)
– beta-adrenergic antagonists (β-blocker) (propranolol)
– calcium channel antagonists (diltiazem)
– clonidine

– cardiac glycosides (digoxin)
– opioids
– organophosphate insecticides (muscarinic


What are the effects of an overdose of calcium channel blockers? What is the antidote? What else is it used to treat?

• Calcium channel blockers in overdose may also lead to bradycardia and heart block along with significant hypotension.

• Ca chloride or Ca gluconate

• Used to treat the severe, life threatening hypocalcemia caused by poisoning by hydrofluoric acid, ammonium bifluoride and other fluoride salts.

• Part of the multi-agent therapy for overdoses of calcium channel blockers.


What is the classic symptom of beta blocker intoxication? What else is it used to treat? What are the side effects?

• Bradycardia is classically seen with beta-blocker intoxication.

• Antidote for beta-blocker poisoning. May be of limited benefit in calcium channel blocker overdose

• Bypasses the blocked ß receptor to switch on adenylyl cyclase which increases production of cyclic AMP and activates more cAMP-dependent
phosphokinase.This in turn enhances calcium flux through calcium channels and increases the rate and strength of myocardial contraction.

• Treats hypoglycemia because it stimulates hepatic gluconeogenesis and glycogenolysis.

• Side effects include nausea and vomiting
and rash.


What are 2 clues that can be gathered from the GI Exam?

• Absence or severe diminution of bowel sounds

– Anticholinergic ingestion
• differentiate it from a sympathomimetic ingestion
as symptoms may be quite similar

– Gastrointestinal distress

• nausea, vomiting, and diarrhea are classic signs
of cholinergic (ACh) excess seen with organophosphate insecticide poisoning


What are 4 toxidromes?

Anticholinergic Toxidrome

Cholinergic Toxidrome(muscarinic & nicotinic)

Extrapyramidal Toxidrome

Opiate Toxidrome


What is the symptomology of anticholinergic toxidrome?

• DRY as a BONE (dry mouth and skin)

• RED as a BEET (flushed skin)

• BLIND as a BAT (dilated pupils and loss of sight


• MAD as a HATTER (central anticholinergic mania)

• HOT as HADES (hot, dry skin less able to release heat)

• FULL as a FLASK (urinary retention and full bladder)


What is the antidote for anticholinergic toxidrome? How is it administered? When should it not be used?

Physostigmine salicylate

• Reversible acetylcholinesterase inhibitor, which can cross the blood-brain barrier because it is an uncharged tertiary amine.
• Antidote to atropine / anticholinergic poisoning. Put patient on cardiacmonitor and administer slowly, because it may induce arrhythmia.
• Very short duration compared to the toxin; repeat dose if serious anticholinergic symptoms recur.
• Should NOT be used in patients with tricyclic antidepressant overdoses because of the risk of lethal arrhythmia.


What is the symptomology of cholinergic toxidrome? What is the antidote?

 Diarrhea
 Urination
 Miosis (small pupils)
 Bradycardia (slow HR)
 Bronchorrhea
 Bronchoconstriction
 Bradypnea (slowed breathing from weakness)
 Emesis
 Lacrimation (tearing)

Atropine is the antidote


What are extrapyramidal toxidrome symptoms? How do D1 and D2 receptors work? What happens to them with neuroleptics? What does that lead to? What are the antidotes? How do they work? Which should be used in children?

• Dystonia
• Torticollis
• Oculogyric crisis
• Gyric tongue movements
• Choreoathetosis

• D1 receptors are excitatory and D2 receptors are
inhibitory and during normal basal ganglia function,
there is a balance between both pathways.

• Neuroleptics (e.g. haloperidol, phenothiazines)
selectively block D2 receptors allowing endogenous
dopamine to stimulate D1 receptors

• Use ANTIDOTE : Benztropine mesylate
(Cogentin®) and Diphenhydramine to Treat drug-induced dystonic or extrapryamidal reactions occurring when therapy is initiated or
dose is increased (50% occur within 48 hours and
90% within 5 days.)
– Agents that balance dopamine blockade with muscarinic M1 receptor blockade are less likely to produce a dystonic reaction
• Benztropine is a centrally acting anticholinergic
agent with antihistamine activity, usually used
therapeutically in Parkinson’s disease.
• Benadryl (diphenhydramine) is a common sedating antihistamine H1 (Should be used in children)


What are the symptoms for opiate toxidrome? What is the antidote? How does it work?

• Pinpoint pupils (miosis)
• Respiratory depression
• Coma

• Pure opiate antagonist for reversal of opiate-
induced respiratory and CNS depression.
– one of most frequently used antidotes in emergency management of overdoses


What are 5 steps in the general approach to the toxic patient?

• Emergency stabilization using the A,B,C's

• Appropriate H & P assessment including toxidrome recognition

• Strategies for decontamination
– Skin
– GI tract (lavage, AC, WBI)

• Strategies for reversal/prevention of toxin
effect (antidotes)

• Strategies for enhancing elimination of absorbed toxins


What are 6 things involved in stabilization?

• Stabilization involves:
– oxygen delivery and assuring ventilation

– vascular access and support of circulation

– evaluate for evidence of cardiac rhythm effects

– recognition and control of seizures

– support airway and perform endotracheal
intubation as indicated

– recognize and treat rigidity and hyperthermia

– Send chemistry laboratory studies

– Can drug absorption be limited, metabolism
altered, toxicity modified, or elimination enhanced?


What are 6 possible ways to decontaminate the GI tract?

• Methods of gut decontamination to consider in poisoned patients:


Single Dose Activated Charcoal

Multi-dose Activated Charcoal


Gastric Lavage

Whole Bowel Irrigation


How is ipecac used today? what are some effects of abuse of ipecac?

Its use has faded...doesn't help to get rid of toxin

• Toxic effects
– dehydration from induced emesis )
– alkalosis
– hypokalemia
– myocarditis


What evidence is there to support gastric lavage?

There is none.


When should activated charcoal be used? How does it work?

• Single-dose AC should not be administered routinely in the management of poisoned patients.
• Based on volunteer studies, the administration of AC may be considered if a patient has ingested a
potentially toxic amount of a poison which is known tobe adsorbed to charcoal) up to one hour previously

• The adsorptive surface of activated charcoal contains carbonyl and hydroxyl groups that chemically adsorb substances with varying affinity.


How does whole bowel irrigation work? When should it be used?

• Whole Bowel Irrigation (WBI): uses a polyethylene glycol solution (PEG-ELS)
• Some volunteer studies have shown substantial decreases in the bioavailability of ingested drugs.

• Based on volunteer studies, WBI may be considered for potentially toxic ingestions of sustained release or enteric coated drugs.

• Case reports suggest benefit for potentially toxic ingestions of iron, packets of illicit drugs, paint chips or other sources of lead.