How effective are “gastric emptying” techniques?

(stomach pumping, ipecac, etc.)

50 % (or less) of material removed if used within 1 h

In the past, ipecac was recommended as part of every family’s first aid medicine kit. Is it considered a good idea for non-medical personnel to administer ipecac?

No –

It is RARELY indicated, and when it is, that needs to be under medical direction (preferably poison control)

It is used in the prehospital phase of care ONLY!

When is it acceptable to use ipecac, in terms of the ingestion?

(6 conditions)

1. Ingestion has serious risk of morbidity or mortality

2. Patient is far away from medical care (>1 h transport time)

3. Large, recent ingestion (<30 min before administration)

4. Substance not bound by charcoal

5. Plant ingestion

6. Not a hydrocarbon or caustic (you don’t want to bring those up again, causing more damage to the structures they pass)

(Note: Ipecac has become SO unpopular that many practitioners think it should never be used. That is not the case, although circumstances for its use are quite limited.)

When is it acceptable to use ipecac, in terms of the patient’s characteristics?

Patient must be capable of protecting the airway & not have any GI contraindications to inducing vomiting

If you give ipecac, what should you expect to happen?

1. Delayed emesis (15–20 min)

2. Prolonged emesis (not one or two bouts!) mainly over the first hour

When is ipecac completely contraindicated?

(1 material item; 3 patient items)

1. Material is toxic if it comes back up (caustics, hydrocarbons)

2. Patient not protecting airway (seizing, not alert)

3. Patient <6 months old

4. Bleeding disorder (risk of Mallory-Weiss tear in the stomach from repeated emesis)

When is “gastric lavage” a reasonable choice?

(2)

1. Recent ingestion of a life-threatening agent (<1 h is best)

2. Charcoal can’t bind the agent

(Note: “To teach the patient not to try that again” is not the answer on the boards! or in real life!)

When should you definitely not use gastric lavage?

(3)

1. Caustics &

Hydrocarbons

(worse to bring them

up than to let them sit)

2. Unprotected airway

3. Nontoxic agents, of

course

To decrease the risk of complications during gastric lavage, how is the patient positioned?

Left lateral decubitus & head 20° downward

When is whole bowel irrigation worth trying?

(4)

1. Sustained release pill ingestion (large)

2. Iron, lithium, or lead

3. Transdermal patch ingestion (whole patch)

4. Drug packers

 (can also be removed surgically)

When you give the first dose of charcoal in a multi-dose charcoal treatment, what should you consider ordering with it, for an adolescent patient?

A cathartic – usually sorbitol

Note: Not recommended in young children, due to risk of dehydration and/or electrolyte imbalance, & lack of proven efficacy in improving GI issues or the toxic ingestion itself

Should you order a cathartic with each dose of charcoal (if you are using multidosing)?

No

(can cause dehydration & electrolyte problems in patients of any age)

Does a single dose of charcoal produce constipation?

No

(only seen with multidosing regimens)

What is a normal osmolal gap?

Less than 10

What are the typical toxins & molecules that produce osmolal gaps?

Alcohols, antifreeze, & ketones

1. Ethanol

2. Acetone

3. Isopropanol

4. Ethylene glycol

5. Methanol

6. Ketoacidosis

How do you calculate the patients osmolality (roughly)?

2× Na + 10

(good rough estimate if BUN and glucose are near normal limits)

How do you calculate the patient’s osmolality precisely?

How can you calculate the osmolal gap?

Measured osmolality – calculated osmolality

(≥10 is abnormal)

Why do we care about the osmolal gap?

It suggests the patient has:

1. ketones

2. antifreeze (a type of alcohol)

3. or some other sort of alcohol

 on board

Which one is sometimes useful in toxic ingestions – urine acidification or alkalinization?

Alkalinization

(acidification is a distractor answer – not currently used)

Why is changing the urine’s pH sometimes a useful strategy?

Certain molecules are “trapped” in the renal tubules with the change in charge, and cannot return to the bloodstream

What three toxins are especially good candidates for urine alkalinization treatment?

1. Aspirin/salicylates

2. INH

3. Phenobarbitol

How is charcoal dosed?

1 g/kg to maximum of 100 g

In general, when is multi-dose charcoal useful? (2)

1. Sustained release preparations

2. Hepatically recirculated meds

Name some common or important overdose medications that you would want to use multi-dose charcoal with.

(4)

1. Theophylline

2. Phenobarbital

3. Carbamazepine

4. Salicylates

When is charcoal not useful in a toxic ingestion?

 (4 cases: 2 patient related2 item related)

1. Metals (e.g., lithium, iron)

2. Caustics, alkali/acid

3. Ileus

4. Obstruction

When is charcoal specifically contraindicated?

For GI reasons:

1. Caustics (not useful & obscures endoscopy view)

2. Ileus

3. Obstruction

What is a normal anion gap?

Less than 13

How is anion gap calculated?

(Na) – (Cl + CO₂) = gap

(positive electrolyte minus negative electrolytes)

The MUDPILES mnemonic goes with anion gap acidosis – What do the letters stand for?

Methanol, metformin

Uremia

DKA

Paraldehyde

Iron & INH

Lactic acidosis

Ethylene glycol

Salicylates

(For lactic acidosis, think of CO or CN as possible causes in tox questions)

How can you remember which anion gap mnemonic is which?

NAGs (non-anion gap) are HARD UP. Therefore MUDPILES must go with anion gap acidosis.

What is the antidote for a calcium channel blocker overdose?

(2)

1. Calcium

2. Glucagon

What is the antidote for a β-blocker overdose?

Glucagon

(isoproterenol is also a possibility)

In a coumadin overdose, what is your first choice to correct coagulation parameters?

FFP

(Fresh Frozen Plasma)

Vitamin K will not correct the bleeding problem fast enough – FFP supplies the missing factors right away!

Vitamin K is also listed as an antidote for coumadin (warfarin) toxicity. What are the problems with vitamin K use?

(2)

1. Unreliable onset of effect & always delayed

2. Can be difficult to regulate later if the patient needs ongoing anticoagulation

On the boards, should you give both FFP & vitamin K for warfarin toxicity?

Yes –

If there is an answer choice with both, it is usually correct

How do patients end up overdosing on warfarin?

(4)

1. Iatrogenic – level gets too high on med regimen

2. Medication dosing errors

3. Child gets hold of med

4. Rat poison

If your patient has ingested rat or mouse poison, what should you watch for, in addition to anticoagulant effects?

If it was the “wheat pellet” sort of poison, it may also contain a CNS depressant (alphachloralose)

Charcoal will bind it

Household detergents come in three classes – what are they & which one is dangerous?

Cationic, anionic, and non-ionic

Generally, only cationic is dangerous

If a patient eats or drinks a household detergent, what is the main toxic effect you should be worried about?

Corrosion of the gastric tissue (or in some cases respiratory tissue), due to the detergent’s pH –

typically the bases are the biggest problem

If a child has eaten a toxic plant, what should you do?

Give charcoal – it binds most plant toxins

There are many potentially toxic plants in the world. What are the typical effects of toxic plant ingestion?

(3 categories)

• Nearly all produce gastric irritation, usually with nausea/vomiting/diarrhea

• Many also produce CNS depression & sometimes seizures, if the ingestion is large enough

• Some produce arrhythmia

Unintentional toxic ingestions are most common in which age group?

Young children <6 years old

(Toddlers & infants are especially inquisitive!)

Unintentional nicotine ingestion is especially common in which pediatric age group?

<1 year old!

(70 % of nicotine ingestions are in this group)

What sorts of tobacco products are most often ingested by children?

#1 is cigarettes

#2 is smokeless tobaccos

(meaning snuff or chewing tobacco)

Electronic or “e-cigarettes” are relatively new. Is there a risk of an e-cigarette toxic ingestion?

Yes –

The fluid used to fill them can be consumed

The labeling on an e-cigarette or its fluid indicates its nicotine content. How should you interpret the milligrams listed?

The milligrams listed are PER CC!

(So if it says 16 mg, that means 16 mg nicotine PER cc!)

What does of nicotine is thought to be the minimum lethal dose for pediatric consumption?

1 mg/kg

(recent evidence suggests that significantly higher amounts can likely be tolerated)

What aspect of liquid nicotine (“vaping”) products should limit their ingestion?

Nicotine is quite irritating to the mucosal surfaces

(but some of the fluids have flavoring which may make them more attractive)

In addition to the nicotine content, are there other toxins you should worry about in a vaping fluid ingestion?

Yes, they often contain highly toxic alcohols & essential oils –

Content varies, but more consistency is likely as regulation of e-cigarettes increases

How do large nicotine ingestions cause death, generally?

“Nicotinic” stimulation leads to respiratory muscle paralysis & death –

Acetylcholine receptors of the nicotinic sort are overstimulated. When the muscle can no longer respond, it is effectively paralyzed & breathing ceases

After ingesting a small quantity of nicotine, what effects would you expect?

Tachycardia & vomiting

With a moderate nicotine ingestion, what effects are typical?

Ataxia & seizure

(ataxia is a somewhat unusual toxicological effect, so good to remember)

At higher doses, what is special about the nicotine toxidrome?

Nicotine activates both nicotinic & muscarinic ACh receptors, causing both sorts of effects!

(SLUDGE is added to the nicotinic effects)

TCA overdose and sympathomimetic overdose look very similar – how can you tell them apart?

TCAs are anticholinergic – no sweating!

Please recite the “anticholinergic mantra.”

Hot as hell (fever)

Blind as a bat (dilated, can’t accommodate)

Dry as a bone (can’t sweat)

Red as a beet (skin flushing)

Mad as a hatter (cognitive & psychotic changes)

Bloated as a bladder (urinary retention & decreased gut motility)

Seizing like a squirrel!

(seizures not uncommon)

How do you recognize the “cholinergic toxidrome?”

(4)

1. The gut moves like crazy (emesis & diarrhea)

2. Everything runs (salivation, urination, defecation, lacrimation, bronchorrhea)

3. Bradycardia

4. Miosis (small pupils)

Remember, this toxidrome is

the opposite of the

anticholinergic toxidrome.

What makes the cholinergic toxidrome dangerous, rather than just annoying?

The typical toxidrome symptoms are muscarinic, but the nicotinic system is also affected →

seizures, muscle twitching and/or weakness leading to respiratory failure

What agents typically cause cholinergic poisoning?

(3)

1. Insecticides (carbamates & organophosphates)

2. Certain mushrooms

3. Nerve gas agents

How can you remember that cholinergic poisoning critically involves the nicotinic receptor?

Insecticides that gave the bug SLUDGE would give you an unhappy bug, but probably not a dead bug

(SLUDGE is salvation, lacrimation, urination, defecation, GI distress/emesis)

How do most cholinergic toxins produce their effects?

They mess up the enzyme that normally breaks down ACh (acetylcholinesterase), so too much is constantly available

What is the first line antidote for any kind of cholinergic poisoning?

Atropine

Why is atropine helpful?

It is a competitive inhibitor of ACh, so binds to the same sites, without producing a response. This reduces the percent of molecules bound to a receptor that produce a response (allowing muscle cells to recuperate)

(Remember, though, that atropine only binds at muscarinic ACh sites!)

What type of poisoning needs 2-PAM (pralidoxime) treatment?

For organophosphate-type poisonings

Why is it important to give pralidoxime in organophosphate-type poisonings?

If it is not given promptly, the AChase is permanently disabled (referred to as “aging”)

(This means your patient will not recover until the body has synthesized all new AChase.)

How do the chemical nerve agents, a possible agent in chemical terrorism incidents & of course war, work?

The same way as the insecticide poisonings – acetylcholinesterase is inactivated, producing both muscarinic & nicotinic effects

If a nerve agent is inhaled, how long will it take to work (in general)?

Not long! Seconds to minutes

How long is required before nerve agent effects are seen, if the agent is absorbed from the skin?

Hours – anywhere from about 2–18 h

If nerve agents are acetylcholinesterase inhibitors, then what is the first line of treatment?

Atropine & pralidoxime (to prevent chemical aging)

As a healthcare worker, do you need to worry about contact with the patient poisoning you, if the patient has been exposed to a nerve agent by breathing it?

Generally not –

Nerve agent vapors generally dissipate rapidly on their own – VX present on the skin might still be an issue

(simple decontamination with soap & water will remove liquid nerve agent present on the skin)

Which nerve agent remains in the environment & is a hazard long after the initial release?

VX

(the others dissipate rapidly)

A chemical agent that causes severe pain & irritation of the skin, eyes, & mucous membranes, with respiratory problems & blister formation following those effects, is likely to be from what class of agents?

Vesicants or blistering agents

What are some examples of chemical agents that cause this skin & respiratory presentation?

Mustard gases (there are several types)

Phosgene (famous for its odor of “freshly mown hay”)

Lewisite

Are vesicant/blistering agents a contact hazard for healthcare workers?

Yes – decontamination should be performed

(both to remove the agent from the patient & to prevent contamination of others)

Do vesicant agents stay in the environment, creating an ongoing risk to others who go there?

Yes

(like the nerve agent VX)

In general terms, how do these blistering agents work?

They form acids on the skin or other bodily surfaces, generating damage

What is special about the eye effects of vesicant/blistering agents?

Corneal damage occurs regularly

Other than decontamination, how do you treat a patient exposed to a blistering agent?

Supportive care & burn-type protocols may be required

Are blistering agents generally persistent in the area where they were released?

Yes –

& that means they are also a risk to healthcare workers until the patient is decontaminated

Some chemical agents act primarily via the lungs, and are called choking or suffocating agents. Some of these are also a concern in industrial accidents. What are the most typical agents in this category?

(4)

Chlorine gas

Hydrogen chloride

Phosgene (also a vesicant/blistering agent)

Nitrogen oxides

Other than irritation to musical & skin surfaces, what are the main effects seen after a choking agent exposure?

Dyspnea & cough

Wheezing & bronchospasm

What is the main mechanism of action for the choking agents?

They are acids or acid formers when in contact with mucosal surfaces – these agents have most of their effects in the respiratory tree, though

Is recovery usually complete if the patient survives a choking agent exposure?

No – chronic respiratory difficulties often follow significant exposures

How is a choking agent exposure treated?

After removal from environment & provision of oxygen – supportive care

How do tear gas & pepper spray affect people?

VERY painful to eyes & makes seeing (temporarily) difficult

(they also react with water to form irritating compounds on mucosal surfaces, especially the eyes)

Are long-term effects expected from an exposure to lacrimation agents (tear gas & pepper spray)?

Generally not

Which chemical agent can be delivered in many different ways, and shuts down cellular protein synthesis?

Ricin

(from castor beans – made famous by espionage assassinations carried out this way)

Do protein synthesis inhibiting agents remain in the environment after release?

Only briefly

What is the usual result of ricin ingestion?

GI symptoms with gut hemorrhage,

Followed by liver & kidney failure

What is the usual result of ricin inhalation or injection?

Flu-like illness in the first day, then –

inhalation form presents with pulmonary symptoms first

injection form tends to go directly to multisystem organ failure

How is ricin exposure treated?

Supportive only –

With significant exposure, high mortality regardless of care

In general, for any patient suspected of being exposed to a chemical agent, what should be done prior to the patient entering the healthcare facility?

Simple decontamination –

Remove clothing & wash with soap & water

(this removes the majority of most agents that do not dissipate on their own)

Which bizarre chemical agent presents with ataxia & anticholinergic effects, sometimes including mass shared hallucinations?

BZ also known as Agent 15 –

It is an “incapacitating agent” because most individuals will not become very ill from the exposure, but the ataxia & cognitive impairment renders them unable to take effective action

What is the mechanism of this odd chemical agent?

It is anticholinergic in both peripheral & central muscarinic neurons, causing delirium & peripheral effects

Is this anticholinergic agent a contact threat for the healthcare personnel?

Yes! It is very persistent!!!

(It is quite potent, and lasts more than 4 weeks in the soil)

How should BZ or Agent 15 be decontaminated?

The usual way –

Remove cloth, wash with soap & water

(particulate matter can be gently brushed away)

Is BZ dangerous in any way?

Yes, two ways –

Patients are a danger to themselves through bizarre behavior (be sure that no weapons are available)

&

Hyperthermia is common

If anticholinergic effects are the problem in BZ intoxication, is it wise to give a medication like physostigmine (a cholinesterase inhibitor) to increase acetylcholine?

Generally not – too many serious side effects (including cardiac arrest)

(It may be used for intractable seizures, tachycardia or agitation not responding to other measures, with caution.)

For control of agitation & bizarre behavior, what medication is recommended in BZ intoxication?

Benzodiazepines

Which common plant ingestions also cause anticholinergic delirium?

(3)

Jimsonweed

Belladonna

Nightshade

What is the antidote to opiate overdose?

Narcan™

(aka naloxone)

What is the “typical” finding in opiate overdose (pupils)?

Pinpoint

(meperidine may dilate)

What opiate source might be in the family medicine cabinet & not considered dangerous by the family?

Lomotil™

(Diphenoxylate)

What are the dangers of opiate overdose?

Apnea!

(& some hypotension – not usually bad except in young children)

Acute toxic effects from the extrapyramidal system are typically seen with which medications?

Antipsychotics (haldol, droperidol, etc.)

&

Thiazines

What two medications can be used to treat extrapyramidal toxic effects?

1. Diphenhydramine (Benadryl™)

2. Benztropine (Cogentin™)

What are the symptoms & signs of extrapyramidal toxicity?

1. Dystonic reaction (oculogyric crisis & torticollis)

2. Akathisia (need to move)

3. Rigidity

4. Dysphagia

5. Laryngospasm

How is a sedative/hypnotic overdose treated?

Supportive care

(and make sure that is the only drug onboard!)

Should you use flumazenil to reverse a sedative/hypnotic overdose?

No – could cause tough to control seizures

What two general categories of medications make up the majority of sedative/hypnotic medications?

Benzodiazepines

&

Barbiturates

Is isolated benzodiazepine or barbiturate overdose dangerous?

Generally not – monitor BP and respiratory rate

(apnea occurs with ETOH & other medication combinations)

How is ETOH withdrawal treated, in terms of medications?

Benzodiazpines

&

Clonidine

Why is it important to treat ETOH withdrawal?

Autonomic instability can be dangerous

In addition to ETOH, what other withdrawal syndromes must be treated?

(4)

1. Benzos

2. Barbiturates

3. Cocaine

4. Clonidine

Amphetamines, cocaine, and PCP all belong to what general medication class?

Sympathomimetics

In general, what is the presentation of someone overdosing on a sympathomimetic?

Like someone having an obvious m.i. –

(anxious, sweaty, tachycardic, hypertensive, dilated pupils)

What medication counteracts the effects of sympathomimetics?

A benzodiazepine

In addition to m.i.-like findings, what other problems may accompany sympathomimetic overdose?

(2)

Seizures

&

Hyperthermia

In mg/kg, how much Tylenol™ (aka acetaminophen, paracetamol, or APAP) will prove toxic?

140 mg/kg

(about 10 g in an adult)

What is the antidote for acetaminophen toxic ingestions?

NAC

(n-acetyl cysteine aka mucomyst)

What is the loading dose for NAC?

140 mg/kg

(same as the toxic dose of APAP)

For patients who cannot tolerate or have contraindications to oral treatment with NAC, what other treatment option do you have?

Administer IV

Known as the “British Protocol” –

150 mg/kg over 60 min then

12.5 mg/kg/h for 4 h then

6.25 mg/kg/h for 16 h

(total treatment time 21 h)

In an APAP ingestion of unknown quantity, how do you know whether APAP will reach toxic levels?

Check the serum APAP level at 4 h & compare to chart

(The chart is also called a “nomogram.” In the case of APAP, the Rumack-Matthew nomogram is the name of the one used.)

Should a higher than usual dose of NAC be given, if charcoal is also given at the same time?

No – this is a change from previous practice!

(Activated charcoal does adsorb some of the NAC, but the impact is so small, that no adjustment is needed.)

After the loading dose, how is NAC dosed?

70 mg/kg × 17 doses

Given 4 h apart

(There is a new NAC formulation that makes the infusion regimen simpler)

What patient group is least likely to develop liver toxicity with APAP?

Young children

Why is NAC helpful in APAP overdose?

It provides a glutathione-like substance that binds the toxin

What are the stages of APAP toxicity?

1. GI symptoms which resolve spontaneously, then

2. Liver & renal dysfunction

3. ↑ LFTs & GI symptoms return

4. Recovery or liver failure

Why is too much APAP (acetaminophen) toxic?

The liver can only detoxify so much APAP at a time – excess amounts saturate glutathione and kill liver cells

Why is ethanol toxicity more dangerous in kids than adults?

It can produce rapid hypoglycemia

(immature liver – limited glycogen stores)

Why is ETOH withdrawal dangerous?

Autonomic dysregulation

(fever, tachycardia, HTN)

When do the potentially dangerous complications of alcohol withdrawal begin?

Typically 2–3 days after the last drink!

What are the dangerous features of alcohol withdrawal collectively referred to as?

DTs

(delirium tremens)

Why are alcoholic patients given “banana bags” of vitamins, thiamine, folate, & magnesium?

In an effort to prevent Wernicke-Korsakoff syndrome

(caused by dietary deficiencies common in alcoholics)

What medication class is primarily used to treat ETOH withdrawal?

Benzos!

What are the stages of ETOH withdrawal?

1. “Shakes” – tremor & agitation

2. Hallucinations

3. “Rum fits” – seizures

4. DTs – autonomic dysregulation (significant mortality)

“Disk hyperemia” on funduscopic exam is a buzzword for toxicity from what substance?

Methanol

Mnemonic:

Picture a red “disk” of methanol being tossed like a Frisbee at a party, and splashing on the players’ eyes when they grab it, producing tunnel vision!

What are the four treatment choices for methanol ingestion?