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EORE Emergency Medicine > Environmental Injuries & Toxic emergencies > Flashcards

Environmental Injuries & Toxic emergencies Flashcards

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1
Q

Approach to the poisoned patient

A

Assess ABCs:
Airway, Breathing, Circulation

Vitals signs
Supportive care

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2
Q

Information to obtain in poisened patient

A

PACT -
Product - what did they take?

Amount - how much (when was pill bottle filled?)

Coingestion - does pt have anything else on board?

Time - how long ago did he/she take it?

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3
Q

Physical Exam components possible poisoning

A

VENAS -

Vitals 
Eye exam 
Neuro exam 
Abd exam 
Skin exam
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4
Q

Eye exam findings - what to look for

A 
Pupil size (pinpoint = opioid) 
Nystagmus (can = ketamine) 
Reactivity to light?
Scleral discoloration? 
Ptosis? Ophthalmoplegia?
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5
Q

Skin Exam Assessment

A 
Temperature
Moisture
Flushed
Cyanotic
Pale
Track marks/abscesses
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6
Q

ABD Exam Assessment

A

Bowel sounds?
Ileus?
Abd cramping?
Diarrhea?

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7
Q

Neuro Exam Assessment

A

Mental status - A&Ox3
Gait
Reflexes
Clonus - shaking/seizing

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8
Q

Anti-Cholinergic Toxidrome

A 
"Hot as hare" (hyperthermia)
"Dry as bone" (dry mm) 
"Red as a beet" (flushed) 
"Mad as hatter" (Confusion) 
"Seizing like squirrel" (seizures)
"Full as flask" (Urinary retention) 
"Tachy as lesiure suit" (tachy)
"Blind as bat" (mydriasis, blurred vision)

Absent bowel sounds - ileus/constipation.

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9
Q

Agitated delirium w/ visual hallucinations & mumbling speech, tachycardia, dry flushed skin, mydriasis, myoclonus, urinary retention, dec bowel sounds

Which Toxidrome?

A

Anticholinergic

Similar to simpathomimetic except simpathomimetic OD (cocaine) = DIAPHORESIS not dry skin & also HYPERTENSION

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10
Q

Sympathomimetic Toxidrome Symptoms

A 
Delusions, agitation
Paranoia
Tachycardia
Hypertension
Hyperpyrexia
Diaphoresis
Piloerection 
Hyper-reflexia

Severe: Seizures/dysrhythmias

Caffeine & Theophyline OD present similarly but don’t have the organic psych manifestations

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11
Q

Causes of Anticholinergic OD

A 
Antihistamines
Anti-parkinsonism meds
Atropine
Scopolamine
Amantadine
Antipsychotics
Antidepressants
Antispasmotics 
Skeletal muscle relaxants 
Many plants - Jimson weed
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12
Q

Causes of Sympathomimetic OD

A

Cocaine
Methamphetamine, MDMA
OTC decongestants (pseudoephidrine, phenylpropanolamine)

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13
Q

Opiate/Sedative OD CP

A
  1. Depressed mental status
  2. Respiratory depression
  3. Miosis

= classic triad for opioids

Bradycardia 
Hypotension
Dec bowel sounds
Hyporeflexia
Needle marks
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14
Q

Causes of opiate/sedative OD

A

Narcotics
Barbiturates
Benzos
Z-drugs (zolpidem, zopiclone, zaleplon)

GHB 
Carisoprodol (Soma)
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15
Q

Cholinergic Toxidrome

A

Confusion
CNS de pression
Weakness

SLUDGE BBB
Salivation, lacrimation, urination, diarrhea, GI cramping, emesis, bronchorrhea (pulmonary edema), bronchospasm, bradycardia

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16
Q

Causes Cholinergic toxidrome

A

Organophosphate & carbamate insecticides

Physostigmine, edrophonium (MG, alzheimer’s meds)

Some mushrooms

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17
Q

Serotonoergic Toxidrome

A

SHIVERS

S hivering, one of the neuromuscular symptoms unique to SS, helps distinguish it from other hyperthermic syndromes

H yperreflexia and myoclonus are frequently seen in mild to moderate cases and are especially notable in the lower extremities; muscular rigidity occurs only in more severe cases

I ncreased temperature, although variable in SS and usually observed in severe cases, is likely caused by muscular hypertonicity

V ital sign instability can present as tachycardia, tachypnea, and/or labile blood pressure

E ncephalopathy—characterized by mental status changes such as agitation, delirium, confusion, and to a lesser extent obtundation—can develop from hyperthermia

R estlessness and incoordination are common because of excess serotonin activity

S weating (diaphoresis) is an autonomic response to excessive serotonin stimulation; by comparison, anticholinergic toxicity usually manifests with hot, dry skin

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18
Q

NMS

A

Similar to SS (SHIVERS) - but develops/progresses over 1-3 days instead of <12 hrs in SS. Also caused by different medications

NMS = HALA
Hyperthermia, AMS, Autonomic instability, Lead-pipe rigidity

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19
Q

Diagnostic Testing in possible overdose - 4 things to order right away

A

Remember - assess ABCs FIRST..then do…

  1. 12-lead EKG
  2. Glucose (AMS)
  3. CMP (anion gap)
  4. ABG/VBG (pH)

Also order:
ASA/APAP level
Pregnancy test
Urine/serum tox screen

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20
Q

Causes of anion gap / metabolic acidosis

A

MUDPILES

Methanol
Uremia 
DKA 
Propylene glycol, propofol 
Isoniazid, iron, infection 
Lactic acidosis 
Ethylene glycol
Salicylates, starvation ketosis, sympathomimetics

Analgesics (ibuprofen, asa, apap), carbon monoxide, cyanide

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21
Q

What causes QRS interval prolongation in OD’s?

A

Agents blocking cardiac fast Na+ channels (QRS >100ms)

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22
Q

What causes QT interval prolongation in ODs?

A

Agents that block cardiac K+ efflux channels

QTc > 440 men
QTc > 460 women

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23
Q

Sedative overdoses mimic which condition which you must rule out first?

A

Intracranial hemorrhage - rule out with CT

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24
Q

Treatment strategies for OD (3)

A
  1. Prevent absorption:
    Emesis, gastric lavage, activated charcoal, cathartics, whole bowel irrigation
  2. Enhance elimination:
    Hemodialysis, urine alkalinization
  3. Block effects
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25
Q

When to use emesis as method of preventing GI absorption

A

Not clinically used 2/2 risk of aspiration

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26
Q

When to use gastric lavage as method to prevent GI absorption of toxin

A

Not clinically used very often

Only used if life-threatening dose/ingestion of substance <1 hr ago for which reliable tx options are limited. Not shown to affect clinical outcomes

Increases risk of aspiration, laryngospasm, and esophageal injury

27
Q

When to use cathartics as method of preventing GI absorption

A

Theory: Speeding up GI transit time = dec absorption - in reality, cathartics = vomiting, abd pain, electrolyte abormalities & do not dec drub absorption or improve outcomes so DO NOT USE

28
Q

When to use whole bowel irrigation in preventing GI absorption

A

MOA: Use PEG to rapidly flush chemicals thru GIT

Indications: Used when pt ingests extended release tabs, radio-opaque tabs/chemicals, substances not well absorbed by charcoal (Lithium, iron, heavy metals), or large packets of street drugs (cocaine bags etc)

Problems: Unless pt is awake & oriented, there is risk of vomiting & aspiration & massive amounts of diarrhea in bed

29
Q

When to use activated charcoal

A

Activated charcoal = most widely used GI decontaminant in OD. Decreases drug absorption Has not been shown to affect clinical outcomes.

Use w/in 1 hour of ingestion. Or longer if ER formulations or very large ingestion.

30
Q

Drugs not well absorbed with charcoal decontamination

A

Lithium, heavy metals, iron, alcohols

31
Q

When is use of charcoal contraindicated?

A

After ingestion of hydrocarbons (won’t help & inc risk of vomiting & aspiration pneumonitis)

After ingestion of alkali/acidic substances - major concern w/ these is mucosal injury not GI absorption so won’t help

Patients w/ trivial or small ingestions (risks of activated charcoal > benefits) or pt that ingested it >1 hour ago

Patients who are not able to protect their own airway

32
Q

Does forced diuresis help in the treatment of acute poisoning?

A

Probably not - few drugs are excreted unchanged in the urine so increasing urine flow is unlikely to help

HOWEVER - if some cases if we manipulate urine pH AND urine flow - we can increase excretion - examples = salicylates & phenobarbitol (called alkaline diuresis) –> contraindicated if pulmonary or cerebral edema

Use of high volume Ns to treat Li intoxication also common - unclear whether forced saline diuresis for lithium is of extra benefit over simply ensuring normal renal flow

33
Q

When to use hemodialysis to enhance elimination of a drug?

A

Drugs that are LMW w/ low volume of distribution, are water soluble & not protein bound - ie if a drugs has rapid and thorough tissue distribution, then HD won’t work - needs to be in vessels unbound (or if highly protein bound, then protein saturation = free amts of toxin that can be removed (valproic acid))

MC used w/ Lithium
Others: ASA, methanol, ethylene glycol, and sometimes theophylline

Benefits: Corrects metabolic acidosis and fluid/electrolyte abnl as it removes the drugs

34
Q

How can dx of drug overdose be made when pt is unconscious?

A

Do bedside glucose or administer glucose - positive response = dx hypoglycemia

Miosis, resp depression - administer naloxone - positive response = definitive dx opioid OD

Examine pill bottles, review medical records (medication list), interview family & friends - call pharmacists where prescriptions were filled - dates

Needle track marks - IV ipioid, crack cocaine, or amphetamine

Physical examination - DRY w/ mydriasis = anticholinergic realm. DIAPHORESIS, HTN, hyperthermia - possible sympathomimetic. Tremor - possible SS.

35
Q

Antidote suspected anticholinergic toxidrome

A

Physostigmine (SOS -help!)

Do not use in TCA overdose or suspected TCA overdose (QRS widening)

36
Q

Antidote cholinergic poisoning

A

Atropine and pralidoxime (2-PAM)

Atropine dries up pulmonary secretions - direct inhibitor of Ach receptor (direct parasympatholytic)

2-PAM prevents skeletal muscle toxicity by preventing maturing of organophosphate bond

37
Q

Antidote for methanol or ethylene glycol overdose

A

Ethanol or fomepizole (F-MP)- alcohol dehydrogenase blocking agents - aka prevent metabolism of methanol/ethylene glycol to toxic metabolites

38
Q

Antidote Digoxin OD

A

Digibind, DigiTAb = DIgoxin immune Fab

MOA: Sequesters all digoxin - can rapidly reverse dysrhythmias and hyperkalemia - full response takes 20 minutes

39
Q

CP Methanol or ethylene glycol poisoning

A

CP Methanol/ethylene glycol OD = CORGI- dogs often drink b/c tastes sweet

C = CNS toxicity -
HA, AMS, confusion

O = Ocular toxicity -
Decreased visual acuity, retinal edema, hyperemia of disc - can progress to blindness & osmol gap (occurs early, but can be normal)
EG also = Oxalate crystaluria

R = Renal failure (late) -
PROFOUND METABOLIC ACIDOSIS = multi-organ failure, kidneys first

GI symptoms - N/V/ ABD pain

40
Q

Treatment methanol/ethylene glycol OD

A

Remember - ABCs ALWAYS first - protect airway if decreased level of consciousness

Gastric lavage & charcoal - not effective b/c sm volume & rabid absorption

Acidosis (pH < 7.2) - treat rapidly w/ sodium bicarb or HD

Antidotes: Ethanol, 4-MP (preferred 2/2 ease of use, less ADRs but slows 1/2 life of EG/M so need to be given over period of days)

Inc final step of metabolism to nontoxic substance - pyridoxine (vit B6) & thiamine for ethylene glycol, folate for methanol

41
Q

Toxic dose of methanol

Toxic dose of ethylene glycol

A

Methanol - 15-30ml (1-2 Tbsp)

Ethylene glycol - 1-2ml/kg

42
Q

Indications for hemodialysis in methanol or ethylene glycol OD

A

HD is most definitive therapy
b/c clears all ethylene glycol/methanol & toxic metabolites from blood & corrects any metabolic acidosis

Indications: Serum pH < 7.2, signs of end organ toxicity (seizures, coma) and renal failure

43
Q

Sx of ASA or salicylate OD

A

ASPIRIN acronym
Agitation, convulsions, delirium, hallucinations, convulsions etc

Sodium bicarb = tx, spots (petechiae) on eyelids

Pyretic (fever)

Increased anaerobic metabolism = lactic acidosis

Rapid breathing (hyperventilation –> respiratory alkylosis - pulmonary edema

Intestinal irritation - vomiting

Noise in ears - ringing/tinitis

Last three (RIN) = classic salicylism

44
Q

Tx Salicylate OD

A

Activated charcoal + cathartic +/- lavage - ASA has zero order kinetics - metab at same rate no matter how much you ingest - repeated charcoal may be necessary even > 1 hr - help prevent gastric concretions w/ ongoing absorption

Alkaline diuresis - Sodium bicarb bolus then infusion - reduces fraction of non-ionized salicylate & increases pH gradient with the CSF (prevents entry into CNS) - make blood more basic so acid is pulled from tissues & into blood stream

Correct for hypokalemia (give 20-40mEq) -

Consider hemodialysis in pt who cannot tolerate volume load

45
Q

Salicylate OD - which lab tests to order?

A

Salicylate level q2 hrs until decreasing trend w/ final level < 20 & pt is asx w/ normal RR

CBC, BMP (look at electrolytes (hypokalemia), BUN/Cr), glucose level, and UA, quantitative APAP level

Consider: PT/INR (coags) and ABG

46
Q

Explain why you could have decreasing serum salicylate and increasing clinical toxicity

A

Serum salicylate levels do not reflect tissue distribution of the drug

Acidic blood means the salicylate remains unionized and can easily penetrate the BBB = CNS toxicity

Therefore salicylate levels should be interpreted in light of the pt;s clinical condition and a concurrent blood pH - an acidotic pH is a/w toxicity regardless of the salicylate level

47
Q

Indications for hemodialysis in salicylate OD

A

Persistent, refractory metabolic acidosis (arterial pH < 7.1), renal failure w/ oliguria, cardiopulmonary dysfunction (pulmonary edema, dysrhythmias, cardiac arrest), CNS deterioration (seizures, coma), serum salicylate level >100 at 6hr mark

CONSULT NEPHROLOGY EARLY if pt ingests > 300mg/kg - predictor of severe toxicity - will probably need HD

48
Q

How do you treat respiratory compromise in pt w/ opioid OD?

A

Resuscitation takes precedence over naloxone administration

Support ventilation w/ bagged mask until naloxone can be administered

Intubate the cyanotic or apneic patient if no response to naloxone

Obtain serum glucose, administer oxygen

49
Q

Which over the counter cold remedy is sometimes abused by teenagers?

A

Dextromethorphan (DM) is the d-isomer of codeine - metabolite stimulates release of serotonin - which accounts for abuse as a hallucinogen

APAP = common co-ingredient in these meds - should get tylenol level

50
Q

CP Sedative hypnotic intoxication

A

Slurred speech, ataxia, loss of coordination

Moderate-severe w/ greater CNS depression, respiratory depression (8-10 breaths/min, esp if mixed w/ opioids/ethanol),

51
Q

Treatment of pt w/ toxicity from stimulants

A

3 C’s - take cocaine - tx = calm, cool, uncover complications

Treat agitation/seizures w/ benzos. Treat chest pain after cocaine w/ benzos (NO BETA BLOCKERS= unoppposed alpha agonism = WORSE HTN & coronary artery vasospasm)

Cool (to treat hyperthermia) with evaporation, cooling blankets, and cool IV fluids)

Complications = rhabdo, pyrexia, acidosis, ICH, pneumomediastinum, abd ischemia, & injection-related complications (abscess, endocarditis, cellulitis) - evaluate for thru history, physical exam, and testing - cocain = more likely to cause complications b/c causes direct vasoconstriction

52
Q

How do you treat HTN from stimulant toxicity?

A

Most HTN from stimulant toxicity is short-lived - treat w/ benzos - if true HTN emergency then add nitroglycerin

53
Q

Which toxic ingestion would cause bradycardia with hypotension (no QRS widening)?

A

Alpha-agonists:
Cclonidine, guanfacine, oxymetazoline, tetrahydrolozine) - inhibit sympathetic outflow in CNS resulting in hypotensino, bradycardia, pinpoint pupils, and somnolence

Beta blockers w/o sodium channel effects, CCBs, cardiac glycosides (digitalis)

Sedative-hypnotics:
Decrease CNS sympathetic outflow - opioids, benzos, barbiturates - usually minimal brady/hypo unless moderate-severe OD

54
Q

Which toxic ingestion would cause bradycardia with hypotension and WIDE complex QRS?

A

Quinidine, procainamide, dispropyramide (class 1a antiarrhythmics)

Lidocaine, tocainide (class 1b anti-arrhythmics)

Propafenone, fecainide (class 1c antiarrhythmics)

BB w/ Na+ channel effects (propanolol, metoprolol)

Severe CCB OD = ventricular escape arrhythmias

Hyperkalemia from cardiac clycosides, BBs, and K-sparring diuretics

55
Q

Which toxic ingestion(s) would cause tachycardia & HTN?

A

Sympathomimietics (amphetamines, cocaine, ephedrine, pseudoephedrine)

Anticholinergics (diphenhydramine & atropine) - decreased vagal tone & agitation from delirium

56
Q

Tachycardia w/ hypotension & wide complex QRS?

A

TCA - amitriptyline, imipramine, cyclobenzaprine (flexeril)

57
Q

Sx of pt w/ BB/CCB toxicity

A

BBs compete w/ endogenous catecholamines for receptor sites = blunts normal adrenergic response = bradycardia, AV blocks, hypotension (decreased heart contractility) - similar to CCB overdose

Propanolol = lipid soluble - crosses BBB and can cause seizures & AMS

Some BBs antagonize sodium channels = widened QRS - propanolol, acebutol)

Sotalol = QT prolongation

CCB toxicity also causes hyperglycemia

58
Q

Signs/sx of TCA overdose

A

MOA: TCA inhibits reuptake of NE & 5HT. Also has anti-histamine, anti-adrenergic, anti-muscarinic and Na+-channel blocking activity

TCA OD si/sx think that the C stands for CARDIAC toxicity & A stands for AMS leading to seizure

Cardiac - tachycardia, prolonged QRS & QT, & PR intervals = torsades (rare), AV block, RBBB, hypotension & myocardial depression –> GET SERIAL EKGs!!!!

Seizures managed w/ benzos

59
Q

Tx TCA Overdose

A

QRS prolongation - sodium bicarb- sodium overwhelms that Na+ receptor to un-do the TCA blocking effects

Torsades - Mg sulfate
Seizures - benzos

Severe TCA OD - Intravenous lipid emulsion therapy

60
Q

Initial treatment BB/CCB OD

A

ABCs - airway, breathing, circulation

Symptomatic bradycardia - atropine or pacing

Hypotension - 2L fluid bolus

Refractory brady/hypotension - GI decontamination
Calcium gluconate or chloride (requires central access 2/2 venous necrosis but is 4x more powerful)

Vasopressors (epinephrine)

Glucagon (activates beta-cells)

HDI (high dose insulin)

ILE (intralipid emulsion therapy)
= “Lipid sink” - only works on highly lipid soluble drugs (amiodorone, amitryptiline, fluoxetine, fentanyl, verapamil, amiodipine, propanolol) - binds offending toxin thereby reversing toxicity

61
Q

Uses of digoxin & MOA

A

Used for CHF and to control ventricular response in atrial tachydysrhythmias

MOA: Inhibits Na+/K+ ATPase - promotes Ca2+ influx via the Na+/Ca2+ exchange pump = increased force of myocardial contraction (positive inotrope)

62
Q

Digitalis toxicity CP

A

Acute dig intoxication -
N/V/ABD pain, confusion, weakness, hyperkalemia

Chronic dig intoxication -
insidious onset of weakness, anhedonia, loss of apetite, N/V/ABD pain, delirium, confusion, drowsiness, HA, hallucinations, seizure, visual disturbances

Also xanthopsia - blurred, yellow-tinted vision/halos

63
Q

Digitalis toxicity EKG changes

A

Sinus bradycardia
High degree AV block (AV dissociation)

ST depression - “reverse check” or “salvador dali”mustache

Signs of hyperkalemia

64
Q

What are the indications for DigiFab?

A

Symptomatic bradycardia, complete heart block, ventricular tachycardia, ventricular fibbrilation

Pt’s who seek tx after acute ingestion w/ hyperkalemia or hemodynamically significan dysrhythmias

Give 10-20 vials empirically if critically ill & unknown amt ingested

EORE Emergency Medicine (15 decks)

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