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Emergency Medicine > poisoning and ingestions > Flashcards

poisoning and ingestions Flashcards

1
Q

initial mgmt when presented with a poisoned pt?

A
  1. Gross decontamination beforehand
  2. ABC, VS
  3. Cont. Cardiac monitoring, ECG
  4. IV access - Large bore or central line
    - HoTN: IV crystalloid bolus
  5. Bedside glucose
  6. ABG
  7. Mental status, Pupil size, Skin check
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2
Q

Toxin-induced QRS interval prolongation can be seen with what medications?

A

Antidepressants, antipsychotics, antihistamines, organophosphate insecticides

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3
Q

SVT can be caused by what meds?

A

Sympathomimetics, Anticholinergics

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4
Q

V Tach can be caused by what meds?

A

Sympathomimetics, TCA

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5
Q

bradycardia can be caused by what meds?

A

cholinergics, opioids, sedative-hypnotics

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6
Q

initial tx for AMS

coma cocktail

A
  1. dextrose
  2. naloxone (Narcan)
  3. thiamine
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7
Q

initial tx for seizures

poisoned pt

A
  1. IV lorazepam - Double the dose if no improvement within a few mins
  2. seizure persists - IV phenobarbital, intubate
  3. Isoniazid-induced - pyridoxine
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8
Q

What medication is ineffective for stopping seizures caused by most poisonings?

A

Phenytoin

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9
Q

how/what to obtain a brief hx about the poisoned pt?

A
  • Pt may be unreliable - correlate with pt’s sx
  • Get hx from others - EMS, police, family, friends, etc
  • Inquire about exposures
  • Other ill contacts - CO, foods, chemical and biological warfare agents
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10
Q

The ____, ____, and ____ help classify the pt into either a state of physiologic excitation or depression

A

mental status, VS, and pupillary examination

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11
Q
  • signs of physicologic excitation?
  • what meds can cause this?
A
  • CNS stimulation, mydriasis
  • Tachycardia, inc BP, RR and temp
  • Etiologic toxidromes: anticholinergic, sympathomimetic, serotonin syndrome, hallucinogens
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12
Q
  • signs of physiological depression?
  • what meds can cause this?
A
  • AMS, miosis, Low BP, RR and temp
  • Etiologic toxidromes: sedative-hypnotic agents, opiates, cholinergics
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13
Q

what meds can cause Mydriasis?

A
  • anticholinergics
  • sympathomimetics

dilated pupils

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14
Q

what meds can cause Miosis?

A
  • cholinergics
  • opioids

small pupils

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15
Q

what meds can cause Nystagmus?

A

Ethanol, phenytoin, ketamine, PCP

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16
Q

what med can cause Excessive lacrimation

A

cholinergics

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17
Q
  • what meds can cause hypersalivation?
  • excessive dryness?
A
  • cholingerics
  • anticholingergics
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18
Q

possible findings of abominal exam from a poisoned pt?

signs and their meds

A
  1. bowel sounds - diminished in anticholinergic and opiates
  2. enlarged bladder - anticholinergic
  3. abdominal tenderness or rigidity - ASA, anticholinergic
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19
Q

what meds can affect muscle tone and tremor or fasciculation

A

cholinergics,serotonin

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20
Q

general w/u for poisoned pt?

A
  1. Abd XR
  2. CXR
  3. Tox screen
  4. Concentrations of common coingestants
  5. UA
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21
Q

When is a tox screening not needed?

A
  • non-intentional ingestion and asx OR
  • clinical findings consistent with MHx
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22
Q

individual tox screening may be needed to determine specific tx for what 2 meds?

A

lithium, digoxin

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23
Q

what 3 specific concentrations should always obtain in any person with unknown ingestion

A

APAP, ethanol, and salicylate

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24
Q

Calcium oxalate crystals may be present with what type of poisoning

A

ethylene glycol (antifreeze)

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25
Q

preferred method of gastric decontamination?

A

Activated Charcoal (AC) 1g/kg

  • absorbs toxins in stomach
  • not able to bind metals, corrosives or alcs
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26
Q

indication for activated charcoal?

A
  • if ingestion < 1 hr prior to arrival
  • can be used after 1 hour if toxins that slow GI transit (anticholinergics) and those that form bezoars (salicylate)
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27
Q

CI for activated charcoal?

A

unable to protect airway

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28
Q
  • removes non-absorbed toxins
  • High risk of aspiration - avoid unless pt is intubated or airway protective reflexes are intact

which type of gastric decontamination?

A

lavage

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29
Q

indications for gastric lavage?

A
  • ingestion has occurred < 1 hr prior to presentation
  • no antidote
  • toxin has a poor response to supportive care
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30
Q

how to perform gastric lavage?

A
  • Insert 36F-40F orogastric tube
  • LLD w/ HOB tilted down
  • 200 ml of warm tap water instilled into stomach and removed via gravity or suction
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31
Q

what gastric decontamination is indicated for:

  • ingestion of chemicals poorly adsorbed to charcoal (lithium, iron, lead)
  • ingestion of drug-filled packets
A

Whole bowel irrigation

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32
Q

how to perform Whole bowel irrigation?

A

Instil a electrolyte polyethylene glycol soln (GoLYTELY) to flush out entire intestinal tract

  • via NG tube, 1–2 L/h (400–500 mL/min in children)
  • Continue until rectal effluent is clear (3–5< hr)
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33
Q

CI of whole bowel irrigation

A

absent bowel sounds or suspected ileus or obstruction

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34
Q

indications, CI, and caution of multi-dose activated charcoal?

A
  • carbamazepine, dapsone, phenobarbital, quinine, and theophylline
  • unprotected airway, absent BS
  • ingestions resulting in reduced GI motility
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35
Q

what method of enchanced elimination ionizes acidotic toxins preventing resorption back across the renal tubule

A

Urinary alkalinization

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36
Q

indications and caution for Urinary alkalinization

A
  • moderate-severe salicylate toxicity
  • hypokalemia will reduce the alkalinity of the urine
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37
Q

how to perform urinary alkalinization?

A
  1. Give IV NaHCO3 +/- KCl
  2. monitor serum K and HCO3 q 2-4 h
    - Serum K goal 4-4.5 mEq/L range
  3. assess urine pH q 15-30 min
    - pH goal 7.5-8.5
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38
Q

which type of Extracorporeal removal is more effective at clearing highly protein-bound drugs and lipid-soluble drugs?

A

hemodialysis

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39
Q

when to use hemoperfusion as a choice for enhanced elimination?

A

for clearing water-soluble low molecular wt substances

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40
Q

4 indications for antidotes?

A
  1. exposure to toxin where a antidote exists
  2. severity of toxicity warrants use
  3. benefits outweigh its associated risk
  4. no CIs
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41
Q

MOAs of antidotes?

A
  1. Prevent absorption
  2. Bind and neutralize poisons directly
  3. Antagonize end-organ effects
  4. Inhibit conversion to more toxic metabolites
42
Q

how to decontaminate for Inhaled Poisons?

A
  1. Give O2
  2. Water aerosol inhalation - dilute irritants in nasopharynx
  3. Be alert for delayed upper airway obstruction or pulmonary edema
43
Q

how to decontaminate/tx contaminated eyes?

A
  • Irrigate eyes w/ plain water or NS ASAP
  • Assess pH of eye after 2 L of irrigated fluid
44
Q

how to manage contaminated skin?

A
  • avoid direct secondary self-exposure
  • Wash immediately with water and dilute soap solution
  • Discard contaminated clothes in a marked plastic bag
45
Q

how can US Poison Control be helpful?

A
  1. Obtain info on unknown pills or chemicals found
  2. immediate assistance in selecting labs
  3. Recommend preferred methods of decontamination, patient-specific care recommendations, or use of antidotes
  4. Advise on pt disposition
46
Q

criteria for a poisoned pt that can be discharged?

A

Asx pts with non-toxic exposures after observation, access to further consultation and a safe DC destination

47
Q

3 questions must be addressed to determine a non-toxic exposure

A
  1. Was exposure unintentional and a clearly identified single substance?
  2. How much of agent was ingested or amount of exposure?
  3. Can Poison Control Center (or other source) confirm substance as nontoxic in reported dose?
48
Q

mainstay for poisoned pt?

A

supportive

“Treat the patient, not the poison”

49
Q

supportive care for poisoned pt?

A
  1. Airway protection, Temp control
  2. HoTN: isotonic saline; +vasopressors if unresponsive
  3. HTN
    - agitated - BZD
    - risk of end-organ damage - CCB, phentolamine, labetalol or nitroprusside
  4. arrhythmia: correct hypoxia, acid-base, and give antidote; NaHCO3 if wide QRS
  5. naloxone (IV, IM, nasal): diagnostic and therapeutic
50
Q

avoid what med in sympathomimetic toxicity d/t unopposed a-adrenergic stimulation causing vasoconstriction when controlling HTN in poisoned pt?

A

B-blockers

51
Q

Temps indicative of hyperthermia and hypothermia?

A
  • core temp >39°C (>102.2°F)
  • core temp < 32°C (<90°F)
52
Q

if aggressive cooling is ineffective for treating hyperthermia, what is the next step?

A

drug induced coma

Drug-induced coma can lead to hypothermia

53
Q

complications of hyperthermia?

A
  1. rhabdo
  2. end-organ failure
  3. DIC
54
Q

how to calc anion gap?
normal value?

A
  • Na - (Cl + HCO3)
  • <10-15 mEq/L
55
Q

caues of metabolic acidosis

anion gap, mneumonic

A
  • C - cyanide, CO
  • A - alcoholic ketoacidosis
  • T - toluene
  • M - methanol, metformin
  • U - uremia
  • D - DKA
  • P - propylene glycol
  • I - inborn errors, iron, isoniazid, infection
  • L - lactic acid
  • E - ethanol, ethylene glycol
  • S - salicylates, starvation ketoacidosis
56
Q

mgmt of anion gap metabolic acidosis

A
  1. Address any lack of rsp compensation first
  2. Address lyte abnormalities
  3. Tx underlying cause
  4. Severe (pH < 7, hemodynamic instability): NaHCO3 0.5 mEq/L/kg
    - raise pH to 7.1
    - No EMB of benefit
57
Q

7 Basic Toxidromes?

A
  1. Opioid
  2. Sympathomimetic
  3. Cholinergic
  4. Anticholinergic
  5. Sedative/hypnotic
  6. Serotonin Syndrome
  7. Hallucinogenic
58
Q

s/s of narcotic toxidome?
mgmt?

mneumonic

A

CPR-3H

  • coma
  • pinpoint pupils
  • rsp depression
  • HoTN
  • hypothermia
  • hyporeflexia

Naloxone 0.04mg, titrate up if needed, rsp support

59
Q

MOA of Sympathomimetics?
Examples?

A

mimic effects of endogenous agonists of the sympathetic nervous system (epinephrine, norepinephrine, dopamine)
Cocaine, Caffeine, Amphetamines, Cathinones (“bath salts”)

60
Q
  • s/s of Sympathomimetics?
  • mgmt?
A

SyMpATHomimetic: physiologic excitation

  • Mydriasis, muscle cell death
  • agitation, arrhythmia, angina
  • tachycardia
  • HTN, hyperthermia, hyperactive BS
  • seizures, sweating

Cooling, IV fluids, BZD if agitated/HTN/seizure

61
Q

CI med for sympathomimetic toxidrome?

A

BB

62
Q

MOA of cholingerics?
examples?

A
  • blocks acetylcholinesterase = inc acetylcholine; Affects muscarinic and nicotinic receptors
  • Organophosphate insecticides, Carbamate insecticides
63
Q

s/s of cholinergic toxidrome?

A

Crying all over, DUMBELLS

  • MC - Salivation, lacrimation, diaphoresis, bronchorrhea, inc urination and defecation, N/V, muscle fasciculations, weakness
  • Additional: Bradycardia, rales, seizures, miosis/mydriasis, rsp failure, paralysis
64
Q

mgmt for cholinergic toxidromes

A
  1. Airway protection and ventilation
  2. Atropine - blocks Ach receptors at muscarinic receptors
  3. Pralidoxime + atropine - reactivate cholinesterase at both muscarinic and nicotine receptors.
  4. Diazepam - seizure, muscle fasciculation
65
Q

MOA of anticholinergics?
examples?

A

block acetylcholine muscarinic receptors = inhibits PS nerve impulses

  • Scopolamine
  • Atropine
  • Antihistamines
  • TCA’s
  • Antiparkinson agents
  • Antispasmodics/Muscle relaxants
66
Q

s/s of anticholinergic toxidrome

A
  • hyperthermia, tachycardia, dry af, AMS, urinary retnetion, mydriasis, flushed/dry skin
  • seizures, dec/absent BS, dysarhythmia, rhabdo, changes in BP
67
Q

how is the presentation of antichoinergic toxidrome different from sympathomimetic?

A

dry skin and dec BS

68
Q

mgmt for anticholinergic toxidrome?

A
  1. Activated charcoal to dec drug absorption - if applicable
  2. Tx complications
    - Wide QRS - NaHCO3
    - Agitation - BZD’s
    - rhabdo - Fluids
    - Hyperthermia - external cooling
  3. Physostigmine - antidote
    - cholinesterase inhibitor increases concentration of Ach at cholinergic receptor
    - indicated if conventional tx fail
69
Q

disposition of anticholinergic toxidrome

A
  • DC if resolve after 6 hrs observation
  • Admit if more significant sx or receiving physostigmine
70
Q

3 classes of sedatives/hypnotics

A
  1. BZD
  2. Non-BZD’s: carisoprodol, alc, hypnotics
  3. Barbiturates
71
Q

s/s of sedative/hypnotic toxidrome

A

physiologic depression

  • MC - slurred speech , lethargy, CNS depression, rsp depression, confusion
  • Additional: Bradycardia, HoTN, hypothermia, bradypnea, hyporeflexia
72
Q

mgmt for Sedative/hypnotic toxidrome

A
  1. Supp: vent/intubate, 2 large bore IVs; bolus for HoTN; Dop/NOR if bolus fails
  2. AC: if applicable
  3. Barbiturates unresponsive to tx - enhanced excretion methods
  4. BZD: flumazenil
    - ONLY IF confirmed OD w/ rsp depression
73
Q

T/F: flumazenil is not used empirically for BZD ODs

A

T - can precipitate seizures

74
Q

disposition for sedative/hypnotic toxidrome

A
  • Admit if symptomatic after 6 hrs of management
  • Consult psych for intentional OD
75
Q

MOA of serotonin syndrome?
examples?

A
  • increased serotonergic activity in CNS
  • MAOI’s, SSRI’s, meperidine (Demerol), dextromethorphan, TCA’s, L-tryptophan
76
Q

s/s of serotonin syndrome

A

H : hyperthermia, HTN
A : AMS, agitation
T : tremor, tone (inc muscle tone), tachycardia, tachypnea
S : seizures

hyperthermia MCC of death

77
Q

mgmt for serotonin syndrome

A
  1. Vent support as needed
  2. External cooling
  3. BZD for agitation, tremors, seizures
    - If failed: cyproheptadine
  4. DC serotonergic drug
  5. admit all
78
Q

examples of hallucinogenics?
s/s?
mgmt?

A
  1. LSD, PCP, shrooms (psilocybin), ecstasy, dextromethorphan, ketamine
  2. physiologic excitation
  3. Symptomatic tx
    - Refractory sx - medically induced coma
    - refractory HTN - Nitroprusside or phentolamine

Admit if persistent sx after adequate tx

79
Q

Persons at increased risk for APAP toxicity

A
  • chronic alcohol use
  • AIDS
  • anticonvulsant
  • anti-TB therapy
80
Q

A toxic exposure to acetaminophen in pt >6 y/o is suggested when…

A
  • > 10g or 200 mg/kg as single ingestion or over 24 hr
  • > 6g or 150 mg/kg per day for at least 2 consecutive days
81
Q

A toxic exposure to acetaminophen in pt < 6 y/o is suggested when…

A
  • > 200 mg/kg as single ingestion or over an 8 h period
  • 150 mg/kg per day for at least 2 consecutive days
82
Q

stages of APAP toxicity

A
  1. Stage 1 (day 1 after ingestion): anorexia, N/V, and malaise; hypokalemia
  2. Stage 2 (days 2-3)
  3. improved 1st sx, RUQ pain; inc transaminases, bilirubin, PT
  4. Stage 3 (days 3-4): liver failure, met acidosis, coagulopathy, renal failure, encephalopathy, pancreatitis and recurrent GI sx
  5. Stage 4 (day >5) - 2 outcomes
    - survives - improvement and recovery
    - continued deterioration to multi-organ failure and death
83
Q

w/u for APAP toxicity

A
  1. serum APAP
    - assessed even in asx: delay in sx
    - peak: 30-120 min after acute ingestion
    - Rumack-Matthew nomogram: determines clinical outcomes, only after acute ingestion 4-24 hrs post ingestion
84
Q

mgmt for APAP toxicity

A
  1. AC (if applicable)
  2. Acetylcysteine
  3. +/- Extra-corporal excretion
    - If severe intoxication who present too late and have hepatic encephalopathy

Admit if needed acetylcysteine
DC after 4-6 h observation and no acetylcysteine

85
Q

MOA of Acetylcysteine

A

prevents metabolite from binding to hepatic cells (if given < 8 hr) and diminishes hepatic necrosis

86
Q

s/s of ETOH toxicity

A
  • ataxia, slurred speech, depressed sensorium, and nystagmus
  • vasodilation = orthostatics and hypothermia
  • hypoglycemia

complications: trauma, rsp depression, pulmonary aspiration, coma

87
Q

w/u for ETOH toxicity

A
  • BAC - if unknown ingestion
  • Glucose level
  • Tox or co-ingestant screening
  • Labs to assess other organs
88
Q

mgmt for ETOH toxicity

A
  1. Supportives and observation
  2. IV dextrose for hypoglycemia
  3. IV thiamine if concerned about chronic alc use and Wernicke’s encephalopathy
  4. Address other s/s: hypovolemia, hypothermia, trauma, rsp distress
    - uncomplicated - observe until sober; no suicidal/homicidal ideations - d/c home
    - Admit if have assoc dx that need admission
89
Q
  • de-icers and antifreeze
  • colorless, odorless and sweet tasting
  • metabolized in liver by alcohol dehydrogenase toxic metabolites (glycolic acid → oxalic acid) = met. acidosis and end-organ damage

what is this?

A

Ethylene Glycol

90
Q

s/s of ethylene glycol toxicity

A
  • Progressive sx
  • 1 hr - CNS depression
  • 12 hrs - HF, pulmonary edema
  • 24–72 hrs - renal tubule necrosis, flank pain, hematuria, and renal failure
91
Q

w/u and findings for ethylene glycol

A
  1. ABG - wide AG met acidosis
    - may show 12-16 hrs after ingestion
  2. UA - fluoresce under Wood’s lamp; Ca oxalate crystals
  3. Ethanol lvl
  4. CMP
  5. serum osmolality gap >50
    - Measure (serum) Osm - Calculated osm = Osmolar Gap
    - Nml: -14 to +10
92
Q

mgmt for ethylene glycol toxicity

A
  1. ABC
  2. IV NaHCO3 only if pH < 7.2
  3. Metabolic Blockade: fomepizole IV; ethanol PO/IV (alt)
  4. +/- Hemodialysis
  5. Adjunctive Vit B - no solid EBM
  6. Admit all EG ingestion
    - If uncertain - observe x 6 h
    - DC if negative ethanol, asx, no osmolar gap or met acidosis
93
Q

MOA of fomepizole

A
  • Inhibits alcohol dehydrogenase
  • an enzyme which catalyzes metabolism of ethanol and ethylene glycol to their toxic metabolites
  • The slowed elimination of EG results in renal excretion
94
Q

indications for hemodialysis for EG toxicity

A

severe acidosis, visual changes, hemodynamic instability, or renal failure

95
Q

Meds that contain salicylate

A

ASA, combo pills with ASA, Pepto Bismol, liniments, flavoring agents

96
Q

salicylate toxicity is at risk for ____ formation due to salicylate impairing gastric emptying

A

bezoar

97
Q

presentation of salicylate toxicity

A
  1. chronic - mistaken for “infection” (F, hyperventilation, AMS w/ volume depletion, acidosis, hypokalemia)
  2. acute - dose dependent
    - < 150: tinnitus, hearing loss, dizziness, N/V
    - 150–300: tachypnea, hyperpyrexia, diaphoresis, ataxia, anxiety
    - >300: AMS, seizure, heart/lung/renal failure, shock
98
Q

w/u for salicylate toxicity

A
  1. salicylate lvl: > 30 mg/dL is toxic
    - peak in acute may not occur for 4-6 hrs: repeat q 1-2 h until peak, then q 4-6 h
  2. CMP + Mg; ABG
    - Early: rsp alkalosis
    - Later: met acidosis
  3. coingestants - APAP, tox screen
  4. CXR and EKG
  5. if bezore suspected: X-ray, US, CT or endoscopy
    - Suspect if salicylate lvl keeps inc despite tx w/ lavage or AC
99
Q

mgmt for Salicylate Toxicity

A
  1. ABC’s
  2. Correct volume depletion and metabolic derangements (hypokalemia)
  3. GI decontamination - single dose AC
  4. Reduce salicylate burden
    - Systemic/urinary alkalinization w/ NaHCO3 - 1st line for mod-severe toxicity
    - Hemodialysis - if unresponsive severe tox or evidence of renal impairment
100
Q

what are Bezoar formations

A

conglomerates of meds or med vehicles that get stuck in GI tract

Emergency Medicine (20 decks)

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