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Module 14 > Approach to Suspected Poisoning > Flashcards

Approach to Suspected Poisoning Flashcards

1
Q

what are the types of poisonings

A
  1. drug overdose
  2. drug interactions
  3. adverse drug reactions
  4. true poisonings – usually accidental
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2
Q

what is important when first assessing a suspected poisoning

A

impossible to know all possible toxins

history taking is vital

supportive care as essential as “antidote”

ask owner to bring product

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3
Q

what are common poisonings (9)

A
  1. ethylene glycol
  2. metaldehyde
  3. rodenticide
  4. paracetamol
  5. xylitol
  6. chocolate
  7. raisins/grapes and lillies - renal
  8. permethrin - neurological
  9. ibuprofen - GI ulceration, renal, neuro
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4
Q

what are the management goals of poisonings

A
  1. stabilize immediate clinical signs
  2. history
  3. prevent continual absorption
  4. antidote
  5. removal of toxin

supportive care and monitoring is key

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5
Q

what is the general approach to a poisoning

A

if toxin confirmed by owner –> antidote if there is one

otherwise –> proceed with decontamination procedures while performing futher investigations

PCV/TP

urea/creatinine

ALT

glucose

electrolytes

urinalysis

ECG

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6
Q

how do you prevent continual absorption from the GIT (5)

A
  1. emetics
  2. gastric lavage
  3. adsorbents
  4. enemas
  5. surgical removal
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7
Q

how do you prevent further absorption topically (2)

A
  1. irrigation of eyes
  2. washing skin/clipping hair: prevent grooming (self and others), clip the coat and buster collar
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8
Q

what patients should you not bathe

A

seizuring animals

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9
Q

how is ocular decontamination done (4)

A
  1. irrigate the eye for at least 15 mins (water/saline)
  2. fluoroscein assessment
  3. corticosteroids only if no ulceration
  4. lubricants/topical antibiotics
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10
Q

when are emetics contraindicated (5)

A
  1. neurological dysfunction: animals that are seizuring or likely to seizure
  2. corrosive ingestion: damage to esophagus (harder to treat than GI damage)
  3. predisposed to aspiration: megaesophagus, laryngeal paralysis, french bulldogs (prone to aspiration)
  4. time post ingestion (> 4hrs?): depends on what it is (paracetamol vs. raisins)
  5. prior vomiting
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11
Q

what substances may prevent emesis

A

marijuana

codeine

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12
Q

what are emetics used in cats and dogs

A
  1. apomorphine (dogs)
  2. xylazine/dexmedetomidine/medetomidine (cats)
  3. hydrogen peroxide (3%)
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13
Q

how is apomorphine administered

A

IV, SC or via the conjunctiva

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14
Q

how long does apomorphine take to have effect

A

5-10 mins

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15
Q

is apomorphine a controlled drug

A

no

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16
Q

what side effects can apomorphine cause

A

sedation –> reverse with naloxone if required

continued nausea

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17
Q

what effects does xylazine/dexmedetomidine/medetomidine cause in cats

A

moderately effective

sedation and cardiorespiratory depression

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18
Q

is apomorphine used in cats

A

no it isn’t effective

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19
Q

what is the dose of hydrogen peroxide used to cause emesis

A

1-2 ml/kg P.O (max 50ml dogs)

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20
Q

what are the adverse effects of hydrogen peroxide

A

mild gastric irritation

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21
Q

can hydrogen peroxide be used in cats

A

yes but more side effects and its less effective

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22
Q

what can be used to reverse side effects of xylazine/dexmedetomidine/medetomidine

A

atipamezole

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23
Q

is repeat administration allowed in hydrogen peroxide

A

no more than once

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24
Q

when is a gastric lavage used

A

neurological patients (metaldehyde)

seizure

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25
Q

how is a gastric lavage done

A

GA

stomach tube: 5-10 ml/kg of warm water and repeat until runs clear

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26
Q

what are the risks of a gastric lavage

A

aspiration –> cuffed ET tube

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27
Q

what are contraindications of gastric lavage

A
  1. corrosive substances
  2. anesthetic risk too high
  3. over 4 hours post ingestion
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28
Q

what absorbents are used

A

activated charcoal

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29
Q

how do activated charcoal work as absorbents

A

bind toxin and stop furhter absorption

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30
Q

which is better liquid and powder or tablets for activated charcoal

A

liquid and powder > tablets

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31
Q

how is activated charcoal administered

A

give in food, via syringe/stomach tube

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32
Q

how often is activated charcoal repeated

A

q 4 hours –> enterohepatic recycling

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33
Q

what needs to be considered when giving oral meds and activated charcoal

A

2 hours between charcoal and oral meds

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34
Q

what should you warn the owners when their pet is given activated charcoal

A

stains feces black

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35
Q

what substances does activated charcoal not work on

A

xylitol, onion, garlic, ethylene glycol

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36
Q

what facrtors are there to consider when using an antidote

A

cost and shelf life

necessity of antidote

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37
Q

what does tox box contain

A

activated charcoal

apomorphine

european adder activation

methocarbamol

acetylcysteine

vitamine K1

intralipid

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38
Q

how can the toxin be removed

A
  1. IVFT
  2. intravenous lipid emulsion
  3. blood purification techniques (dailysis)
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39
Q

why are intravenous fluids helpful (3)

A
  1. increase renal elimination: theobromine
  2. support kidneys: lillies, raisins, nephrotoxins
  3. GI loss, hypotension
40
Q

what is the intravenous lipid emulsion

A

liquid sink for lipophilic toxins

41
Q

what is the intravenous lipid emulsion used for

A

toxins with short half-life –> ivermectin, permethrin, local anesthetics, ibuprofen, cannabis

42
Q

what are adverse reactions associated with intravenous lipid emulsion (5)

A
  1. pancreatitis
  2. anaphylaxis
  3. volume overload
  4. coagulopathies
  5. bacterial contamination
43
Q

what can intravenous lipid emulsion interfere with

A

diazepam, phenobarbital

44
Q

what are specific poisonings (7)

A
  1. paracetamol/acetaminophen
  2. metaldehyde (slug/snail pellets)
  3. vitamin K antagonist (rodenticide)
  4. ethylene glycol (anti-freeze)
  5. theobromide (chocolate)
  6. xylitol (chewing gum)
  7. raisins/grapes
45
Q

what does paracetamol toxicity cause

A

hepatic metabolism

  • liver overwhelmed –> accumulation of toxic metabolites and oxidative damage
  • hepatocellular necrosis
  • methemoglobin formation (chocolate blood)

heinz body anemia

dry eye

46
Q

why are cats more susceptible to paracetamol

A

cats lack the glucuronide conjugation pathway

47
Q

what is the absorption time of paracetamol

A

rapid

48
Q

what are the clinical signs of paracetamol toxicity <24 hrs (5)

A
  1. cyanosis/muddy brown mucus membranes
  2. tachycardia, tachypnea, lethargy
  3. facial and paw edema
  4. vomiting
  5. anemia
49
Q

what are the clinical signs of paracetamol >24 hours (5)

A
  1. liver failure
  2. icterus (yellow mucous membranes)
  3. seizures/coma
  4. renal failure
  5. hematuria/hemoglobinuria
50
Q

when is paracetamol treatment recommended

A

>10 mg/kg (cats) or >100mg/kg (dogs)

51
Q

what is the recommended treatment for paracetamol toxicity

A

emetics if <1-2 hours post ingestion

absorbents

supportive care –> IVFT, oxygen, blood products

antidotes

52
Q

what are the antidotes for paracetamol toxicity

A

N-acetylcysteine –> glutathione precursor

S-adenosylmethionine (S-AME)

ascorbic acid (vit C)

cimetidine (dogs) - inhibits conversion to toxic metabolite

53
Q

what is metaldehyde

A

slug bait

pellets or solutions

54
Q

what is the onset of metaldehyde

A

rapid

30-3 hours

55
Q

what clinical signs does metaldehyde cause

A

hyperesthesia

tremors

seizures

hyperthermia

56
Q

how does metaldehyde cause death

A

respiratory arrest/seizures

liver failure after 2-3 days

57
Q

what is the treatment of metaldehyde toxicity

A

treat regardless of dose ingested

emetics if asymptomatic and observe

activated charcoal

if seizures: diazepam (propofol if non-responsive)

+/- gastric lavage

methocarbamol: muscle relaxer

IVFT and nursing care

58
Q

what is the effects of rodenticides

A

blocks vitamin K activation

–> depletion of clotting factors II, VII, IX, X

defect in secondary homeostasis

59
Q

how are rodenticides absorbed

A

slowly absorbed from GIT

60
Q

what are examples of rodenticides

A

first and second generation

warfarin, brodifacoum, bromodiolone

61
Q

what is the plasma half life of rodenticides

A

long half life

varies for different compounds

62
Q

what are the clinical signs of rodenticide ingestion (6)

A

coagulopathy

  1. lethargy
  2. body cavity hemorrhage (hemothorax dyspnea, hemoabdomen)
  3. epitaxis
  4. GI bleed - melena/hematemesis
  5. joint pain
  6. anemia
63
Q

how are anticoagulant rodenticides diagnosed

A
  1. prolonged prothrombin time (PT) occurs first (factor VII shortest half life, extrinsic pathway)
  2. prolonged APTT
  3. platelets: normal or decreased
  4. PIVKA: proteins induced by vitamin K antagonism
  5. anemia
64
Q

how are asymptomatic anticoagulant rodenticide animals treated

A

emesis & activated charcoal

check coags 24, 48, 72 hours

if PT prolonged treat with vitamin K1 for up to 6 weeks

repeat coags after finish treatment

1st dose S/C

oral bioavailability imrpoved with a fatty meal

clotting factors improve within 6 hours

65
Q

how are symptomatic rodenticide animals treated

A

immediate support –> oxygen +/- transfusion (plasma and red cells)

vitamin K1

66
Q

how is ethylene glycol (anti-freeze) absorped

A

very rapid absorption

GI decontamination only effective in first 2 hours

67
Q

what is the prognosis of ethylene glycol ingestion

A

poor prognosis

>90% mortality in cats

68
Q

at what dose of ethylene glycol are fatalities seen

A

> 1ml/kg in cats

> 4.4 ml/kg in dogs

69
Q

when is treatment effective in animals that have ingested ethylene glycol

A

within 3-4 hours

70
Q

what is the pathway of ethylene glycol that causes damage to the kidneys

A
71
Q

when is euthanasia recommended after ethylene glycol ingestion

A

if the animal is azotemic

72
Q

what are the clinical signs of ethylene glycol in the first 12 hours

A
  1. neurological signs (ataxia, twitching, seizures)
  2. GI signs
  3. acidosis
73
Q

what are the clinical signs of ethylene glycol in the first 12-24 hours

A
  1. cardiac/respiratory system affected
74
Q

what are the clinical signs of ethylene glycol in 24-72 hours

A

renal:

azotemia

anuria

hyperkalemia

75
Q

how is ethylene glycol diagnosed (8)

A
  1. history/clinical signs
  2. metabolic acidosis
  3. hypocalcemia
  4. azotemia (from 12hours) –> hyperkalemia, hyperphosphatemia
  5. calcium oxalate crystals in urine
  6. glycosuria, proteinuria, urine casts
  7. medullary rim sign on US
  8. in house tests
76
Q

what is shown here

A

medullary rim signs from ethylene glycol toxicity

77
Q

how is ethylene glycol treated

A

emetics not useful unless early on

diazepam for seizures

correct acidosis

IVFT - monitor urine output and electrolyte

78
Q

what is the antidote for ethylene glycol

A

block alcohol dehydrogenase

20% ethanol (vodka): dilute it to 20% –> stomach tube or IV

4-methylpyrazole (fomepizole): less side effects, limited availability

79
Q

what are the doses of theobromine that cause GI signs, hyperactivity, panting, shaking

A

~20mg/kg

80
Q

what are the doses of theobromine that cause cardiotoxicity (arrhythmias)

A

~50mg/kg

81
Q

what are the doses of theobromine that cause seizures

A

~60mg/kg

82
Q

what is the theobromine content in white chocolate

A

negligible

83
Q

what is the theobromine content in milk chocolate

A

~1.4mg/mg

84
Q

what is the theobromine content of dark chocolate

A

~5.3mg/g

85
Q

what is the theobromine content of cocoa powder

A

38 mg/g

86
Q

what amount of milk chocolate ingestion should you treat

A

>14g/kg

87
Q

what amount of dark chocolate ingestion should you treat

A

if >3.5g/kg

88
Q

what are the treatments for theobromine toxicity

A
  1. emesis, activated charcoal
  2. IVFT: diruresis, consider urinary cathertization
  3. continuous ECG and seizure monitoring
  4. supraventricular tachycardia –> beta blocker
  5. ventricular tachycardia –> lidocaine
  6. symptomatic treatment of seizures and GI signs
89
Q

what effects does xylitol have

A

stimulates insulin release –> hypoglycemia, hypokalemia, hypophosphatemia

90
Q

what is the toxic dose of xylitol

A

> 50mg/kg (1 piece of extra gum in a 20kg dog)

amounts of xylitol in gum brands differs

91
Q

at what dose of xylitol can hypoglycemia be seen

A

>100mg/kg see from 30 mins

92
Q

at what dose of xylitol can hepatic necrosis be seen

A

>500 mg/kg

delayed up to 72 hours

coagulopathy

93
Q

how is xylitol toxicity treated

A

decontamination

rapid absorption –> emesis?

charcoal of questionable use

monitoring: glucose (minimum of 12 hours), ALT, total bilirubin, potassium, phosphorus, clotting times

supportive care: fluids/dextrose

liver protectants: S-AME

94
Q

what occurs in raisin ingestion

A

idiosyncratic reaction

some are fine but some are severely affected

not dose dependent

95
Q

when is treatment recommended for raisin ingestion

A

recommended at any ingestion

96
Q

what can raisins cause

A

GI signs: vomiting, diarrhea

acute renal failure

97
Q

how is raisin toxicity treated

A

decontamination: emesis, charcoal
monitoring: urea, creatinine, electrolytes, phosphorus, calcium –> baseline and after 48 hours, +/- after stopping fluids

supportive care: IVFT for 48-72 hours

Module 14 (29 decks)

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