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Y4 SA - GI & hepatic disease > Toxins - general approach & common examples > Flashcards

Toxins - general approach & common examples Flashcards

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1
Q

Basic principles of treating known ingestion/exposure

A
  • decontamination
  • assessment of effects
  • tx of symptoms
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2
Q

How can a toxin be absorbed?

A

Eaten
- therefore absorbed either across mm (rapid e.g. alcohol) or absorbed across the intestinal mucosa after transiting the stomach (slower)

Skin exposure
- e.g. spot-on products (quick)
- some toxins not absorbed, but groomed and ingested

Inhalation
- rare

Metabolised
- many compounds aren’t inherently toxic until they’ve been metabolised e.g. by the liver

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3
Q

Toxins absorbed across mm

A
  • rapid
  • already missed the boat on presentation
  • however, if its something caustic (e.g. bleach) rinsing the mouth can be useful to prevent more oral burns
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4
Q

How to prevent gastric absorption

A
  • induce emesis or gastric decontamination
  • window of opportunity: 2-8h in dogs, 2-12h in cats
  • apomorphine: licensed in dogs, v effective
  • alpha-2 agonist e.g. xylazine, medetomidine: not licensed but can be used in cats (moderately effective)
  • avoid neurological compromised pts e.g. obtunded due to aspiration risk
  • avoid caustic substances e.g. hydrogen peroxide and causing oesophagitis and potential major complications
  • stomach lavage; OG tube placed and warmed saline or Hartmann’s used to flush the stomach
    – ALWAYS KINK THE TUBE on removal to avoid aspiration
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5
Q

How to prevent intestinal absorption

A

Arguably could try to reduce intestinal transit time e.g. with laxatives but this will likely cause fluid and electrolyte losses unnecessarily

Adsorbants - activated charcoal
- doesn’t work for all toxins (in the unknown toxin always worth trying)
- activation makes the charcoal massively porous which increases the SA hugely
- carbon is reactive, and as a result some molecules will react with this surface and resultantly ‘bind’ to the surface of the carbon (adsorption)
- causes black poo -> warn O
- licensed in tube and liquid in UK
- powder available off license

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6
Q

Skin exposure decontamination

A
  • washing the skin is primarily performed with water
  • can apply activated charcoal topically before washing off but messy
  • lipid soluble toxins can be removed easily with soap e.g. fairy liquid
  • prolonged washing e.g. several minutes can increase absorption of some chemicals (‘wash in effect’)
  • don’t use dilute bleach
  • take care when drying -> absorption through abrasions
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7
Q

Inhalation decontamination

A
  • very rare
  • realistically decontamination for the pt is not possible
  • be careful yourself
    – e.g. attending a scene to retrieve an animal
    – washing the pt and aerosolising any toxin
  • appropriate PPE e.g. mask and gloves always a good idea
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8
Q

Metabolised toxins decontamination

A

Once toxins are in the blood stream we still have the opportunity to prevent them being metabolised

The solution to pollution is dilution
- the simplest approach is fluid therapy
- increase GFR and promote renal excretion
- increase organ perfusion and transit of compounds
- e.g. 2xM in the normally hydrated pt

Lipid infusion
- works well for lipid soluble compounds
- some evidence in humans for improved outcomes in non-lipid soluible
– fatty acids are a cardiac energy source
- minimal side effects -> pulmonary lipid embolus, ? ARDS

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9
Q

The unknown toxin - assessment

A

Neuro
- seizures
- ataxia
- sedation

Cardiovascular
- arrhythmias
- tachycardia/bradycardia
- hypo/hypertension

GI
- v+
- d+

Renal
- azotaemia
- inappropriate USG

Hepatic
- jaundice
- elevations in ALT, ALP, bile acids

Haematological
- clotting: prothrombin time, activated partial thromboplastin time, thromboelastography, point-of-care US
- anaemia: PCV, HCT

Cardiovascular
- ECG

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10
Q

Unknown toxin - tx

A

Primary symptomatic based on the system

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11
Q

Unknown toxin tx - neuro

A

Seizure control

Diazepam IV x3
- diazepam vs midazolam: whilst midazolam has shown some promise for being superior to diazepam it is not licensed in vet med
- IV vs rectal diazepam: rectally is variable in its absorption
- diazepam IV: give it, wait 10 mins, if hasn’t worked give another dose, … if the 3 doses don’t work go more aggressive
- even in the refractory pt the seizure severity is reduced, bringing the temp down, etc the pt will be getting a bit better

Levetiracetam, phenobarbital IV
- sedative
- good at reducing seizure activity, but animal knocked out as a result

Propofol CRI
- if these all fail use propofol CRI
- induced coma
- need to ventilate and breathe for this pt
- not simple.

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12
Q

Unknown toxin tx - hepatic damage

A

Supportive in nature
- SAMe
- ursodeoxycholic acid
- silybin (milk thistle)
- ^ these antioxidants usually given as a 3-way combo

The liver is a very regenerative organ so support it over the next 24-48h and it should heal

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13
Q

Unknown toxin tx - AKI

A
  • IVFT ± diuretics depending on urine output
  • dialysis

Key:
- keep them polyuric
- maintain their losses
- keep them maintained from a hydration POV
- if they start to become oliguric and you think their hydration status is good but their kidneys are starting to shut down: add in diuretics
– care with furosemide as is technically nephrotoxic in the poorly hydrated pt
- if pt becomes anuric the kidneys are basically dying
– long term dialysis will help get them back, but they don’t do well at this point
- fluid therapy rely and aggressively when it comes to AKI

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14
Q

Unknown toxin tx - Cardiovascular & respiratory

A

BP management
- fluid therapy
- vasopressor (e.g. noradrenaline)
- or anti-hypertensives (e.g. amlodipine)

Oxygen therapy

Ventricular tachycardia:
- lidocaine or amiodarone (anti-arrhythmias)

Supraventricular tachycardia
- filling will reduce, stroke volume will reduce, CO will suffer
- give beta-blocker (e.g. propranolol) -> slows HR down to improve filling

Bradycardia
- usually because the toxin has stimulated the vagal system
- e.g. certain snake toxins and mushrooms
- can cause v inappropriately low HR, output drops, heart will stop
- give atropine
– should see quick response back to normal
– but doesn’t have a long T1/2, so may need repeated doses

Amlodipine
- calcium channel blocker
- vasodilator
- reduces resistance in the system as a whole and brings BP down

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15
Q

Unknown toxin tx - GI

A

V+
- may not want to stop in the acute phase
– trying to decontaminate itself

Irrectractable v+
- anti-emetic (e.g. maropitant, metoclopramide, ondansetron) and fluid therapy

D+
- fluid therapy
- GI diet

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16
Q

Unknown toxin tx - haematological

A

Clotting
- vitamin K1
- plasma

Anaemia
- packed RBCs / whole blood

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17
Q

Examples of respiratory problems caused by toxins

A
  • non-cardiogenic pulmonary oedema
  • direct inflammatory issues of the lung if inhaled (rare)
  • more likely to have perfusion ventilation mismatch (neurological effects causing hypo/hyperventilation, or things affecting bp and perfusion to the lungs)
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18
Q

Ibuprofen/NSAID toxicity - what are they? what effect does this have?

A

COX inhibitors -> reducing prostaglandin production

PGE2 & PGI2 play important roles in:
- maintaining afferent renal blood flow
- maintaining GI mucus production, mucosal blood flow and cell turnover

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19
Q

Ibuprofen/NSAID toxicity - CS

A
  • haemorrhagic v+/d+
  • AKI
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20
Q

Ibuprofen/NSAID toxicity - how much is needed to cause a problem?

A

Ibuprofen
- 10mg/kg GI signs
- 100mg/kg renal signs

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21
Q

Ibuprofen/NSAID toxicity - specific tx

A

H2 blockers
- ranitidine/cimeditine

Proton pump inhibitor
- omeprazole

Prostaglandin analogue
- misoprostol
- not in the pregnant pt

Intralipid infusion
- side effects but overall probably a good idea

^ on top of supporting the v+/d+ and AKI

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22
Q

Aspirin toxicity - what effect does it have?

A
  • very similar to other NSAIDs but may have greater inhibition of Thromboxane in addition to prostaglandin inhibition
  • Thromboxane (TXA2) is important for platelet function
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23
Q

Aspirin toxicity - CS

A
  • thrombocytopathy: bleeding, e.g. prolonged BMBT, petechiae
  • other NSAID associated
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24
Q

Aspirin toxicity - tx

A
  • as for NSAIDs
  • bleeding is unlikely to be significantly associated with death before other damage
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25
Paracetamol (Acetaminophen/APA) toxicity - what effect does it have?
Mechanism of action is believed to be via COX but there are other theories - metabolised by the liver, primarily by glucuronidation then sulphate conjucation - those pathways can become saturated, cytochrome P450 oxidises the excess into N-acetyl-p-benzoquinone (NAPQI) (which is really horrible) - NAPQI is de-toxified by glutathione, but glutathione stores can be exhausted - another potential metabolite produced is para-aminophenol (PAP) (which is also horrible) NAPQI causes: - hepatic cell necrosis - nephrotoxicity PAP causes: - methemoglobinaemia -- prevents haemoglobin releasing oxygen
26
Paracetamol (Acetaminophen/APA) toxicity - CS
- brown mm (methemoglobin) - jaundice - abdominal pain - lethargy - v+ - (direct hepatic damage) - AKI - signs of hypoxia to tissues -- brady/tachyarrhythmias - peripheral oedema (esp the neck in dogs) (due to endothelial damage -> leaky vascular endothelia) - resp distress
27
Paracetamol (Acetaminophen/APA) toxicity - diagnostic clue
- brown blood - in cats, Heinz body anaemia is suggestive - potentially also brown mm
28
Paracetamol (Acetaminophen/APA) toxicity - tx
*N-acetyl cysteine* - glutathione procures which binds the toxic metabolites H2 receptor antagonists - e.g. ranitidine - may reduce CP450 oxidation - evidence limited but won't harm to give Ascorbic acid (vit C) - may reduce methaemoglobin to haemoglobin - evidence limited/inconclusive - realistically short erm won't cause damage Liver support - SAMe - UDA Silybin AKI support - IVFT GI support
29
Chocolate (Theobromine & caffeine) - what effect does it have?
Both examples of methyl-xanthines: - increase catecholamine release - increases cAMP -> increased intracellular calcium in cardiac and skeletal muscle - inhibits adenosine receptors Primary affects the cardiac rhythm and CNS
30
Chocolate (Theobromine & caffeine) toxicity - CS
- hyperactivity - v+/d+ - arrhythmias (usually tachy) with VPCs, tachypnoea - seizures - coma - death When get arrhythmias should get worried as next stage is seizures
31
Chocolate (Theobromine & caffeine) toxicity - tx
As per system with some specifics: - entero-hepatic recycling -> charcoal every 4-6h - severe cases may need intubation and urinary catheterisation
32
Xylitol toxicity - what is it and what is it commonly seen in?
- it is a sugar-alcohol, that mimics glucose but without a caloric contribution - commonly as a result of dogs eating chewing gum, can be found in other things including some peanut butters
33
Xylitol toxicity - what effect does it have and what CS?
Stimulates insulin release and hepatotoxic: - prolonged hypoglycaemia: 12-48h - liver failure: within 72h - weakness, collapse, seizures, coma, death - jaundice
34
Xylitol toxicity - diagnostic clues
- hypoglycaemia - elevated ALT
35
Xylitol toxicity - specific tx
Hepato-protectants - sAME - UDA - silybin Glucose supplementation - oral vs IV - bolus vs CRI - try to avoid causing further insulin spikes - if the dog is eating, give it orally - constant small meals: little but often, producing no dramatic spikes - bolus will definitely cause big insulin spikes but CRI is difficult to maintain the glucose at 5% - monitor glucose: every hour, if happy stable drop to every 2h, for a least 24-48h
36
Pyrethroids (e.g. permethrin) toxicity - what is it found in?
- found in insecticides such as 'Raid' and ant powders, as well as some old school flea products
37
Pyrethroids (e.g. permethrin) toxicity - which animals are particularly susceptible? why?
- cats are particularly susceptible as they lack the enzyme glucuronyl transferase required for the glucuronidation pathway
38
Pyrethroids (e.g. permethrin) toxicity - what effect do they have? CS?
Primarily act on neural axons (sodium channels): - ataxia, tremors, disorientation and seizures - dyspnoea and resp arrest - hypersalivation and v+ - uncontrolled seizing can cause rhabdomyolysis and subsequent AKI
39
Pyrethroids (e.g. permethrin) toxicity - diagnosis
- usually based on known exposure and CS
40
Pyrethroids (e.g. permethrin) toxicity - tx
- generally principles - decontamination may involve the skin e.g. flea products - intralipid is excellent as permethrin is highly lipophilic
41
Cleaning product toxicity - examples
- many household cleaning products contain either strong acids or alkalis
42
Cleaning product toxicity - what effect do they have?
- damage is primarily due to surface contact, in the case of ingestion this will be the mucosa, particularly oral, oesophageal and gastric
43
Cleaning product toxicity - CS
- oral pain - dysphagia - regurgitation - v+
44
Cleaning product toxicity - tx
Gastric decontamination is dangerous - risk of worsening oesophagi's Dilution - oral water, or washing exposed surfaces with water
45
Cleaning product toxicity - complication
- severe oesophagi's can develop post exposure including strictures
46
Ethylene glycol (anti-freeze) toxicity - what effect does it have?
- it is sweet tasting and similar in structure to alcohol -> it's tasty and rapidly absorbed - it is metabolised into glycoaldehyde, glycolic acid and oxalic acid - glycoaldehyde is neurotixic - glycolic acid produces a severe acidosis - oxalic acid binds calcium leading to calcium oxalate crystal formation in several organs - mortality is high - cats are particularly susceptible (1.5ml/kg compared to 6.6ml/kg for dogs)
47
Ethylene glycol (anti-freeze) toxicity - CS
<12h - v+ - lethargy - ataxia (looking drunk) 12-24h - tachyarrhythmias - tachypnoea - hypocalcaemia 24-72h - AKI & death
48
Ethylene glycol (anti-freeze) toxicity - diagnosis
1. increased osmolality of blood due to EG <1h; not often available in 1st opinion 2. acid/base analysis: profound normochloraemic metabolic acidosis 3. hypocalcaemia (ionised preferentially) 4. renal damage: azotaemia, hyperkalaemia 5. urinalysis: 3-6h may find calcium oxalate monohydrate crystals 6. woods lamp on paws/mouth: some anti-freeze contains fluorescein dye 7. ethylene glycol point of care tests are available
49
Ethylene glycol (anti-freeze) toxicity - specific tx
Have low expectations -> be realistic with O Slowing the production of toxic metabolites is key - alcohol dehydrogenase - medical ethanol (20%) - vodka diluted with saline (20%) - 2-3d of repeated prolonged boluses - dialysis has improved outcomes -> referral - assess QoL at 7d mark, if hasn't worked then -> PTS
50
Rat poison / Warfarin toxicity - what effect does it have? CS?
- inhibit vitamin K epoxide reductase i.e. inhibits vit K synthesis - vit K is important in production of clotting factors II, VII, IX and X - coagulopathy 36-72h post ingestion
51
Rat poison / Warfarin toxicity - diagnosis
- PT prolongation initially (factor VII has the shortest T1/2) - aPTT prolongation follows - cavitatory (large) bleeds e.g. haemothorax - petechiae are unlikely to be present
52
Rat poison / Warfarin toxicity - tx
Vit K1 injectable initially, followed by oral - up to 8w Fresh frozen plasma transfusion in severe cases - for clotting factors
53
Raisins/grapes/sultanas/currants toxicity - what effect does it have? CS
- toxic substance is not known -- tartaric acid has been implicated - resultantly there is no known toxic dose, so any exposure should be considered serious - however, retrospective reviews have highlighted a low degree of AKI developing after exposure - CS: AKI - more commonly see self limiting v+/d+
54
Raisins/grapes/sultanas/currants toxicity - tx
General principles IVFT - for 48-72h in non-azotaemic animals Dialysis - improved outcomes where AKI is confirmed
55
Cocaine - CS
- hyperactive - hyperthermia - tachyarrhythmias - v+ - ataxia - seizures
56
Cocaine - tx
- general principles - don't forget the hyperthermia
57
Marijauna - CS
- v+ - 'paranoia', which can lead to aggression - ataxia - depression - coma - urinary incontinence
58
Marijauna - tx
- general principles - urinary catheter - intralipid fusion - anxiolytics
59
Opiates (e.g. heroin) - CS
- depression - lethargy - v+ - constipation - hypoventilation
60
Opiates (e.g. heroin) - tx
- general principles - reversal: naloxone - consider ventilating short term
61
Ketamine - CS
- ataxia - hallucinations - aggression - cataplexy (K-hole - essentially anaesthetise themselves) - loss of patent airway
62
Ketamine - tx
- general principles - consider intubation
63
Lily toxicity - what effect does it have?
- toxic substance is not known (probs a steroidal glycoalkaloid) - cats are very sensitive: minimal ingestion can lead to AKI - dogs are less sensitive: usually just GI signs - any part of the plant is toxic
64
Lily toxicity - tx
- as per AKI - dialysis has improved outcomes - decontamination should also involve clipping/washing paws and around the mouth to prevent further exposure through grooming
65
Onion, garlic, leek, chive toxicity - what effect do they have?
- large quantities need to be eaten for toxicity to develop - cats may be more sensitive Sulphur containing compounds which can cause - oxidative damage to RBCs - haemolysis - Heinz-body anaemia
66
Onion, garlic, leek, chive toxicity - v+/d+
- tachycardia - tachypnoea - pale mm (anaemia)
67
Onion, garlic, leek, chive toxicity - tx
- general principles - in severe cases consider a transfusion - keep an eye on RBCc, haematocrit & PCV
68
Tremorgenic mycotoxins - what effect do they have
- fungal metabolites (Penitrem A) that are neurotoxic - usually found on mouldy food
69
Tremorgenic mycotoxins - CS
- muscle tremors, esp intention tremors (i.e. on action they tremor more) - hyperaesthesia - seizure, coma, death
70
Tremorgenic mycotoxins - tx
- general principles - diazepam is ineffective for tremors, instead methocarbamol (Robaxin) should be used, but is off licence - intralipid may be useful as Penitrem A is considered lipid soluble Prognosis is usually good but they can look severe.

Y4 SA - GI & hepatic disease (14 decks)

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