Intoxications.module 15 Flashcards
Describe the phone triage of suspected intoxication cases
What, when, how much, route of access, bring in packaging.
Discuss the decontamination methods for intoxicants and associated complications and contraindications
WASHING;eg. permethrin toxicity in cats (the dog permethrin formulation applied as a spot on to cats). Decontamination involves warm soapy water bath to remove as much of the toxic compound as possible. Shaving the fur is often helpful in these cases.
INDUCTION OF EMESIS;
Dogs;
Apomorphine (0.03-0.05mg/kg IV or 0.05-0.1mg/kg SC) or a crushed tablet placed in the conjunctival sac (6.25mg) or a tablet placed over the gingiva (6.25mg).
Cats;
Xylazine (0.44-1.0mg/kg IM)
or
Dexmedetomidine (7.0 mcg/kg IM or 3.5mcg/kg IV)
Both medications are effective approximately 50% of the time. Both medications can be reversed with atipamezole. (dexmedetomidine IS DIFfERENT to medetomidine)
Emesis will result in removing 20-60% of gastric contents when performed within 4 hours of ingestion. In 2018, a study involving 7 dogs found that 10-77% of ingested brodifacoum was recovered when emesis was induced within 60 minutes. Human medicine does not tend to induce emesis.
Contraindications to emesis;
Any patient showing clinical signs that predispose them to aspiration of vomited material (e.g. patients experiencing sedation, altered mentation, severe weakness, tremors, seizures)
Any patient with compromised swallowing mechanisms (e.g. LMN paralysis, megaoesophagus, laryngeal paralysis)
Ingestion of caustic substances (acids or alkalis) or sharp objects
Ingestion of substances with a high aspiration potential (e.g. petrol/kerosene)
Other medical conditions that could be exacerbated by forceful vomiting (e.g. increased intracranial pressure, coagulopathies, recent abdominal surgery, ocular pathology).
GASTRIC LAVAGE; Under ga. Et tube must be positioned. Then place large bore stomach tube. Flush repeatedly with warm water. Not as effective as emesis.
ACTIVATED CHARCOAL;I “activated “ b/c has been super-heated and so has greater number of binding sites. Usually combined with sorbitol, which will decrease gut transit time and promote colonic evacuation. Can be useful for absorbtion and elimination of most organic toxins. It is NOT useful for alcohol, xylitol, petrol, nitrates and nitrites. CAN be useful for methylxanthines and NSAIDs intoxications.
Activated charcoal can be given to an animal that has ingested a potentially toxic dose of a substance if:
The substance is known or thought to be absorbed by activated charcoal,
Ingestion was very recent, the substance is known to undergo enterohepatic circulation, or if the agent is a sustained release agent,
The animal is in a clinical condition where it can tolerate activated charcoal, and
The animal does not require immediate administration of oral medication (as active charcoal will affect its absorption).
I/V FLUIDS;-once corrected any fluid deficits, just maintenance rates can help renal excretions of toxins.
INTRALIPID (i/v fat emulsion) may be used in extreme cases of lipid-soluble toxins such as beta blockers, anaesthetics, ivermectin etc. Provides extra energy source and acts as a “lipid sink”. Sometimes also used for i/v nutrition. Beware may cause phlebitis and anaphylaxis, pancreatitis..
The current dosing for 20% lipid solution is 1.5ml/kg IV bolus over 1-2 minutes, followed by
0.25ml/kg/min for 30 to 60 minutes. Useage is still controversial and not widely accepted as efficacious.
Discuss the common intoxications, including clinical signs, diagnosis, stabilisation, and management of patients affected:
Metaldehyde intoxication
Synthetic pyrethrin intoxication
Anticoagulant rodenticide intoxication
Lily plant intoxication
Non-steroidal anti-inflammatory drug (NSAID) intoxication
Chocolate/Caffeine intoxication
Ethylene glycol intoxication
Grape & Raisin intoxication
METALDEHYDE;green snail bait pellets. Causes profound seizures which may lead to hyperthermia and organ failure.Tx by emesis if able, otherwise control seizures as per;
Control seizures/muscle tremors
* NOTE: A combination of these medications is often required to reduce the tremors to
an acceptable level; it is often not possible to eliminate them completely.
* Methocarbamol 44mg/kg IV initially - can repeat this dose up to a maximum of
330mg/kg per 24 hours to control tremors.
* Diazepam 0.5mg/kg IV in event of grand mal seizure - give up to three doses
* Midazolam as a CRI @ 0.1-0.5mg/kg/hr if methocarbamol is ineffective as a sole agent
* Phenobarbitone 4-6mg/kg IV as a loading dose to control seizures
* Levetiracetam 20mg/kg IV can be used as a second line for control of seizures
refractory to diazepam/phenobarbitone.
* If seizures cannot be controlled with the medications listed above, anaesthesia should be
induced with propofol, titrated to effect, followed by placement of a cuffed ET tube to
protect the airway. The patient should then be maintained on a CRI of Propofol (0.1-
0.6mg/kg/min) and Midazolam (0.1-0.5mg/kg/hr).
Provide cooling, gastric lavage and usually repeated colonic irrigation. Run bloods, liver supports if necessary, clotting times if suspect dic.Activated charcoal at end of gastric lavage. Intralipid has occasionally also been used.
SYNTHETIC PYRETHRIN;Cats are considered exceptionally sensitive to permethrin toxicosis compared with dogs, rats or humans. This is thought to be due to a deficiency of hepatic glucuronosyltransferase. Products
formulated for dogs contain 0.054% to 65%, products formulated for cats should contain less than 0.2% permethrin.
clin signs range from mild twitching to protracted vomiting and diarrhoea, marked depression, ataxia or generalised muscle tremors, seizures and death.
Tx;
Control of muscle tremors/seizures. It is not always possible to stop tremors
completely. Rather, the goal is to reduce to a level that is compatible with life.
o The majority of these patients can be managed with methocarbamol (44mg/kg
IV initially - up to a maximum of 330mg/kg/day)
o Seizure activity is uncommon in these cases but should be treated appropriately.
o Adjunctive therapies – although not strictly directed at reducing tremors, antiseizure medication can reduce excitation and help augment methocarbamol,
especially when high levels have not had sufficient control.
▪ Benzodiazepines (e.g. diazepam or midazolam)
▪ Phenobarbitone 2-6mg/kg IV q6 to 8 hours can help alleviate symptoms
even though these are not strictly seizures
o Acepromazine 0.01mg/kg IV every 6 to 8 hours can reduce stress and anxiety.
Decontaminate coat, i/v supportive fluids, don’t use activated charcoal as administration only increases stress. In rare unresponsive cases may use intralipid.
RODENTICIDE;Rats and mice have developed a resistance to first generation rodenticides (warfarin and others), thus 2nd generation produced (brodifacoum and others).Works by antagonising the enzyme vitamin K epoxide reductase, which is
responsible for recycling Vitamin K. Vitamin K is essential for the conjugation of clotting
factors II, VII, IX and X. When the body’s stores of vitamin K1 and the circulating clotting
factors have been consumed (which can take 3-5 days), the patient develops a secondary
coagulopathy.Prothrombin time (PT) is the first blood test to be prolonged with acute long-acting
anticoagulant ingestion (as Factor VII has the shortest half-life). This will usually take 36-48
hours to occur after ingestion.
Tx; emesis if appropriate.
If coagulopathic;
Vitamin K1 should be administered as soon as possible for patients with known
ingestion. This can be given orally at 5mg/kg for one dose followed by 2.5mg/kg BID
for 4 weeks (second generation) or 2 weeks (first generation). Oral Vitamin K1 is
better absorbed with a fatty meal. If the oral route is not possible, Vitamin K can be
given as a subcutaneous injection (this can cause haematoma formation) or
intravenously (this carries a high incidence of anaphylaxis).
Fresh frozen plasma if clinically haemorrhaging at 10ml/kg is
recommended before rechecking ACT or aPTT, and repeated if required. The body
takes 6-12 hours to synthesise enough clotting factors to halt bleeding, so patients
should be hospitalised and monitored for at least 24 hours.
For patients with clinical bleeding:
o ACT every 6 to 12 hours, can be used to monitor improvement in clotting
times. However, it should be noted that ACT and PT/aPTT has not been
correlated with risk of haemorrhage.
o PCV/TP should be performed every 6 to 12 hours if there is suspicion of
ongoing bleeding.
Packed rbc’s may also be required.
If dyspnoiec, Tfast scan and may need chest drain although risky if done prior to correcting clotting factors.
Other supportive meds eg painrelief, sedation/anti-anxiety, padded cages etc.
LILY PLANT;
Cats are particularly susceptible to the lilium spp. (true lilies) and Hemerocallis spp. (daylily).Note that this does not include the peace lily, which is a common house plant.
causes renal failure. 1-2 leaves fatal.
if in time, might be best to r/o via gastroscope. Polyuria may occur within 12 hours, and
anuria and renal failure can occur within 24-48 hours.
may also cause v+ initially just as gastric irritant. need to know if have vomitted the lily leaves up.
tx is emesis/gastric retrieval/gastric lavage, activated charcoal, fluids.If anuric, try low dose frusemide, but if no response, hopeless px.
NSAID; Nsaids usually inhibit cycloxygenase. Cycloxygenase (1 or 2) converts Arachidonic acid to thromboxanes or prostaglandins.
Generally COX-1 Prostaglandin have protective effects. It increases gastric mucous production and
enhances local blood flow. COX-2 – stimulated when damage occurs and produces PG that
play important role in mucosal healing. Therefore NSAID side effects are gastric ulceration
and inhibit ability of ulcers to heal.
Normally when perfusion to kidneys decline GFR decreases. As a protective mechanism, the
JGA releases prostaglandins that vasodilate afferent renal arterioles to maintain renal blood
flow and GFR. Also stimulate renin from JGA (see RAAS). These are mediated by COX-1
and COX-2 enzymes. Therefore when NSAIDs are administered (particularly to a
hypovolaemic patient) – prostaglandin mediated effect of local vasodilation is diminished or
lost. ➔ damage.
However will still see renal damage with high doses in patient with normal blood volume.
There is also an immune-mediated response in kidneys (interstitial nephritis).
Haematologic Adverse Effects: Inhibition of thromboxane - resulting in reduced platelet
aggregation.
Hepatic adverse effects: Idiosyncratic – does not depend on dose or duration.Formation of reactive metabolites that cause hepatocellular injury by binding to cellular
macromolecules or disrupting organelle functions, activation of apoptotic mechanisms,
haptenization of hepatocellular membrane components that triggers an immune-mediated
attach and release of drug modified macromolecules that trigger an immune response.
TX;emesis within 4 hours, activated charcoal, fluids, gastro protection (Proton pump inhibitor (e.g. esomeprazole 1mg/kg IV every 8-12 hrs If ulcers are suspected to be present, sucralfate 0.25-1g/dog orally every 12 hrs),Misoprostol is a synthetic prostaglandin that has mucosal protective properties. Dose at
2-5 mcg/kg PO TID. This medication can cause abortions in pregnant women and
owners/staff should be warned about this (It is recommended to wear gloves when
handling the medication).
**Literatures did not find increased benefit in using Misoprostol compared to other
GA protectants for NSAID toxicity.
* Blood transfusions are occasionally necessary due to uncontrolled gastric bleeding.
* Surgical intervention is required in cases of gastric/duodenal perforation.
CHOCOLATE/CAFFEINE;
Chocolate contains
theobromine, which, along with caffeine, is a source of methylxanthines. Methylxanthines
can cause CNS stimulation (seizures, tremors), cardiac muscle stimulation (tachycardia,
arrhythmias), diuresis (PU/PD) and relaxation of smooth muscle. Caffeine is absorbed more
rapidly than theobromine, with clinical signs typically occurring after 1-2 hours and 6-12 hours
respectively. Many chocolate products contain both theobromine and caffeine.
TX; emesis (chocolate can remain in stomach for up to 12 hours), fluid support,
control of seizures/tremors;
* Methocarbamol 44mg/kg IV initially - can repeat this dose up to a maximum of
330mg/kg per 24 hours to control tremors.
* Diazepam 0.5mg/kg IV in event of grand mal seizure - give up to three doses.
* Midazolam as a CRI @ 0.1-0.5mg/kg/hr if methocarbamol is ineffective as a sole
agent.
* Phenobarbitone 2-6mg/kg IV as a loading dose to control seizures.
* Levetiracetam 20mg/kg IV can be used as a second line for control of seizures
refractory to diazepam/phenobarbitone.
* If seizures cannot be controlled with the medications listed above, anaesthesia should
be induced with propofol, titrated to effect, followed by placement of a cuffed ET tube
to protect the airway. The patient should then be maintained on a CRI of Propofol (0.1-
0.6mg/kg/min) and Midazolam (0.1-0.5mg/kg/hr).
Cooling, activated charcoal, urinary catheter flushing as methylxanthines can be re-absorbed from bladder and in dwelling urinary catheter so not accumulating.
Cardiac care if req;
* Control arrhythmias if present:
o In the presence of ventricular arrhythmias (ventricular tachycardia where the
heart rate is >180bpm or R on T phenomenon) lignocaine @ 2mg/kg IV bolus
repeated every 5 minutes to a max of 6mg/kg then followed by a CRI of 20-80
mcg/kg/min.
o Persistent supraventricular tachycardia that results in perfusion deficits can be
controlled with beta blockers (esmolol, give a loading dose of 0.25-0.5mg/kg
followed by CRI at 10-100mcg/kg/min, starting at the lower dose and titrating
to effect).
ETHYLENE GLYCOL;Ethylene glycol is in products such as anti-freeze for cars.
Ethylene glycol is metabolised via a series of pathways to oxalic acid. Serum calcium binds to
oxalic acid – resulting in calcium oxalate crystal formation. These crystals cause severe renal
damage in the tubules. Ethylene glycol that is not metabolised is excreted in the urine – is a
gastrointestinal irritant, central nervous system depressant and osmotic diuretic and is
significantly less toxic than its metabolite.
CLIN signs;Metabolic acidosis
o With increased AG
o Hypocalcaemia, hyperglycaemia
o Azotaemia
o Calcium oxalate crystalluria
* Ultrasound
o Renal echogenicity – hyperechoic – ‘halo sign’
TX;Emesis only if within 1 hour as is rapidly absorbed. Gastric lavage.
Fluids. Urinary catheter.
Specific antidotes are
1. Ethanol Inhibitor of alcohol dehydrogenase (inhibits formation of oxalic acid)
IV CRI – 1.3ml of 30% ethanol/kg bolus then CRI of 0.42ml/kg/hr for 48
hours
OR
2. Fomiprazole also an alcohol dehydrogenase inhibitor. Esp recommended for cats but must commence within 3 hours.
Cats 125mg/kg slow i/v at time o then at 12 and 24 hours, then 31.25mg/kg at 36 hours. (yes cats need much higher doses).
Dogs initially 20mg/kg slow i/v at time o, then 15mg/kg slow i/v at 12 hours and 24 hours, then 5mg/kg at 36 hours.
Note that unmetabolised ethylene glycol which can thus spare kidneys, can still have cns depressant effects.
Px is guarded esp if already showing clinical signs. Anuria can occur quite quickly.
GRAPE/RAISIN Possible nephrotoxic
agent (tartaric acid is proposed) or idiosyncratic reaction leading to hypovolaemic shock and
renal ischaemia in dogs.Large variability in dogs’ tolerance for the Vitus fruits;
o Estimated quantity of raisin causing toxicity
▪ 2.8-36.4g/kg
o Estimated quantity of grapes causing toxicity
▪ 19.6-148g/kg
o Suspected that toxicity increases with increasing amount ingested but some pets
were asymptomatic after ingestion of 1kg of raisins
o One pet was reported to have clinical signs after eating 4-5 grapes (8kg dog)
CLIN signs;Vomiting, anorexia, diarrhoea, lethargy, abdominal pain
* Oliguria, anuria.Acute renal failure (elevated BUN and creatinine)
* +/- hypercalcaemia, hyperphosphataemia
* Histopathologically – acute tubular necrosis (especially proximal tubules)
TX;emesis, activated charcoal, fluids (up to 48-72 hours post ingestion), monitoring.
Discuss ‘serotonin syndrome’, including clinical signs, diagnosis, stabilisation, and management of affected patients
Serotonin syndrome occurs following overstimulation of serotonin receptors (5-HT). A variety
of drugs from different classes can cause serotonin syndrome. These include tryptophan,
amphetamines, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, tricyclic
antidepressants and others. The most prescribed veterinary medications causing serotonin
syndrome are for pain or behaviour modification (tramadol, fentanyl, amitriptyline and
selegiline). Clinical signs can include the following:
* Autonomic signs - Diarrhoea, mydriasis, tachycardia, tachypnoea, hypertension,
diaphoresis, fever
* Neuromuscular signs - Hyperreflexia, myoclonus, tremors, rigidity, seizures, secondary
hyperthermia, respiratory muscle compromise
* Altered mentation - Agitation, disorientation, vocalisation, excitement
TX;emesis, seizure /tremor control as listed previously, heart monitoring., gastric lavage, activated charcoal, (intralipid shown useful for trammadol intoxication).
Specific antidote of Cyproheptadine is a serotonin receptor (5HT-2A) antagonist and should be given at
1.1mg/kg PO q6-8h until clinical signs resolve.
Propranolol possesses some 5-HT antagonist
properties and possibly ideally used if persistent hypertension/tachycardia.
