Toxicology Module 1 Flashcards
What are the types of decontamination?
- Ocular - irrigate for 20-30mins using tepid water or saline
- Dermal - clip/clean/lavage/lipophilic substances
- GIT - Emesis, gastric lavage, whole bowel irrigation, MDAC
Use of emesis for decontamination?
Not always complete evacuation
Less effective if 2-3 hours post ingestion
Not to be done if caustic toxin ingested (petroleum)
Use of gastric lavage for decontamination?
Can delay absorption if emesis contraindicated - Needs GA
May not be worth it - 15-20min post ingestion, yields 33% of poison load
complications: hypothermia, hypoxaemia, dysrhythmias, laryngospasm, GI perf, electrolyte imbalances
Whole bowel irrigation for decontamination?
May be more effective at removal but no studies to show better than MDAC
Good for slow release capsules/toxins
Similar complications to gastric lavage
Nasogastric tube placed and polyethyleen glycol solution administered till rectal effluent is clear
enemas can be used
MDAC for decontamination?
- Carbon granules with large surface area allowing lots of area to bind and create a intraluminal sink
Not good for ethylene glycol (alcohols), iron compounds, strong alkali - Administered orally or via nasogastric tube
- Complication: vomitting/aspiration
- Similar effects to emesis - 70-90% if <30mins post ingestion
- can have cathartics such as sorbitol that enhance expulsion from GIT
What are principles when dealing with a toxin?
Can it be decontaminated?
Can elimination be enhanced?
Is there an antidote?
Methods to enhance elimination?
Encourages removal of the agent form the plasma by enhancing normal means of excretion (urine/feces) or using medical means
1. Forced diuresis - Increase filtration through kidneys - phenobarbs, bromides, lithium, - not for lipophilic meds
2. Ion-trapping - altering pH of urine to trap highly charged molecules in urine and increase excretion
3. Cholorectics - lipophilic toxins undergo entero-hepatic circulation where certain molecules/metabolites after initial conversion by liver in to bile into the bowel and then resorbed in to small intestines - DESTOLIT : increase bile flow use with MDAC
4. Intralipid - lipophilic LogP >2 - lipid sink
5. Peritoneal/haemodialysis - useful for cardiac/real causes, ibuprofen, NSAID, ethylene glycol
6. Plasma exchange - good for IMHA, ehrlichia, hyperbilirubinaemia- NSAIDs
What are the toxic metabolites of ethylene glycol?
Glycoaldehyde (resp depression/hyperglycaemia) and glyoxalate (acute tubular necrosis) per weight and glycolic acid has the most cumulative toxic effects
Rapidly absorbed from GIT w/n 30mins, peak w/n 3 hours
Metabolism in liver with small amount in kidneys, stomach and excreted in urine
What are the clinical signs of ethylene glycol toxicity?
Stage 1: 30mins of ingestion
- GI signs v+/d+
- neuro: seizures, muscle fasciculations, ataxia
- PUPD
Stage 2: related to metabolites
- cardiopulmonary: increased RR, HR, pulm edema
- renal effects - 12hrs in cats - azotaemia, anuric renal failure
Treatment for glycolic acid toxicosis?
Rapid treatment needed
Emesis w/n 1-2 hrs
Fluid therapy
Antidose: ethanol - ideally given within 6-8hrs, fomipezole (competitive inhibitor of alcohol dehydrogenase)
haemodialysis
Diagnosis of ethylene glycol?
History
Metabolic acidosis (glycolic acid)
Woods lamp for fluorescence in urine around face
calcium oxalate crytalluria (w/n 3-6hrs) - marked azotaemia 6-12hrs, isosthenuric urine
RIM sign in kidney (corticomedullary sign)
Point of care kit
What is the mechanism of paracetamol toxicity?
NAPQI: normally binds with sulphdryl groups of endogenous glutathione - if glutathione depletes then NAPQI accumulates
- causes hepatocellular death with centrolobular necrosis, direct acute tubular necrosis in proximal tubules in kidneys
- oxidative damage to cell membranes and binding to Hb = methhaemoglobin, heinz body anaemia and haemolysis
- Lack of n-acetyltransferase in canine and feline erythrocytes leading to build up of para-aminophenol rather than NAPQI- metHb
Clinical signs of paracetamol toxicity?
Depression, vomitting, lethargy, anorexia, muddy mm, tachycardia, facial/paw edema
Treatment of paracetamol toxicity
- Emesis
- Activated charcoal
- O2 therapy
- pRBC transfusion (methHb)
- Supportive care with fluids
- Frozen plasma +/- vit K
- N-acetylcysteine - glutathione precursor - oral or IV
Coumarin Rodenticides MOA, CS, Dx, Tx
MOA: inhibit vit K epoxide reductase (inhibits recycling in the liver), decrease levels of vit K which is needed to activate coag factors
- 1st and 2nd generation anticoags have the same effect and second generation has a longer period of action
CS: after 3-5 days CS of bleeding become evident
Dx: check clotting factors 48hrs-72hrs post ingestion can check clotting factors - factor 7 (shortest halflife) so PT will be prolonged before aPTT
Tx:
-Emesis and MDAC very effective if instituted within 4hrs of ingestion
- no value to giving vit K prior to 48-72hrs
- Vit. K s/c or blood products if bleeding
- check clotting 48-72hrs post stopping tx