HEPATOTOXICANT TABLE
TOXIN
SOURCE
MECHANISM OF ACTION
CLINICAL SIGNS
CLIN PATH
TOX TEST
TREATMENT
PROGNOSIS
May be seen as soon as 30 minutes after ingestion but typically occur within 3 to 5 hrs GI (vomiting, diarrhea) and CNS (hyperesthesia, incoordination, hyperthermia, seizures) signs Liver damage and cirrhosis may occur 2-3 days after exposure Death from respiratory failure may occur within 4-24 hrs after exposure
Known as a molluscicide, used for the control of slugs and snails (although recently replaced by less toxic iron phosphate)
• Decontamination, if appropriate • Gastric lavage with inflated ETT should be performed if the patient is symptomatic and evidence of pellets still in stomach on radiograph; administration of 1 dose of charcoal if gastric lavage performed • Stabilization of vital signs, IV fluids, anti-emetics, acid-base monitoring, methocarbamol/anticonvulsant therapy, respiratory and CV system monitoring, supportive care
Acidosis, liver value abnormalities
Acute median LD values are 210 to 600 mg/kg for dogs and 207 mg/kg for cats Prognosis is good if survival is > 24 hrs from ingestion with early treatment
Characteristic odor of formaldehyde
Results in the disruption of the GABAergic system Monoamine oxidase, 5-hydroxytryptamine, and norepinephrine may also be involved in the toxic mechanism
Metaldehyde
may be present in the stomach contents along with bait material No consistent and pathognomonic gross or histological lesions occur in metaldehyde poisoned animals
Coins, feeds, solutions, wire, jewelry, food
• Chelation with penicillamine or trientine • Supportive care for other derangements
Increasing zinc in diet can aid in prevention
Quantitative hepatic copper values; genetic testing (some breeds)
Breeds that are homozygous for a recessive gene (Bedlington Terrier, Skye Terrier, West Highland White Terriers, Labrador Retrievers, Doberman Pinschers) have excessive copper storage in the liver
Copper
Lethargy, anorexia, vomiting, weight loss, jaundice
Sedation, malaise, ataxia, jaundice
Oral diazepam (valium) and alprazolam (not seen with parenteral administration); typically seen with chronic oral dosing
Markedly ↑↑↑ ALT ↑ T-bili, PT/PTT
Acute hepatic necrosis in 5-11 days of oral treatment
Benzodiazapines (oral) CATS ONLY
Amanita spp., Galerina spp., Conocybe spp., Lepiota spp.
• Decontamination is often too late – gastric lavage +/- activated charcoal, bathe (use protective gear) • PCV/TS/BG • Baseline Chem, CBC PT/PTT • Decontamination (emesis and AC if < 2 hrs post ingestion) • IV fluids, sequester amatoxin bile in gallbladder with octreotide CRI, NPO), ultrasound-guided bile aspiration
Alpha amanitin LD 50 (human) = 0.1 mg/kg Easily found in one mushroom
↑↑ Liver enzymes within 48-72 hrs
Microcystin binds to protein phosphatase in cytoskeleton, disorganization of actin leads to cellular collapse, intrahepatic hemorrhage, death Inhibit DNA and RNA transcription and protein synthesis; bind to actin filaments, deform cytoskeleton → hepatocyte death
Centrilobular hemorrhagic necrosis
Develop GI signs within 6-24 hrs “False” recovery period, followed by fulminant liver failure and AKI in 36-48 hrs
Amatoxin Mushrooms
Death in hrs to days with hepatotoxin GI (e.g., vomiting/diarrhea), CNS (e.g., weakness, ataxia, tremors, seizures), cardiac (e.g., collapse, pallor, tachycardia, respiratory failure, hemorrhagic and hypovolemic shock) Very acute clinical signs with neurotoxin (death can occur in minutes to hrs) – CNS signs and SLUDGE-like signs
Cyanobacteria Hepatotoxins ( Microcystis spp., Nodularia spp.,
Toxic dose – 50-11,000 mcg/kg
↑↑ Liver enzymes within a few to 24 hrs; ↑↑ PT/PTT; anemia
Diffuse hepatic necrosis
Blue-Green Algae
Prognosis – often grave
Oscillatoria spp. most common; Anabaena spp. less often) Can also contain neurotoxins
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