HEPATOTOXICANT TABLE
TOXIN
SOURCE
MECHANISM OF ACTION
CLINICAL SIGNS
CLIN PATH
TOX TEST
TREATMENT
PROGNOSIS
Centrolobular and mid-zonal coagulative hepatic necrosis
GI signs (vomiting, diarrhea) within 15 minutes to several hrs, CNS signs (lethargy, seizures) (48-72 hrs), liver failure (24-72 hrs)
Cycads ( Cycas spp., Macrozamia spp.) (SE, South central or tropical areas of US usually) but can be found as bonsai household plant Multivitamins, iron supplements, fertilizers, snail/slug bait
• Baseline bloodwork, PT/PTT • PCV/TS/BG/liver panel q 24 hrs x 2-3 days
↑↑ Liver enzymes (24-72 hrs)
All parts of the plant are poisonous, but seeds contain largest amount of toxin
1-2 seeds can lead to severe signs Grave prognosis once hepatoxicity seen Toxicity dependent on amount of elemental iron 20-50 mg/kg = GI signs 50-80 mg/kg = GI ulcers > 80 mg/kg = liver and other systemic effects
Sago Palm
GI signs (e.g., vomiting, hematemesis, melena, diarrhea) within 0.5-6 hrs; liver failure 12-24 hrs later With large doses can see hypovolemic shock, coagulopathy and acidosis
Fluid therapy, anti-emetics, blood work monitoring, hepatoprotectants, symptomatic and supportive care antiemetics, GI protectants/antacids, hepatoprotectants, deferoxamine (chelator), supportive care, blood work monitoring • MgOH can be given while iron is still in the GI tract • Emesis if appropriate. Activated charcoal does not bind and should not be used • Other treatment includes
↑↑ Liver enzymes; ↑↑ PT/PTT if liver necrosis
Metabolized into reactive epoxide, binds to hepatocytes Large acute exposures = hepatic necrosis; smaller chronic exposures = neoplasia Stops cellular protein synthesis in multiple organs Hepatotoxicity thought to be from inhibition of mitochondrial function When serum iron exceeds the binding capacity of transferrin and ferritin, free iron causes lipid peroxidation and damage to liver, heart and brain Iron is also caustic to the GI mucosa
Iron
Serum iron levels; chelate warranted if iron > 400 mcg/ dl)
Vomiting, anorexia, lethargy, icterus, coagulopathy
Mycotoxin (mold) found in corn, peanuts, cottonseed, rice and potatoes
↑↑ Liver enzymes; ↑↑ PT/PTT
Aflatoxins
Acute – diffuse hepatic necrosis Chronic – fatty liver
GI (e.g., anorexia, vomiting, melena, stomach ulcers), lethargy, icterus
NSAID pain medication
Fluids, anti-emetics, antacids, gastroprotectants, hepatoprotectants
↑↑ Liver enzymes
Dogs > 400 mg/kg for liver effects
Aspirin
Centrilobular hepatic necrosis
GI (e.g., anorexia, vomiting), lethargy, anorexia, icterus, weakness, tremors, death
Castor bean (Ricinus communis) , Precatory bean (Abrus precatorius) , Black locust ( Robinia spp. ) , Mistletoe (Phoradendron) Pennyroyal oil, melaleuca (tea tree) oil
Fluids, anti-emetics, symptomatic and supportive, hepatoprotectants
↑↑ Liver enzymes
All parts of plants are toxic. Seeds are most toxic part of Ricinus and Abrus . Seeds must be chewed to release the toxin. Usually associated with application of 100% oil to open wound, ear canal or oral ingestion
Lectins (toxalbumins)
Vomiting, lethargy, ataxia, hind limb weakness, icterus
Symptomatic and supportive (fluids, hepatoprotectants)
↑↑ Liver enzymes
Unknown
Essential oils
isoniazid, ketoconazole, lomustine, methimazole, melarsomine, mitotane, sulfonamides, trazodone, zonisamide
• Discontinuation of drug • Hepatoprotectants • Symptomatic supportive care
Veterinary drugs associated with hepatotoxicity (albeit rare)
Abbreviations: AKI: acute kidney injury; CNS: central nervous system; DIC: disseminated intravascular coagulation; GI: gastrointestinal; LD: lethal dose; LES: liver enzymes; Meth: methemoglobin; NAC: N-acetylcystine; PT: prothrombin; PTT: partial thromboplastin time
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