HEPATOTOXICANT TABLE
TOXIN
SOURCE
MECHANISM OF ACTION
CLINICAL SIGNS
CLIN PATH
TOX TEST
TREATMENT
PROGNOSIS
Vomiting, abdominal pain, liver and kidney damage
Paradichlorobenzene (PDB) (NOTE: Make sure to differentiate from naphthalene)
• Prompt GI decontamination • Fluid administration to induce diuresis • Symptomatic response to adverse signs • Supportive care of vital functions • Seizure control with parenteral benzodiazepines • Immediate discontinuation • Treatment for hepatic failure • Hepatoprotectants (SAMe or NAC)
Hemolytic anemia Hemolysis
Organochlorine insecticide
Organochlorine insecticide with an LD 50 of approximately 500 mg/kg
Mothballs
Methemoglobinemia (rare in dogs and cats; reported in humans)
DOG DOSES: > 20 mg/kg: vomiting, GI ulcers > 40 mg/kg: AKI
Carprofen Deracoxib
↑↑ LES (AST thought to be most sensitive) MetHb, Heinz bodies, chocolate-brown appearance to blood ↑↑↑ ALT GI and AKI related findings: • anemia • hypoproteinemia • azotemia • hyperphosphatemia, etc.
Inhibit PG synthesis → mostly GI and renal effects, reported liver effects as well (chronic)
DOGS: 100 mg/kg hepatotoxicity; 200 mg/kg methemoglobinemia CATS/FERRETS: 10 mg/kg methemoglobinemia KCS can occur in dogs after even therapeutic doses DOG DOSES: Hepatotoxicity, when observed, typically develops with chronic dosing (e.g., 5-30 days of chronic use; median 19 days) > 0.1 g/kg → hypoglycemia > 0.5 g/kg → acute hepatic necrosis
NSAIDs
Idiosyncratic liver toxicity (1.4 cases out of 10,000)
DOG: GI signs, CNS depression, hepatotoxicity (icterus, coagulopathy); metHb can occur at higher doses (cyanosis, dyspnea) but not as common as in cats CAT: Respiratory distress, hypoxemia, cyanosis, edema of face and paws, metHb Clinical signs develop in as short a time as 30 to 60 minutes Weakness, ataxia, collapse, and seizures from hypoglycemia may last 12 to 24 hrs, perhaps caused by the slow xylitol release from the ingested formulations and its absorption Liver injury (within 24 hrs), including signs of melena, hepatic encelopathy, hemorrhage
Analgesic and antipyretic derived from paracetamol ( Note: Not an NSAID)
NAC replenishes glutathione, provides sulfur and will directly bind NAPQI Others: • Vitamin C • SAMe • IV Fluids
Metabolized to NAPQI, binds to macromolecules and causes lipid peroxidation of membranes; induces direct cell injury and death leading to hepatic necrosis Oxidative damage in cats, resulting in metHb, Heinz body formation Induces hypoglycemia by stimulating insulin secretion from the pancreas of dogs Hepatic necrosis thought to be from decrease ATP production (xylitol uses pentose phosphate pathway instead of TCA [Kreb’s] cycle)
Acetaminophen (APAP)
Plasma, urine or tissue
Methylene blue has been described, but not recommended, especially in the cat (due to Heinz body formation)
Sweetener in sugar- free products, such as chewing gum and baking products
• Stat BG and treatment for hypoglycemia; emesis if recent ingestion and normoglycemic • Activated charcoal not indicated • Fluid support and glucose support (dextrose can correct hypoglycemia and is liver supportive by providing ATP) even in the face of euglycemia • Response from clinical effects is usually rapid and within 12 to 24 hrs • Recheck liver values at 24 and 48 hrs to evaluate for liver involvement • SAMe for 1-2 weeks if hepatotoxic dose ingested
Hypoglycemia, ↑↑ LES, DIC, coagulopathy
Xylitol
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