Introduction

• Selective herbicides that mimic plant growth hormones. Available as soluble concentrates or emulsions. These are a family of chemicals that are structurally similar, that are carboxylic acids in an acid or salt form.
• Signs: common signs include dermal or ocular irritation, nauseas, vomiting and diarrhea - signs are usually self-limiting and respond well to minimal symptomatic and supportive care; high dose exposures in dogs can lead to myotonia; prolonged exposures may lead to renal or hepatic damage. 
• Diagnosis: history of exposure, clinical signs, response to treatment.
• Treatment: detoxification if appropriate, intravenous fluids to maintain hydration and assist in renal excretion, anti-emetic medications for persistent vomiting, bland diet.
• Prognosis: excellent - renal/hepatic damage and fatalities are rare.

Pathogenesis

Etiology

• Ingestion of herbicide.
• Ingestion of treated plants.
• Exposure to treated areas before herbicide has dried can result in percutaneous absorption.

Pathophysiology

• Ingestion causes local irritation to and possible ulceration of mucous membranes of the mouth, pharynx and gastrointestinal tract. 
• Compounds are readily absorbed from the gastrointestinal tract, skin and lungs.

• Not significantly stored in fat.
• Renal excretion is rapid except in dogs. 
• Limited biotransformation to less toxic substances; majority of compounds are excreted unchanged in the urine.
• Relatively low toxicity: acute oral LD50 in dogs is 100 mg/kg.
• Uncouples oxidative phosphorylation, depresses ribonuclease synthesis, and increases paranitrophenyl phosphatase.

Timecourse

• Most patients respond positively within 24-72 hours following acute exposures.

Diagnosis

Treatment

Prevention

Outcomes