Household and Environmental Toxicoses – BCSE Study Guide

Overview and Clinical Importance

Household and environmental toxicoses represent some of the most common emergency presentations in small animal practice. Understanding the mechanisms of action, clinical presentations, and appropriate treatments for these toxins is essential for entry-level veterinarians and heavily tested on the BCSE examination.

Ethylene Glycol Toxicity

Ethylene glycol (EG) is the primary toxic component in automotive antifreeze, representing one of the most life-threatening toxicoses in companion animals. Its sweet taste makes it attractive to pets, and even small amounts can be fatal.

Sources and Toxic Doses

Common sources include: automotive antifreeze (95% EG concentration), brake fluid, windshield deicing agents, heat exchange fluids, and some paints/solvents.

Memory Aid - EG Toxic Doses

"Cats are 3x more sensitive" - Cats need only 1.4 mL/kg (about 1 teaspoon for a cat) vs dogs at 4.4-6.6 mL/kg. Treatment window is also shorter: 3-4 hours in cats vs 8-12 hours in dogs.

Mechanism of Toxicity

Ethylene glycol itself has relatively low toxicity. The danger lies in its hepatic metabolism via alcohol dehydrogenase (ADH) to toxic metabolites:

• Glycoaldehyde - causes CNS depression
• Glycolic acid - causes severe metabolic acidosis
• Glyoxylic acid - the most toxic metabolite
• Oxalic acid - binds calcium, forms calcium oxalate crystals in renal tubules

Three-Phase Clinical Presentation

Memory Aid - EG Phases

"Drunk, Then Dying" - Phase 1 looks like alcohol intoxication (stumbling, vomiting), then progresses to cardiopulmonary distress, then irreversible kidney failure. Remember cats progress faster!

Diagnosis

• History of exposure or witnessed ingestion
• Severe metabolic acidosis with increased anion gap (develops within 3 hours)
• Hyperosmolality (serum osmolality increases within 1 hour)
• Isosthenuria (USG 1.008-1.012) due to osmotic diuresis
• Calcium oxalate monohydrate crystals in urine (appear 6-8 hours post-ingestion)
• Hypocalcemia (calcium bound by oxalic acid)
• Positive EG test kit (best run 1-10 hours post-ingestion)

Treatment Protocol

Chocolate and Methylxanthine Toxicity

Chocolate toxicity is one of the most common canine poisonings. The toxic principles are theobromine (3,7-dimethylxanthine) and caffeine (1,3,7-trimethylxanthine), both methylxanthines that inhibit phosphodiesterase and antagonize adenosine receptors.

Methylxanthine Content by Chocolate Type

Memory Aid - Chocolate Toxicity Ranking

"DARK is DANGEROUS" - Remember: Darker = More Theobromine. White chocolate is essentially non-toxic for theobromine (fat content is the concern). Baking chocolate and cocoa powder are most dangerous.

Toxic Doses and Clinical Signs

Mechanism of Action

• Phosphodiesterase inhibition - increases cAMP, causes catecholamine release
• Adenosine receptor antagonism - CNS stimulation, tachycardia, diuresis
• Stimulates myocardial and skeletal muscle contraction
• Increases gastric acid secretion

Treatment

• Decontamination: Induce emesis if less than 1-2 hours post-ingestion (chocolate absorbs slowly), repeat activated charcoal due to enterohepatic recirculation
• Cardiac arrhythmias: Beta-blockers (atenolol, metoprolol), lidocaine for ventricular arrhythmias
• Seizures: Diazepam or phenobarbital
• Supportive care: IV fluids, urinary catheter to prevent reabsorption, monitor ECG

Memory Aid - Chocolate Treatment

"ACID" - Activated charcoal (repeated), Cardiac monitoring, IV fluids, Diazepam for seizures. No specific antidote exists - treatment is supportive.

Rodenticide Toxicoses

Rodenticides encompass four major classes with distinct mechanisms, clinical presentations, and treatments. Accurate product identification is critical as treatment differs dramatically between classes.

1. Anticoagulant Rodenticides

Most commonly encountered. Inhibit vitamin K epoxide reductase, preventing activation of vitamin K-dependent clotting factors (II, VII, IX, X).

Clinical Signs

Signs delayed 3-5 days (time for clotting factor depletion): lethargy, exercise intolerance, dyspnea, epistaxis, hemoptysis, hematemesis, hematuria, melena, pale mucous membranes, lameness (hemarthrosis), sudden death.

Diagnosis and Treatment

• PT prolonged (first factor depleted is VII with shortest half-life of 6 hours)
• PIVKA test (Proteins Induced by Vitamin K Absence)
• Treatment: Vitamin K1 (phytonadione) 3-5 mg/kg/day PO divided BID with fatty food (increases absorption 4-5x)
• Duration: 2-4 weeks (first gen) to 4-6 weeks (second gen)
• Blood transfusion if severe hemorrhage
• Recheck PT 48-72 hours after stopping vitamin K1

Memory Aid - Anticoagulant Rodenticides

"PIVKA for K" - Test: PIVKA or PT. Treatment: vitamin K1 with Fat. Remember factors 2, 7, 9, 10 (1972 - "1972 was a good year for clotting"). Factor VII depleted first (shortest half-life).

2. Bromethalin

Neurotoxin that uncouples oxidative phosphorylation in CNS, causing cerebral edema. NO ANTIDOTE. Cats more sensitive than dogs.

Treatment

• Aggressive decontamination with repeated activated charcoal (q6-8h for 24-48 hours)
• Anticonvulsants (diazepam, phenobarbital) as needed
• Mannitol and corticosteroids for cerebral edema (efficacy unproven)
• Supportive care - prognosis guarded to poor once neurological signs develop

3. Cholecalciferol (Vitamin D3)

Causes severe hypercalcemia and hyperphosphatemia leading to soft tissue mineralization, especially kidneys. Very toxic - effects seen at doses as low as 0.5-2 mg/kg.

Clinical Signs (18-36 hours post-ingestion)

• Depression, anorexia, PU/PD, vomiting
• Progressive kidney failure
• Cardiac arrhythmias, hypertension
• Soft tissue calcification (metastatic mineralization)

Treatment

• IV saline diuresis (dilute calcium, promote excretion)
• Furosemide (calciuresis)
• Corticosteroids (reduce intestinal calcium absorption, promote calciuresis)
• Calcitonin or pamidronate disodium (inhibit bone resorption)
• Low-calcium diet, oral phosphate binders
• Treatment may be needed for 2-4 weeks or longer

4. Zinc Phosphide

Used primarily for moles/gophers. In stomach acid, releases phosphine gas which is toxic to both pets AND humans (handle vomit carefully!).

Clinical Signs (rapid onset within 1 hour)

• Severe GI pain, vomiting (garlic/fish odor from phosphine gas)
• Respiratory distress, pulmonary edema
• Seizures, cardiovascular collapse
• Liver and kidney failure if survives acute phase

Memory Aid - Four Rodenticides

"ABCZ" - Anticoagulants (Vitamin K), Bromethalin (No Antidote, repeated charcoal), Cholecalciferol (hypercalcemia, saline diuresis), Zinc phosphide (phosphine gas, emesis outdoors).

Heavy Metal Toxicoses

Lead Toxicity

Sources include paint chips (pre-1978 housing), lead fishing sinkers, batteries, plumbing materials, linoleum, and golf balls. Young animals more susceptible.

Clinical Signs

• GI signs: anorexia, vomiting, abdominal pain, diarrhea/constipation
• Neurological signs: behavioral changes, seizures, blindness, ataxia
• Hematologic: nucleated RBCs (metarubricytosis), basophilic stippling

Diagnosis

• Blood lead level greater than 0.4 ppm (40 mcg/dL) diagnostic
• Radiographs may show radio-opaque material in GI tract
• Nucleated RBCs without anemia is highly suggestive

Treatment

• Remove lead source (surgical if large objects in GI)
• Chelation: Calcium EDTA 25-50 mg/kg SC divided QID for 5 days (or CRI)
• Alternative: Succimer (DMSA) 10 mg/kg PO TID for 10 days
• Thiamine supplementation (may reduce CNS signs)
• Control seizures with diazepam

Zinc Toxicity

Most common cause in dogs is ingestion of pennies minted after 1982 (97.5% zinc = 2,440 mg zinc/penny). Other sources include galvanized metal, nuts/bolts, board game pieces, zinc oxide ointments.

Two-Phase Clinical Presentation

Treatment

• Remove zinc source via endoscopy or surgery
• Antacids (calcium carbonate) q2-4h until removal (reduces zinc leaching)
• IV fluids to protect kidneys from hemoglobin
• Blood transfusion if severe anemia
• Chelation with D-penicillamine 110 mg/kg/day PO divided q6-8h if needed

Copper Toxicity

Acute toxicity is rare. More commonly seen as chronic accumulation in certain dog breeds (Bedlington Terriers, Dobermans, Labrador Retrievers, West Highland White Terriers) with inherited copper storage disorders.

Clinical Signs

• Acute: vomiting, diarrhea, hemolysis, hepatocellular necrosis
• Chronic: progressive hepatopathy, icterus, ascites, hepatic encephalopathy

Treatment

• D-penicillamine (chelation) 10-15 mg/kg PO BID
• Zinc supplementation (induces metallothionein, reduces copper absorption)
• Hepatoprotectants: SAMe, milk thistle (silymarin)
• Low-copper diet

Memory Aid - Heavy Metal Chelators

"Lead to EDTA, Zinc to Penicil-LAME" - Lead: Calcium EDTA or succimer (DMSA). Zinc: D-penicillamine. Copper: D-penicillamine. Remember EDTA also chelates zinc, so supplement zinc during lead treatment!

Human Medication Toxicoses

NSAIDs (Ibuprofen, Naproxen)

Among the most common poisonings reported to animal poison control. Dogs are more sensitive than cats to GI effects; cats are more sensitive to renal effects.

Mechanism

COX-1 and COX-2 inhibition reduces prostaglandin synthesis, leading to decreased GI mucosal protection, decreased renal blood flow, and impaired platelet function.

Toxic Doses

Clinical Signs

• GI: vomiting, hematemesis, melena, diarrhea, abdominal pain
• Renal: oliguria, azotemia, isosthenuria
• CNS (high doses): seizures, ataxia, depression

Treatment

• Decontamination (emesis, activated charcoal - repeat doses due to enterohepatic recirculation)
• GI protectants: sucralfate, H2-blockers, PPIs, misoprostol
• IV fluids for renal protection
• Monitor renal values and stool for blood

Acetaminophen (Paracetamol)

Species Differences

Mechanism

Acetaminophen is metabolized to NAPQI (N-acetyl-p-benzoquinoneimine), a toxic metabolite normally conjugated with glutathione. When glutathione is depleted, NAPQI causes hepatocellular damage and oxidizes hemoglobin to methemoglobin.

Treatment

• N-acetylcysteine (NAC): Loading dose 140-280 mg/kg IV/PO, then 70 mg/kg q4-6h for 7 treatments
• NAC provides sulfhydryl groups, replenishes glutathione, binds NAPQI directly
• SAMe (S-adenosylmethionine) as glutathione precursor
• Vitamin C (ascorbic acid) to reduce methemoglobin (cats)
• Oxygen supplementation, blood transfusion if severe
• Cimetidine may inhibit P450 metabolism (controversial)

Memory Aid - Acetaminophen Antidote

"NAC saves CATS" - N-Acetylcysteine is the antidote. Remember cats are extremely sensitive due to deficient glucuronidation. Classic cat sign: chocolate-brown mucous membranes from methemoglobinemia.

Insecticide and Pesticide Toxicoses

Organophosphates and Carbamates

These compounds inhibit acetylcholinesterase (AChE), causing accumulation of acetylcholine at muscarinic and nicotinic receptors. Organophosphates bind irreversibly; carbamates bind reversibly.

SLUDGE/DUMBELS Mnemonic for Muscarinic Signs

Nicotinic Signs

Muscle tremors, fasciculations, weakness, paralysis, tachycardia, hypertension, mydriasis (late)

Treatment

Memory Aid - OP Treatment

"A-P-D" - Atropine first (muscarinic blockade), Pralidoxime second (reactivate AChE - OPs only), Diazepam third (seizures). Remember: 2-PAM must be given within 24-48 hours before the enzyme "ages" and becomes irreversible.

Pyrethrins and Pyrethroids

Pyrethrins are derived from chrysanthemum flowers; pyrethroids are synthetic derivatives (permethrin). CATS ARE EXTREMELY SENSITIVE due to deficient glucuronidation.

Mechanism

Pyrethroids prolong opening of voltage-gated sodium channels, preventing depolarization and causing hyperexcitability of nerves.

Clinical Signs in Cats

• Muscle tremors, fasciculations (especially ears)
• Hyperesthesia, hypersalivation
• Ataxia, seizures
• Hyperthermia or hypothermia
• Onset: 1-72 hours post-exposure; duration: 2-7 days

Treatment

• NO SPECIFIC ANTIDOTE - treatment is supportive
• Decontamination: Bathe with dish soap (not insecticidal shampoo) - use lukewarm water to avoid hypothermia
• Muscle relaxants: Methocarbamol 44-220 mg/kg IV slowly (give half rapidly, remainder to effect)
• Seizure control: Diazepam, propofol, or phenobarbital
• IV lipid emulsion may be beneficial (pyrethroids are lipophilic)
• Temperature regulation, IV fluid support

Memory Aid - Pyrethroid Cat Toxicity

"CATS Can't Conjugate" - Cats lack glucuronyl transferase to metabolize pyrethroids (same reason for acetaminophen sensitivity). Classic sign: ear twitching. Treatment: Methocarbamol for tremors.

Xylitol Toxicity

Xylitol is a sugar alcohol sweetener found in sugar-free gum, candies, peanut butter, baked goods, toothpaste, and medications. It causes severe, potentially fatal toxicity in DOGS (cats are not affected).

Mechanism of Toxicity

In dogs, xylitol causes rapid, dose-dependent insulin release (3-7x normal) leading to profound hypoglycemia. At higher doses, xylitol also causes acute hepatic necrosis through an unknown mechanism (possibly ATP depletion or reactive oxygen species).

Toxic Doses

Clinical Signs

Hypoglycemia (onset 30-60 minutes, may be delayed 12-18 hours)

• Vomiting (often first sign)
• Weakness, lethargy, ataxia
• Seizures, collapse, coma

Hepatotoxicity (onset 24-48 hours)

• Elevated liver enzymes (ALT, AST, ALP)
• Icterus, coagulopathy (DIC)
• Note: Liver failure can occur WITHOUT preceding hypoglycemia

Treatment

• Decontamination: Induce emesis ONLY if asymptomatic and within 30 minutes (hypoglycemia can occur rapidly)
• Activated charcoal NOT effective (does not bind xylitol well)
• Dextrose: Bolus 0.5-1 mL/kg of 50% dextrose diluted 1:4, then CRI 2.5-5% dextrose
• Monitor blood glucose q1-2h for 12-24 hours
• Monitor liver enzymes q24h for 72 hours
• Hepatoprotectants: NAC, SAMe, silymarin (milk thistle)
• Fresh frozen plasma if coagulopathy develops

Memory Aid - Xylitol Toxicity

"X marks the spot for dogs" - Xylitol is X-tremely dangerous to dogs (not cats). Causes "Sugar crash" (hypoglycemia from insulin surge) and "Liver crash" (hepatic necrosis). No charcoal (X-ray/activated charcoal doesn't help). Dextrose is key treatment.