Household toxicosis (Theory) and heavy metal poisoning (Pract) 38.pptx

About toxicosis

1. House-hold Toxicosis (Theory)

2. Household Toxicosis Household chemicals ( e.g. alcohols, bleaches, or corrosives ) Alcohols Metabolic acidosis Hypothermia CNS depression Etiology: Ethanol, methanol, isopropanol, drug elixirs, fermenting bread dough. Methanol: commonly found in windshield washer fluids (windshield “antifreeze”). Lethal oral dose of methanol in dogs: 4–8 mL/kg. Isopropanol: is twice as toxic as ethanol. Found in alcohol-based flea sprays for pets. Oral dosages of isopropanol ≥0.5 mL/kg may result in significant clinical signs in dogs . Pathogenesis: Alcohols rapidly absorbed via GIT and dermally Toxicosis from over-spraying pets with alcohol-based flea sprays is common Alcohols reach peak plasma levels within 1.5–2 hr and are widely distributed throughout the body Metabolized in liver to acetaldehyde (ethanol ), formaldehyde (methanol), and acetone (isopropanol ) These intermediate metabolites then converted to acetic acid, formic acid, and carbon dioxide Accumulation of formic acid results in retinal and neuronal damage Alcohols are eliminated via the urine as parent compound as well as metabolites. In dogs, 50% dose of methanol eliminated unchanged via lungs .

3. GI irritants, vomiting inducer and hypersalivation CNS depressants, affecting neurotransmitters within the nervous system Metabolites (acetaldehyde) stimulate the release of catecholamines , which can affect myocardial function. Metabolic acidosis results from the formation of acidic intermediates Hypothermia develop due to peripheral vasodilation, CNS depression, and interference with thermoregulatory mechanisms Hypoglycemia develops (high isulin secretion) Clinical Findings and Diagnosis: Begin within 30–60 min of ingestion: vomiting, diarrhea, ataxia, disorientation, depression, tremors, and dyspnea. Severe cases may progress to coma, hypothermia, seizures, bradycardia, and respiratory depression. Death due to respiratory failure, hypothermia, hypoglycemia and metabolic acidosis. Pneumonia secondary to aspiration of vomitus.

4. Treatment Stabilization of severely symptomatic animals Adequate ventilation Cardiovascular and acid-base abnormalities should be corrected Seizures: diazepam (0.5–2 mg/kg, IV). For asymptomatic animals: induction of emesis in first 20–40 min after ingestion. Activated charcoal is not thought to appreciably bind small-chain alcohols and is not often recommended. Bathing with shampoo is recommended for dermal exposures. Supportive care: thermoregulation and fluid diuresis to enhance alcohol elimination. Yohimbine (0.1 mg/kg, IV) has been used to stimulate respiration in severely comatose dogs with alcohol toxicosis .

5. Chlorine Bleaches GI , dermal and ocular irritation or ulceration, respiratory irritation Caged birds are at increased risk of succumbing (death) to fumes from bleaches and cleaning agents . Etiology: Used as household cleaners and pool sanitizers. Contain sodium hypochlorite at 3%–10%, and pH range from 9 (mildly irritating) to >11 (corrosive). Pool treatments may contain lithium, calcium, or sodium hypochlorites at concentrations up to 70%–80%, with pH that may range from acidic to alkaline. Pets may be exposed by containers of undiluted product, drinking from buckets containing product diluted in water or swimming in recently treated pools.

6. Pathogenesis: Depends on concentration of hypochlorite, pH, and dilution of the product . Hypochlorite <10% are mild irritants pH >11 or <3.5, alkaline or acid corrosive injury may occur. Mixing of hypochlorite and ammonia produces highly toxic chloramine gas that can cause acute respiratory distress or delayed onset of pulmonary edema within 12–24 hr of exposure . Clinical Findings and Lesions: Vomiting , hypersalivation , depression, anorexia and diarrhea. Concentrated (>10%) bleach products or products with pH > 11: GI corrosive injury. Hypernatremia , hyperchloremia , and metabolic acidosis. Acute inhalation: coughing, gagging, sneezing, retching . Concentrated chlorine fumes: pulmonary edema 12–24 hr after exposure. Ocular exposures: epiphora ( lacrymation ), blepharospasm (pain in eyes during movement of eyelid), eyelid edema, and corneal ulceration. Dermal exposure: dermal irritation and bleaching of the hair coat. Respiratory lesions: tracheitis , bronchitis, alveolitis , and pulmonary edema.

7. Treatment: For oral exposures: emesis and activated charcoal are contraindicated; instead, dilution with milk or water is recommended. Vomiting causes electrolyte or hydration abnormalities: fluid therapy. Respiratory exposures: moved to fresh air area and monitored for dyspnea. Stabilization of severely dyspneic animals: pulmonary  edema. Dermal exposures: Bathing with shampoo Ocular exposures: 10–20 min of ocular irrigation with physiologic saline, followed by fluorescein staining of the cornea to detect corneal injury

8. Corrosives Acid or alkaline corrosives: burns of skin, cornea, mucosa of oral cavity, esophagus, and stomach. Heavy coats may provide some protection from dermal exposure. Etiology: Divided into acid and alkaline corrosives. Acidic household products: anti-rust compounds, toilet bowl cleaners, gun-cleaning fluids, automotive batteries, swimming pool cleaning agents, and etching compounds. Alkaline corrosive agents: drain openers, automatic dishwasher detergents, toilet bowl cleaners, radiator cleaning agents, and swimming pool algicides and “shock” agents. Alkaline products with pH >11 pose risk of significant corrosive injury.

9. Pathogenesis: Acids produce: coagulative necrosis of tissue and pain on contact. Alkaline agents produce: liquefactive necrosis of tissue. Burns from alkaline products tend to be deeper and more extensive than burns from acidic agents. Burns from alkaline agents may take up to 12 hr after exposure to become fully apparent Whereas the extent of acid burns is usually evident shortly after contact. Esophageal burns are more common with alkaline agents Full-thickness ulceration of the esophagus may result in pleuritis or peritonitis due to leakage of ingesta into body cavities. Esophageal burns result in stricture formation during healing, resulting in dysphagia, megaesophagus , and aspiration pneumonia. Gastric ulceration and perforation. Respiratory distress, tracheobronchitis , or pneumonitis. Dermal or ocular exposures result in severe ulceration of dermis or cornea .

10. Clinical Findings: Hypersalivation , lethargy, polydipsia, vomiting (with or without blood), abdominal pain, dysphagia, pharyngeal edema, dyspnea, and oral, esophageal, and/or gastric ulceration. In severe cases, shock may develop rapidly after exposure. Lesions: Milky white to gray but turn black as eschar (dead tissue) formation occurs. Necrotic tissue may slough within days of exposure. Dyspnea, cyanosis, and pulmonary edema may occur secondary to inhaled corrosive agents. Dermal exposure may result in significant burns, with local pain, erythema, and tissue sloughing. Ocular exposure may cause blepharospasm , epiphora , eyelid edema, conjunctivitis, or corneal ulceration. Burns of skin, cornea, and GI mucosa range from mild ulceration to full-thickness necrosis with extensive tissue sloughing. Peritonitis or pleuritis may develop secondary to perforating ulcers of esophagus or stomach. Respiratory lesions may include tracheitis , bronchitis, pneumonitis, pulmonary edema, or aspiration pneumonia.

11. Treatment: Stabilization of animals presenting dyspneic, in shock, or with severe electrolyte abnormalities is always a priority. Oral exposures: immediate dilution with water or milk. Emesis should not attempt (risk of further mucosal exposure to corrosive material). Gastric lavage: contraindicated because of risk of perforation of weakened esophageal/gastric walls and the risk of further exposure of mucosa to the corrosive material. Attempts to chemically neutralize an acid with weak alkali (or alkali with weak acid) are also contraindicated because of the production of exothermic reactions that can result in thermal burns. Activated charcoal is ineffective in cases involving ingestion of corrosives, and the presence of charcoal on damaged mucosa may impede wound healing. Endoscopic evaluation of the esophagus and stomach for ulceration should be performed ~12 hr after exposure. Use of corticosteroids with significant esophageal mucosal injury is controversial. Corticosteroids decrease inflammation and may aid in minimizing stricture formation, but they also suppress the immune system and may enhance susceptibility to secondary infection. In animals with significant oral and/or esophageal burns, gastrostomy tubes may be necessary to provide nutrition while affected tissues heal . Dermal or ocular exposures should be managed by flushing with copious amounts of water or physiologic saline Eyes should be flushed for a minimum of 20 min, followed by fluorescein staining. Standard topical treatments for dermal or ocular burns should be instituted as needed.

12. Alkaline Batteries GIT corrosive injury Foreign body obstruction Dogs are most commonly involved Etiology: Alkaline batteries present in electronic products, including remote controls, hearing aids, toys, watches, computers, and calculators. Most alkaline dry cell batteries use KOH or NaOH to generate currents. Nickel-cadmium and lithium batteries contain alkaline material . Pathogenesis: Alkaline gel in batteries causes liquefactive necrosis of tissues on contact, resulting in burns that can penetrate deeply into tissue.  Lithium disk or “button” batteries may lodge in the esophagus and generate a current against the esophageal walls, resulting in circular ulcers that have the potential to be perforating. Some battery casings contain metals such as zinc or mercury, posing hazards of foreign body obstruction and metal toxicosis if they remain in the stomach for prolonged periods. Small batteries (especially disk batteries) inhaled and pose a choking hazard.

13. Clinical Findings: Vomiting , anorexia, abdominal discomfort, or tenesmus. Respiratory obstruction due to battery inhalation may present acute onset of dyspnea and cyanosis. Mucosal burns within the oral cavity, esophagus, and less commonly, stomach. Perforation of the esophagus lead to secondary pyothorax Gastric perforation result in acute blood loss and/or peritonitis . Diagnosis: Radiographs: to confirm the location of the battery Differential diagnoses: GI or respiratory foreign bodies and oral, dermal, ocular corrosive agents.

14. Treatment : Emesis should not be induced if any possibility of battery casing punctured . 20 mL boluses of tap water every 15 min decrease the severity and delay the development of current-induced esophageal ulceration. The decision on whether to remove a battery from the stomach depends on the size of the animal, battery size, and evidence of battery puncture. Serial radiography to verify battery location is recommended until the battery is expelled. Batteries that do not pass through the pylorus within 48 hr of ingestion are unlikely to pass on their own and may require surgical or endoscopic removal. Endoscopic removal is not recommended in cases in which it is suspected that the battery casing has been punctured. Dermal or ocular exposures to alkaline gels should be managed by copious rinsing of the area with tap water (skin) or physiologic saline solution (eyes). The affected areas should be monitored for development of ulcers.

15. Cationic Detergents Local corrosive tissue injury as well as severe systemic effects. Cats are at increased risk of oral exposure because of grooming habits. Etiology: Present in algicides , germicides (including quaternary ammonium compounds), sanitizers, fabric softeners (including dryer softener sheets), and liquid potpourris. Concentrations of cationic detergents ≤2% associated with oral mucosal ulcers in cats. Pathogenesis: Dermal , ocular, and mucosal injury similar to that of alkaline corrosive agents. CNS depression to pulmonary edema . Clinical Findings and Lesions: Oral exposure: ulceration, stomatitis, pharyngitis, hypersalivation , swollen tongue, depression, vomiting, abdominal discomfort, and increased upper respiratory noises within 6–12 hr of ingestion. Fever and increases in WBC counts. Systemic effects: metabolic acidosis, CNS depression, hypotension, coma, seizures, muscular weakness and fasciculation, collapse, and pulmonary edema. Dermal: Irritation, erythema, ulceration, and pain. Ocular exposure: Conjunctivitis, blepharospasm , eyelid edema, lacrimation, and corneal ulceration Lesions: GI, ocular, or dermal irritation or ulceration.

16. Treatment: Diazepam (0.5–2 mg/kg, slow IV) for seizures Fluid therapy for hypotension Induction of emesis and administration of activated charcoal are contraindicated with cationic detergents. Oral exposures: milk or water can be given for dilution Dermal and ocular exposures: thorough flushing of affected area with tepid water or physiologic saline.

17. Detergents, Soaps, and Shampoos Products containing anionic and nonionic detergents cause mild GI irritation. Etiology: Mild detergents, soaps, and shampoos contain anionic and nonionic detergents; Products included: human and pet shampoos, liquid hand dishwashing soaps, bar bath soaps (except homemade soaps, which may contain lye), laundry detergents, and household all-purpose cleaners. Most are of moderate pH, but agents with pH >11 ( e.g. electric dishwasher detergents) are alkaline corrosives. Pathogenesis: No appreciable systemic absorption of these agents Toxicity is limited to ocular, oral, or GI irritation, which is mild and self-limiting. Cats exposed to shampoos containing sodium lauryl sulfate develop significant respiratory compromise after inhalation during grooming, including dyspnea, increased bronchial secretions, and mild pulmonary edema. Mechanism: Detergent interfere the normal pulmonary surfactants. Clinical Findings: Nausea, vomiting, and diarrhea. Secondary dehydration and electrolyte imbalance (vomiting or diarrhea). Mild ocular irritation (lacrimation and blepharospasm ). Cats grooming after application of sodium lauryl sulfate–containing products may develop moist respiratory sounds, cyanosis, and dyspnea within 1–3 hr of exposure .

18. Treatment: Dilution with milk or water Antiemetics : ( e.g.  metoclopramide, 0.2–0.4 mg/kg, PO, SC, or IM, qid ). Parenteral fluid therapy to correct electrolyte or hydration abnormalities due to protracted vomiting or diarrhea . Ocular exposures: Irrigation of eyes using tepid water or physiologic saline for 5 min will usually suffice. Cats: that have respiratory compromise, supplemental oxygen and general supportive care are recommended; in most cases, signs resolve within 24 hr.