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CA poison-related emergencies
• If corrosive or toxic substance in contact with eyes and skin: immediately wash them with warm water or saline
• If paint or tar (small deposits): clip the hair.
• For larger deposits: soak the areas with vegetable oil for 24 hours.
This will soften the tar, which then can be removed by shampooing
• Never use gasoline, kerosene, turpentine, organic solvents: severe skin burns, toxicities
• Pine pitch (resin): vegetable oil/butter
if poison ingestion occurred recently (max 4 hrs):
Induce vomiting:
– Cooking salt: 1-3 tbs in a glass of water; vomiting in 5-10 min; hematemesis
– Hydrogen peroxide solution (3%): 2-5 ml in a glass of water; vomiting in 10 min, gastric irritation; it can be repeated after 30 min
corrosive substance
If corrosive substance, kerosene, turpentine, chlorine bleach ingestion occurred: AVOID inducing vomiting
• Milk, water to dilute the toxic substance
• Activated charcoal (capsules, granules): within 30 min
administration of activated charcoal
Activated charcoal does not bind all agents: alcohol, petroleum products, corrosive acids/bases, fluoride, cyanide and metals such as iron and lithium (alkaline batteries) → Activated charcoal is of no use
acidic and alkaline ingestion
• Common acidic corrosive products: anti-rust compounds, toilet bowl cleaners, gun-cleaning fluids, automotive batteries, swimming pool cleaning agents, etching compounds
• Common alkaline corrosive products: drain openers, automatic dishwasher detergents, radiator cleaning agents, swimming pool algaecides
Because corrosive agents act so quickly, much of the damage occurs before treatment can be started
Anticoagulant Rodenticides: Warfarin and Congeners
• Inhibition of the enzyme vitamin K epoxide reductase, which normally reactivates vitamin K (a crucial component in several normal clotting factors)
• Potentially dangerous to all mammals and birds
• Intoxications: contamination of feed with anticoagulant concentrate, malicious use of these chemicals, feed mixed in equipment used to prepare rodent bait, poisoned dead rat/mouse (secondary poisoning)
• The “first-generation” anticoagulants (warfarin): multiple feeding for toxicity
• The “intermediate” anticoagulants: fewer feedings
• The “second-generation” anticoagulants: a single feeding
→ Vitamin K1 is antidotal
metaldehyde poisoning
• Active component in molluscicides to control slugs and snails; wet coastal areas worldwide
• Liquid, dust, granular, or pelleted formulations
• Alterations of a variety of neurotransmitter concentrations and enzyme activities: ↓ GABA (inhibitory neurotransmitter → CNS excitation); ↓ brain serotonin, norepinephrine ↓ the threshold for convulsions; ↑ monoamine oxidase activity, ↑ muscle activity, severe electrolyte disturbances, metabolic acidosis
• Neurologic manifestations within 1-3 hour after ingestion.
• Severe muscle tremors, anxiety, hyperesthesia, ataxia, tachycardia, hyperthermia; depression, hyperpnea (metabolic acidosis)
• Opisthotonos: a state of severe hyperextension and spasticity; continuous tonic convulsions unresponsive to external stimuli (in contrast to those in strychnine poisoning)
• Emesis, diarrhea, hypersalivation, colic, cyanosis, mydriasis, nystagmus (cats): often reported
• No specific treatment; aggressive symptomatic treatment during the first 24 hr: full recovery within 2-3 days; activated charcoal, diazepam; gas anesthesia, IV fluids sodium lactate/sodium bicarbonate
chocolate toxicosis in dogs
Potentially life-threatening cardiac arrhythmias and CNS dysfunction (stimulation)
• Indiscriminate eating habits, readily available sources of chocolate; livestock fed cocoa by-products, animals consuming mulch from cocoa-bean hulls
• Theobromine (3-10 x), caffeine (insignificant source in white chocolate)
• LD 50 caffeine and theobromine: 100–200 mg/kg, but severe signs and deaths may occur at much lower dosages (individual sensitivity varies)
One ounce of milk chocolate per pound of BW is a potentially lethal dose in dogs
• Clinical signs: within 6-12 hour of ingestion; polydipsia, vomiting, diarrhea, abdominal distention, restlessness, polyuria, ataxia, rigidity, tremors, seizures, tachycardia.
• Death is generally due to cardiac arrhythmias, hyperthermia, or respiratory failure; high fat content of chocolate products: pancreatitis in susceptible animals
• No specific lesions may be found in animals succumbing to chocolate toxicosis; hyperemia, hemorrhages, or congestion of multiple organs may occur as agonal changes
ethylene glycol toxicosis
• All animals are susceptible to ethyleneglycol (EG) toxicity: most common in dogs and cats
• Ingestion of antifreeze: typically 95% EG (diluted ~50% with water when used in vehicle cooling systems); some heat-exchange fluids used in solar collectors, ice-rink freezing equipment, some brake and transmission fluids
• Widespread availability, sweet taste, small minimum lethal dose, lack of public awareness of the toxicity (e.g., improper storage and disposal)
• Cutaneous absorption from topical products that contain EG: toxicity in cats
• Most commonly in temperate and cold climates (seasonal): antifreeze to ↓ the freezing point and to ↑ the boiling point of radiator fluid
ethylene glycol toxicosis clinical signs + treatment
• Clinical signs: dose- and time-dependent (prognosis)
• The onset of clinical signs: almost immediate; nonspecific multisystemic clinical signs
• Dogs and cats: vomiting (GI irritation), polydipsia, polyuria, neurologic signs (CNS depression, stupor, ataxia, knuckling,↓ withdrawal and righting reflexes)
• Polydipsia: osmotic stimulation of the thirst center; polyuria: osmotic diuresis and ↓ production and release of ADH
• As CNS depression increases: dogs/cats drink less, but the osmotic diuresis continues (dehydration); dogs transiently recover from CNS signs ~12 hours after ingestion
• Treatment: to ↓ absorption of ingested EG, ↑ excretion of unmetabolized EG, preventing metabolism of EG, correcting the metabolic acidosis
• Gastric lavage within 1-2 hours of ingestion; vomiting should not be induced in dogs/cats exhibiting neurologic signs (risk of aspiration); activated charcoal is not likely ↓ absorption of EG; excretion of EG is ↑ by fluid therapy (to correct dehydration, ↑ increase urine production)
strychnine poisoning
• Indole alkaloid from the seeds of Strychnos nux-vomica
• Strychnine-containing baits restricted-use pesticides: currently labelled for below-ground use (control of pocket gophers); its sale is forbidden in a number of states; as indoor pesticides (rats, mice) eliminated since 1989
• Highly toxic to most domestic animals; very low toxic/lethal dose
• Grain-laced or pelleted commercial baits: often dyed red or green
• Most poisonings: non-target species consume commercial baits (young and large-breed, intact male dogs are more likely to be involved)
• Most poisonings are reported from the western USA
strychnine poisoning- inhibitory
• It inhibits competitively/reversibly the inhibitory neurotransmitter glycine at postsynaptic neuronal sites in the spinal cord and medulla: reflex stimulation of motor neurons affecting all the striated muscles (hyperexcitation)
• The extensor muscles are relatively more powerful than the flexor muscles: generalized rigidity and tonic-clonic seizures
• Death: anoxia (asphyxiation during seizure) and exhaustion
strychnine poisoning- clinical signs
• Clinical signs: onset very fast (30-60 min)
• Food in the stomach can delay onset; early signs: apprehension, nervousness, tenseness, stiffness
• Severe tetanic seizures may be spontaneous or initiated by stimuli as touch, sound, a sudden bright light
• Extreme extensor rigidity : “sawhorse” stance; hyperthermia (104°-106°F) often present in dogs
• The tetanic convulsions sec to ~1 min; respiration may stop momentarily
• If untreated, the entire syndrome may last only 1-2 h; rapid rigor mortis
strychnine poisoning - treatment
Treatment: decontamination, control of seizures, prevention of asphyxiation, and supportive care.
• Seizures should be controlled, and symptomatic animals stabilized before decontamination is attempted.
• Decontamination: emesis/gastric lavage, activated charcoal (to bind the remaining bait in the GI tract)
• Seizures: pentobarbital, IV to effect, repeated as necessary; diazepam, propofol; muscle relaxants
Severely affected dogs should be intubated, and artificial respiration provided
azaleas and rhododendrons
Anorexia, vomiting, increase rate of defecations
BULBS
• Non-specific gastroenteritis
IVY FRUITS
• Hypersalivation (sialorrhea), intense thirst, vomiting, abdominal pain, diarrhea
mistletoe
Nausea, vomiting, gastroenteritis
poinsettia
Conjunctivitis, stomatitis, gastroenteritis
dieffenbachia
Oral irritation, intense burning and irritation of mouth, tongue and lips, excessive drooling, vomiting, difficulty swallowing
stinging nettle
Muscular weakness, tremors, hypersalivation, burning mouth, slow and irregular heart beat
yew (english, european, japanese, etc)
Drooling, vomiting, weakness, difficulty breathing, life-threatening changes in heart rate and blood pressure, mydriasis, tremors, seizures, coma, death
avocado
• Myocardial necrosis (mammals, birds), sterile mastitis (lactating mammals)
• Parts of an avocado contain an oil-soluble toxin called persin: the fruit’s seed, bark and leaves are composed of this toxic, fatty acid derivative.
• Dogs and cats: relatively resistant; rabbits, guinea pigs, rats, budgerigars, canaries, cockatiels. Caged birds: more sensitive
• Birds: lethargy, dyspnea, anorexia, subcutaneous edema of the neck and pectoral regions, and may die
bread dough
• Raw bread dough made with yeast poses mechanical and biochemical hazards when ingested: gastric distention, metabolic acidosis, CNS depression
• Any species is susceptible, but dogs are most commonly involved (indiscriminate eating habits)
• Yeast fermentation products include ethanol, which is absorbed into the bloodstream, resulting in inebriation and metabolic acidosis
• Emesis or gastric lavage
macadamia nuts
Ingestion of macadamia nuts by dogs: nonfatal syndrome; vomiting, ataxia, weakness, hyperthermia, depression. Dogs are the only species in which signs have been reported
grapes or raisins
• Anuric renal failure in some dogs: death or euthanasia
• It is not known why many dogs can ingest grapes or raisins with impunity while others develop renal failure after ingestion
xylitol
• A sugar alcohol used to sweeten sugar-free products (gums, candies, baked goods)
• Ingestion of xylitol or xylitol-containing products by dogs: hypoglycemia (rapid, dose-dependent insulin release, hepatic injury and/or failure (higher doses); dogs: the only species
permethrin toxicosis in cats
• Permethrin: insecticide (pyrethroid, synthetic compounds from pyrethrins -Chrysanthemum flowers-)
• Neurotoxins: binding to and blocking Na+ channels on the surface of nerve cells, which interferes with nerve function.
• Because insects are much more susceptible to the effects of pyrethroids than mammals, these chemicals are widely used as insecticides, and are sometimes used for control of fleas and ticks on animals
• Australian cats: most cases of intoxication to directly treating cats with permethrin spot-on products (primary intoxication), but a small number resulted from close contact between cats and recently treated dogs (secondary intoxication)
• It is recommended that cats are kept away from dogs for at least 72 hours after a concentrated permethrin spot-on has been used on a dog
• Low price and widely available
• Lack of knowledge (shop)
gastric dilatation and volvulus (GDV) or gastric torsion or bloat
• Acute, life-threatening condition that primarily affects large- and giant-breed dogs
• The animal’s stomach dilates and then rotates, or twists, around its short axis
• The etiology of GDV is unknown
• Advanced age; lean body condition, deep/narrow thoracic conformation, history of GDV, stress, aggressive/fearful behavior, once daily feeding, dry food, rapid consumption of food, previous splenic disease, gastric ligament laxity
• Symptoms: anxious behavior, depression, abdominal pain and distention, collapse, excessive drooling, vomiting (unproductive dry heaving; tachycardia; dyspnea (labored breathing), weak pulse, pale mucous membrane
GDV treatment
• Cardiovascular stabilization (restoring circulating volume -decreased perfusion-)
• Gastric decompression: orogastric intubation (a tube is inserted through the patient’s mouth into the stomach)
• Surgical measures: to return internal organs (e.g., stomach and spleen) to their normal positions.
• Permanent gastropexy: the patient’s stomach is surgically secured to prevent future improper rotation
heat stroke or heat exhaustion
Summertime; mostly pets with thicker fur or coats
• Dogs eliminate heat by panting; some sweat glands in the footpads -only minimally-
• Remove the dog from the hot environment immediately If it is unconscious: no water in the nose/mouth; no aspirin
• Give water to the dog
• Check for signs of shock
• T must drop below 103F (39.4C)
• Go to the Vet: brain, kidney issue
• Abnormal clotting of blood