Common and Not So Common ToxicitiesCommon and Not So Common Toxicities Peter Lands, DVM Saint...
Transcript of Common and Not So Common ToxicitiesCommon and Not So Common Toxicities Peter Lands, DVM Saint...
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Common and Not So Common
Toxicities
Peter Lands, DVM
Saint Francis Veterinary Center
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Summary
Decontamination
Specific Toxicities• Acetaminophen
• Rodenticide
• Chocolate
• Grape/Raisin
• Pyrethrin
• Lily
• Marijuana
• Xylitol
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Take Away Points
●Treatments
●Monitoring
●Clinical Signs/Presentation
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Decontamination
●Emptying the GI tract to reduce toxin exposure or increase
elimination.
●4 Methods
–Emesis
–Gastric Lavage
–Enemas
–Activated Charcoal
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Induction of Emesis
●Performed if recent toxin
exposure (2-4 hours)
●Do NOT perform if ingestion of
caustic substance
–Cleaning agent, petroleum
products, or detergents
●Do NOT induce if patient is
comatose, dyspneic, or
obtunded
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Induction of Emesis - Dogs
●Hydrogen Peroxide – 1 tablespoon/20 lbs
–Can be repeated
–No more than 3 tablespoons per dose
●Apomorphine – 0.03mg/kg IV or 0.25mg/kg
subconjunctival
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Induction of Emesis - Cat
●Xylazine – 0.44mg/kg IM
–Takes about 30 minutes
–Can reverse with yohimbine 0.1 mg/kg IV
●Dexdomitor - 10mcg/kg IM or SQ
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Gastric Lavage
●Performed in patients where emesis is contraindicated
–Ingestion of caustic material
–Increased risk of aspiration
–Actively seizuring
●General anesthesia with properly inflated ETT
●Measure stomach tube to last rib and mark
●Pass the tube into the stomach
●Check to ensure it is properly in the stomach
●Infuse large amounts of warm water
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Enema
●Used to clear toxins from lower GI tact
●Helps prevent enterohepatic recycling by
increasing GI transit time
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Activated Charcoal
●Binds charged molecules in the GI tract
●Do NOT mix with food, will become inactive
●Toxiban – 6-10ml/kg
●UAA – 1-3ml/kg
●Repeat dose 4-6 hours for toxins with enterohepatic
recycling
●Start oral medications at least 2 hours after
administration
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Toxiban Caveats
●Patients may have black feces for 24-48 hours
●Toxiban will cause positive on ethylene glycol
tests
●Very Messy!!!
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●Acetaminophen
●Amphetamines
●Anthelmintics
●Antibiotics
●Aspirin
●Atropine
●Barbiturates
●Camphor
●Cantharides
●Carbamazepine
●Carbamates
●Chlordane
●Chloroquine
●Chlorpheniramine
●Cocaine
●Diazepam
●2,4-D (dichlorophenoxy acetic acid)
●Digitalis
●Digitoxin
●Ethylene glycol
●Fungicides
●Hexachlorophene
●Ipecac
●Isoniazid
●Malathion
●Mefenamic acid
●Meprobamate
Activated Charcoal
●Methylene blue
●Methyl salicylate
●Morphine
●Muscarine
●Narcotics
●Nicotine
●Nortriptyline
●Organic iodine
●Organic metal compounds
●Organochlorine insecticides
●Organophosphorus insecticides
●Parathion
●Phenobarbitol
●Phenothiazine
●Phenylbutazone
●Phenylpropanolamine
●hydrochloride
●Phenytoin
●Quinacrine hydrochloride
●Quinidine
●Quinine
●Rodenticides
●Salicylamide
●Salicylates
●Strychnine
●Sulfonamides
●Theophylline
●Tricyclic antidepressants
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Acetaminophen (Tylenol)
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Acetaminophen
●One of the most commonly seen toxicities
●Generally given by owner or sought out by patients
●Available in many strengths
–80mg, 325mg, 500mg, ect.
●Toxic dose:
–Cat – 10mg/kg
–Dog – 150-200mg/kg
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Mechanism of Action
●Absorbed via GI tract
●Poorly protein bound
●Primarily metabolized by the liver
●Eliminated by two major pathways:
–Glucuronidation
–Sulfation
●If pathways are deficient or saturated an alternative pathway
converts to NAPQI
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Mechanism of Action
●NAPQI is a free radical
●Damages hemoglobin, RBCs, and kidney cells
●Binds to hepatocytes causing injury and death
●Causes oxidative stress to RBCs
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Clinical Signs
●Seen within 1-4 hours of ingestion
●General signs
–Anorexia, salivation, dyspnea, hypothermia,
depression, weakness
●Chocolate colored mucus membranes, blood, and
urine
●Facial and forelimb edema – mechanism unknown
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Clinical Signs
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Diagnosis
●Based on history
●PE findings
●Methemoglobinemia - Co-oximetry
●Heinz bodies
●Elevated liver enzymes
●Metabolic acidosis
●Compare drop of patients blood to normal blood on
white paper
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Treatment●Decontamination
–Emesis – within first 2 hours
–Activated charcoal
●Oxygen therapy
●N-acetylcystine (Mucomyst) = antidote
–Binds NAPQI and serves as glutathione precursor
–Dose – 140mg/kg IV or PO, then 70mg/kg q6h for 7 treatments
–Dilute to a 5% solution with D5W
●Blood transfusions
●Vitamin C – 30mg/kg PO or SQ QID
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Prognosis
●Cats – guarded to poor if not treated within 24 hours
●Poor prognostic indicators
–Progressive methemoglobin concentrations
–Methemoglobin concentrations >50%
–Rising liver enzymes
●Resolution of signs from methemoglobinemia within 72 hours
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Rodenticide Toxicosis
●3 Common Rodenticides:
–Anticoagulants
–Bromethalin
–Cholecalciferol
●Different rodenticides require different treatments
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History
●Sweet-clover (dicoumarol) poisoning in cattle led to
development of anticoagulants
●Cattle suffered from internal bleeding
●Dicoumarol tested as rodenticide
●First generation (Warfarin) created in 1940-50s
●Second generation (brodifacoum, difethialone,
difenacoum, bromadiolone)
–More palatable, more effective, faster, longer acting
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Anticoagulant
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Pathophysiology
●Interfere with production of clotting factors
–Produced in the liver
–II,VII, IX, X
●Anticoagulants inhibit Vitamin K1 Epoxide Reductase
●Leads to depletion of active Vitamin K1
●Halts the production of active clotting factors
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Clinical Signs
●Takes 36-72 hours for depletion of clotting
factors and clinical signs
●Hemorrhage
●Dyspnea, coughing, lethargy, hemoptysis
●Cavity bleeds are common (chest, abdomen,
joints, ect.)
●Can bleed into brain or spinal cord
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Diagnosis
●History
●Elongated PT
●CBC – anemia, thrombocytopenia,
hypoproteinemia
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Treatment
●Decontamination
●Activated Charcoal
●Vitamin K1 – 3-5 mg/kg PO divided over BID
–Short acting anticoagulants (warfarin and pindone) treat for 14 days
–Bromadiolone treat for 21 days
–All others treat for 28 days
●If Asymptomatic have 2 options
–1: Begin treatment with K1
–2: Monitor PT
●Baseline then repeat in 48-72 hours
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Treatment
●Symptomatic Patients – Treat symptomatically
–Oxygen therapy
–Blood transfusion (whole blood or plasma +/-
pRBC)
–Hospitalize until PT WNL
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Prognosis
●Depends on severity of toxicity
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Bromethalin
●Neurotoxin
●Inhibits mitochondrial energy (ATP) production in the
brain
●Absorbed from GI tract
●Plasma levels peak within 4 hours
●Metabolized by the liver
●Undergoes enterohepatic recirculation
●Slow excretion through bile
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Clinical Signs
●Presents as 2 different syndromes
●1: High dose can cause a “convulsant syndrome”
–Hyperesthesia, hyperexcitability, tremors,
seizures, circling, vocalization, mild/severe CNS
depression, hyperthermia, death
–Signs occur 4-18 hours after ingestion
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Clinical Signs
●2: Low dose can cause a “paralytic syndrome”
–Signs may take 1-7 days to develop and progress over 1-
2 weeks
–Ataxia, CNS depression, hind limb paresis
–GP deficits, UMN signs, loss of nocioception
–May become comatose
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Diagnosis
●Based on clinical signs and history
●Green colored feces
●BW is unremarkable
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Treatment
●Decontamination
●Activated charcoal – q8h
–Monitor Na levels
●Fluid therapy
●Symptomatic treatment
–Seizure – mannitol, anticonvulsants
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Prognosis
●Good if decontamination is successful
●If neurologic signs present prognosis is poor to
grave
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Cholecalciferol
●Cholecalciferol=Vitamin D3
●Toxicity increased serum calcium and phosphorus
●Increases intestinal absorption of Ca and transfer of
Ca and P from bone to plasma
●Prolonged increased plasma levels result in tissue
mineralization
●Renal mineralization leads to AKI and failure
●Decreased functioning of GI tract, skeletal, and
cardiac muscles, blood vessels, and ligaments
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Clinical Signs
●Vomiting, lethargy, muscle weakness, anorexia,
depression
●Acute renal failure can occur within 24-72 hours
–PU/PD
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Diagnosis
●May notice bait in stool
●Chemistry – HyperPHOS, HyperCA (total and
ionized), HyperBUN, HyperCREAT,
●UA – Isosthenuria
●Radiology – may show mineralization of soft tissue
in symptomatic animals
●25-hydroxycholecalciferol -15x above normal
●PTH – low, iCa - high
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Treatment - Asymptomatic
●Decontamination
●Activated Charcoal – repeated doses
●Cholestyramine in dogs – 0.3-1g/kg PO TID for 4
days
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Treatment - Symptomatic
●Treatment aimed at correcting hypercalcemia
●Rehydration with NaCl
●Loop diuretics when rehydrated
–Furosemide enhances Ca excretion from kidneys
●Glucocorticoids
–Suppresses bone resorption of Ca
●Phosphate binders – for HyperPHOS
●Pamidronate – 1.3-2 mg/kg, diluted in saline IV over 2-hours
–Lowers Ca in 24-48 hours
May repeat dose in 5-7 days
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Chocolate Toxicity
●Contains caffeine and theobromine
●Caffeine is found in coffee, tea, chocolate, colas, ect.
●Theobromine is found in chocolate, cocoa beans, cocoa
bean mulch, colas, and tea
●Common around holidays
–Halloween, Christmas, V-Day, Easter
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Toxicity
●Central nervous system stimulant
●Absorbed from the GI tract and undergoes enterohepatic
circulation
●Half-life of caffeine – 4.5 hours
●Half life of theobromine – 17.5 hours
●Many chocolate products contain high fat and cause GI
upset and/or pancreatitis
●Unsweetened baker's chocolate > semisweet chocolate >
milk chocolate > white chocolate
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Clinical Signs
●Restlessness and hyperactivity → tremors and
seizures
●Vomiting and diarrhea
●PU/PD
●Rapid heart rate
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Diagnostics
●Based on history and clinical signs
●Online Chocolate Toxicity Calculator or Poison
Control Hotline
●Comorbidities possible
●No definitive test
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Treatment
●Decontamination
–Emesis
–Activated charcoal q4-6h up to 72 hours
●Intravenous fluids
●Anti-emetics – Cerenia, Anzemet
●Gastric protectants – Protonix, Pepcid
●Frequent walks - q4h
●Symptomatic care – Tachycardia – B-Blocker
(esmolol/propranolol/metoprolol)
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Prognosis
●Most cases recovery in 24-48 hours
●Guarded prognosis if large amounts are ingested
or if patient exhibiting severe signs
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Grape/Raisin Toxicity
●First identified in 1989
●Unsure of causative agent
●Studies on type of grape, seed/seedless, region
of US, brand, ect.
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Grapes/Raisin Toxicity
●Toxic dose – 0.41-1.9 oz/kg
●Lowest documented dose
–0.7 oz/kg grapes
–0.11 oz/kg raisins
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Clinical Signs
●GI and Renal signs
●Vomiting
●ARF within 18-36 hours
–Oliguria, Anuria
–Dehydration
–Depression
–Abdominal pain
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Clinical Presentation
●Recently ingested = NORMAL
●Vomiting and Diarrhea
●Lethargy
●Anorexia
●Ataxia, trembling
●PU/PD progressing to oliguria or anuria
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Diagnostics
●History!
●CBC/CHEM/UA
–Azotemia
–HyperPHOS
–HyperALT/ALKP
–Isosthenuria
–Hyper/Hypo K
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Diagnostics
●Abdominal Ultrasound
–Enlarged Kidneys
–Hyperechoic renal cortices
–Decreased corticomedullary distinction
●Blood Pressure - Hypertensive
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Differential Diagnosis
●Leptospirosis
●Ethylene Glycol Toxicity
●NSAID Toxicity
●Addisonian Crisis
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Treatment●Decontamination
–Emesis
–Activated Charcoal q4-6h
●Antiemetic
●Antacid
●Phosphate Binders
–Aluminum hydroxide at 30-100 mg/kg/day PO with meal
●Antihypertensives
–Amlodipine at 0.5mg/kg PO q12-24h
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Treatment
●If no Clinical Signs
●Intravenous fluids at 90-120 ml/kg/day for at least
48 hours
●If BUN/Creat WNL 3 days after ingestion, likely
no adverse consequences
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Treatment
●If Clinical Signs
–Intravenous fluids at 90-180 ml/kg/day for at least 48-72 hours
–Monitor BUN/Creat
–If Oliguric/Anuric
●Mannitol at 0.5-1 g/kg IV over 20 minutes q8h
●Furosemide at 2-6 mg/kg IV or CRI at 0.25-1 mg/kg/min
●Dopamine CRI at 1-3 ug/kg/min IV
–DIALYSIS
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Monitoring
●BUN/Creat and Phos q24h
●E-lytes q24h or sooner if severe changes
●Weigh q12-24h
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Prognosis
●Great if:
–Early onset of therapy
–Continued normal urine output
–Eating
–Response to therapy
●Poor/Guarded if:
–Delayed onset of therapy
–Decreased/absent urine output
–Ataxia or weakness
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Pyrethrins
●Commonly used in flea/tick preventatives
●Available as dips, powders/dusts, sprays, collars,
gels, aerosol bombs, ect.
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Diagnosis
●Based on:
–History
●Topical most common
●Dog treatment on cat
–Clinical signs
–Exclusion of other differentials
●Blood work WNL
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Clinical Signs
●Seen within minutes to hours
●May be delayed up to 72 hours
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Clinical Signs●Mild/Moderately Affected Cats:
–Hypersalivation
–Mild tremors
–Hyperexcitability or depression
–GI signs (vomiting, diarrhea)
●Severely Affected Cats:
–Disorientation
–Hyperthermia
–Muscle fasiculations
–Generalized tremors
–Seizures
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Clinical Signs
VIDEO
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Treatment
●Decontamination
–Topical
●Bathe in warm water with lipophilic soap
–Oral
●Induce emesis
●Activated charcoal
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Treatment
●Methocarbamol IV
–40-50 mg/kg IV BOLUS, then CRI at 10mg/kg/hour
–May give additional bolus if needed
–Do not exceed 330mg/kg/day
●Diazepam/Midazolam IV
–0.5mg/kg IV as needed
●Propofol IV
–4mg/kg IV to effect or 1.5-19mg/kg/hr CRI
●Intravenous Lipid Emulsions (ILE)
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Prognosis
●Excellent if treated fast and aggressively
●Most pets leave the hospital in 24-96 hours
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Lily Toxicity
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Lily Toxicity
●Easter Lily
●Tiger Lily
●Rubrum Lily
●Stargazer Lily
●Japanese Show Lily
●Day Lily
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Lily Toxicity
●Toxic to CATS
●Causes Renal Failure
●ALL parts are considered toxic
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Presenting Complaint
●Lily Ingestion
●Vomiting
●Lethargy
●Anorexia
●PU/PD
●Common around Easter (March and April)
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Diagnostics
●CBC – WNL
●CHEM
–Azotemia
–Hyperkalemia
–Hyperphosphatemia
●Urinalysis
–Isosthenuria
–Glucosuria in absence of hyperglycemia
–Urinary Casts
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Treatment
●Decontamination
–Emesis
–Activated Charcoal q4-6h
●Fluid Therapy
–120ml/kg/day
–At least 48 hours
–Monitor body weight BID-TID
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Alternative Treatment
●If Oliguric (<2ml/kg/hr)
–Furosemide 2mg/kg IV
–If oliguric in 1 hour, give 4mg/kg IV
–If oliguric in 1 hour, give 6mg/kg IV
●Hyperkalemia
–Bicarbonate (0.5-2 mEq/kg) IV
–Glucose (1-2ml/kg of 50% dextrose diluted) IV
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Alternative Treatment
●Peritoneal Dialysis
●Hemodialysis
●Renal Transplant
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Supportive Treatment
●Antiemetic
●Antacid
●Phosphate Binders
●Pain medication
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Monitoring
●Weights
●BUN and Creat
●Phosphorus
●Potassium
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Prognosis
●Good if:
–Able to produce urine
–Able to concentrate urine
–Decreasing azotemia
–Appetite
●Poor if:
–Anuric
–Isosthenuria
–Increasing azotemia
–anorexia
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Marijuana Toxicity
●Main toxic principle is 9-tetrahydrocannabinol (THC)
●Intoxication after ingestion of marijuana leaves,
baked products, smoke inhalation
●Lethal dose – 3g/kg
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Diagnosis
●History
●Clinical Signs
●Urine Test
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Clinical Signs
●Occur within 30-90 minutes after ingestion
●Neurologic
–Depression, ataxia, tremors, seizures, mydriasis,
disorientation, hyperesthesia, bradycardia,
hypersalivation, weakness, hypothermia, urinary
incontinence
●GI - Vomiting
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Treatment
●Decontamination
–Emesis
–Activated Charcoal q8h for 24 hours
●Intravenous Fluids
●Hospitalization for 24-72 hours
●Diazepam at 0.25-0.5 mg/kg IV as needed for agitation
and/or seizures
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Prognosis
●Great
●Most recovery completely in 24-72 hours
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Xylitol
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Xylitol
●Manufactured sweetener in sugar-free candy and
gum, baked good, beverages, cereals, and
toothpaste
●Toxic to DOGS
●Toxic dose
–>0.1 g/kg causes hypoglycemia
–>0.5 g/kg causes hepatotoxicity
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Xylitol
●Peak plasma levels in 30 minutes, may be delayed
●Increased insulin levels in Dogs by 2.5-7x (also rabbits, baboons,
cows, and goats)
●Causes severe hypoglycemia
●Hepatotoxic:
–Idiosyncratic reaction
–Liver enzyme elevation
–Hepatic necrosis
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Clinical Signs
●Vomiting
●Hypoglycemia:
–Usually within 30-90 minutes
–May be delayed for up to 12-48 hours
–Altered mentation, dullness, weakness, recumbency, ataxia, seizures
●Hyperglycemia secondary to somogyi
●Icteric
●Petechiae/Ecchymosis
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Diagnostics
●Hypoglycemia
●Hypokalemia – intracelluar shift
●HyperALT
●HyperTBILI
●HypoPLT
●Prolonged PT/PTT
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Treatment
●Decontamination
–Emesis
–Activated Charcoal – does not bind xylitol but is still recommended
●Monitor BG q2h for at least 12 hours
●Monitor K/Phos q4-6h
●Monitor Liver enzymes q24-72h
●If 0.1-0.5 g/kg ingested
–Hypoglycemia 0.5cc/kg 50% Dextrose IV, then 2.5%-5% CRI
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Treatment
●If >0.5 g/kg ingested
–0.5cc/kg 50% Dextrose IV, then 2.5%-5% CRI
●Liver protectants and antioxidants
–N-acetylcysteine
–S-adenosylmethionine
–Vitamin E
●Coagulopathies treated with FFP
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Prognosis
●Good if develop uncomplicated hypoglycemia
●Guarded to poor if develop hepatotoxicosis and
liver failure
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QUESTIONS?
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Work Cited
●Common Rodenticide Toxicoses in Small
Animals. DeClementi, Ca and Sobczak, Br. Vet
Clin Small Animal 42 (2012) 349-360.
●VIN -
●Grape and Raisin Toxicity in Dogs. Savigny,
Michelle and Macintire, Douoglass. Standards of
Care (2007) Volume 9.1.
●Lily Toxicoses in Cats. Jill Richardson. Standards
of Care (2002) Volume 4.4.