common and not so common toxicitiescommon and not so common toxicities peter lands, dvm saint...
TRANSCRIPT
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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.