JEN LOEWEN, DVM, DACVECC
Transcript of JEN LOEWEN, DVM, DACVECC
Approach to oral toxins
JEN LOEWEN, DVM, DACVECC
ASSISTANT PROFESSOR, WESTERN COLLEGE OF VETERINARY MEDICINE
Overview
General Approach to Intoxications
Specific Intoxications
Objectives
Describe and implement general treatment of
toxicities
List some specific antidotes
List resources for toxicities
Terminology
Poison / toxicant:
A solid, liquid, or gas that can interfere with homeostasis of an organism or life processes of its cells by its own inherent properties.
Toxin:
Poison that originates from a biological source (AKA biotoxin)
Toxic:
Used to describe the effects of a toxicant (i.e. the “toxic” effects of substance X)
Toxicosis:
The syndrome of adverse effects that result from exposure to a toxicant. Interchangeably used with poisoning and intoxication.
Small Animal Toxicology (Peterson)
General Approach to
Intoxications
Goals
Gather information about exposure and patient
Learn about the toxin
Decontamination
Provide toxin antidote when possible
Decrease toxin absorption
Enhance toxin elimination
General supportive therapy
Ultimate goal: inhibit or minimize further toxicant absorption
and to promote excretion or elimination of the toxicant
from the body
General Approach to
Intoxications: Historical info
Known or suspected intoxication:
Information about toxin
Active ingredient
Route of exposure
How much was ingested?
When was the toxin ingested?
Patient information
Body weight
Clinical signs noted since ingestion
Pre-existing disease/illness
Current medical therapy or supplements administered
***Ask client to bring remainder of package/label***
General Approach to
Intoxications
Other helpful questions
Learn more about patient’s environment
Access to garage, neighbor’s yard, farmland, etc.
Patient examination
Triage examination: ABCs (+ N)
Full physical examination
Learn about the toxin
Important information
Toxic dose
Mechanism of action
Is emesis safe/indicated?
Is there an antidote?
Treatment / Prognosis
References
ASPCA pet poison- (888) 426-4435
Pet poison hotline- (855) 764-7661
*fees apply
Specific therapy:
Is there a known antidote?
Types of antidotes
Direct reaction with toxicant
Chelation of heavy metal ions
Interaction with the toxicant’s receptor
Naloxone = μ-opioid receptor antagonist
Alter metabolism
Inhibition of metabolic pathway
4-MP inhibits alcohol dehydrogenase
Provide alternative substrate for enzymes
Ethanol competes w/ ethylene glycol for alcohol dehydrogenase
Small Animal Toxicology, Ch 24
Examples of known antidotes
Toxicant Antidote
Acetaminophen N-Acetylcysteine
Anticoagulant Rodenticides Vitamin K1
Benzodiazepines Flumazenil
Cadmium, Iron, Lead Chelation (D-penicillamine)
Digitalis Digoxin immune Fab
Ethylene glycol4-methylpyrazole (4-MP),
ethanol
Organophosphates /
Carbamates
2-Pralidoxime (2-PAM),
atropine
Opiods (morphine,
hydromorphone, fentanyl,
heroin)
Naloxone
Small Animal Toxicology, Ch 24
Decontamination
Considerations
Route of exposure
Dermal
Ocular
GI
Respiratory
Risks/benefits of decontamination procedure
Decontamination
Dermal Exposure
Lipophilic toxicants, surfactants are more readily absorbed
Standard method: rinse with water or bathe patient with mild
dish soap.
**Caution: may cause patient distress, use care with obtunded
patients, prevent hypothermia, avoid human exposure
Ocular Exposure
Copious ocular irrigation with tepid tap water, saline, or distilled
water.
Flush laterally (avoid contamination of other eye)
***Caution: Contact lens solutions may cause further irritation
SACCM, Ch 77
Decontamination
Gastrointestinal Exposure
Emetics
Gastric Lavage
Whole Bowel Irrigation
SACCM, Ch 77
GI Decontamination
Emetics
Encouraged
Emesis
Encouraged
Immediately after toxin ingestion
Within 1-2 hours of toxin ingestion
In the alert patient
Product known to last in stomach for prolonged period
Contraindicated
Caustic products
Petroleum products, Acid/alkali
Altered mentation
Risk of aspiration
Toxins that increase risks of aspiration: gasoline, kerosene, motor oil
Laryngeal paralysis, megaesophagus
etc.
Toxins rapidly absorbed:
acetaminophen
SACCM, Ch 77
Only allows retrieval of a fraction of gastric contents
GI Decontamination
Emetics
Centrally Acting (CRTZ)
Apomorphine
Opiate, stimulates dopamine receptors
***Emetic of choice in dogs***, unreliable in cats
Dose: 0.03 mg/kg IV or 0.04 mg/kg IM → can repeat
dose also subconjunctival administration
Side Effects: Protracted vomiting, restlessness,
excitement, CNS depression.
Naloxone to reverse SE (not emesis)
SACCM, Ch 77
GI Decontamination
Emetics
Centrally Acting (CRTZ)
Xylazine
α-2 agonist
***Often used in cats, unreliable in dogs
0.44 mg/kg IM or SQ.
Reverse with yohimbine (0.25 -0.5 mg/kg IM) following emesis
Side Effects: Sedation, bradycardia, arrhythmias, muscle
tremors
α-2 agonists contraindicated in animals with structural heart
disease
SACCM, Ch 77
GI Decontamination
Emetics
SACCM, Ch 77
Xylazine (0.36-0.64 mg/kg IM): 9/21 (43%)
Dexmed (6-18 mcg/kg IM): 15/26 (58%)
Equal effects
Xylazine (0.4-0.5 mg/kg): 11/25 cats
Dexmedetomidine (0.96-10 mcg/kg IM ): 13/16
Hydromorphone (1 mg/kg SQ) – 9/12 vomited
Dexmedetomidine (7 mcg/kg IM)- 7/12 vomited
GI Decontamination
Emetics
Local Irritants
3% Hydrogen Peroxide
1-2 ml/kg PO (max dose 50-150 ml/large dog
Repeat once if ineffective
May result in persistent vomiting/gastritis
In cats: anecdotally 25% develop severe hemorrhagic gastroenteritis
Others (NOT RECOMMENDED)
Dishwashing liquid
Table salt
Stimulation of gag reflex
SACCM, Ch 77
GI Decontamination
Gastric Lavage
Administration and evacuation of liquid through orogastric tube
Encouraged
Within 1-2 hours of toxin ingestion
Depressed mental state/loss of gag (vs emesis)
Contraindicated
Ingestion of hydrocarbons or corrosive substances
In patients with risk of hemorrhage/GI perforation
More than 2h after ingestion
SACCM, Ch 77
GI Decontamination
Gastric Lavage
Procedure
Anesthetize and intubate patient with cuffed ETT
Position patient with head slightly lower than thorax
Premeasure large bore gastric tube from nose to last rib
Lubricate tube and gently pass down esophagus into stomach to marked distance.
Check positioning
Aspirate gastric contents
Insufflate with air while ausculting stomach
Abdominal radiograph to confirm placement if unsure
Lavage with 5-10ml/kg of warm water or saline
Allow to drain from tube via gravity, then repeat until fluid is clear
Kink off tube prior to removal
SACCM, Ch 77
GI Decontamination
Gastric Lavage
Toxin Recovery
Mean recovery of 29-38% of toxin within 15-20
minutes of ingestion.
8.6-13% recovery after 60 minutes have elapsed.
Risks
Aspiration pneumonia (ETT is critical!)
Injury to/perforation of esophagus/stomach
SACCM, Ch 77
GI Decontamination
Whole Bowel Irrigation
Procedure
Administration of large amounts of balanced polyethylene glycol
electrolyte solution through NE tube until bowel movements resemble
fluid administered.
Human Med: Used for ingestion of sustained release or enteric coated toxins
Encouraged
?? Unknown utility in veterinary patients
Improved removal of paraquat in dogs (experimental intoxication)
Contraindicated
GI hemorrhage, obstruction, compromised airway, intractable
vomiting, hemodynamic instability
Complications in humans: nausesa, vomiting, cramping, bloating
SACCM, Ch 77, Mizutani 1992
Decrease Toxin Absorption:
Adsorbents
Activated Charcoal
Does not absorb every toxin
Factors: temperature, solubility of toxin,
ionization of toxin, pH, presence of other
gastric contents
Not effective for: alcohols, ferrous sulfate,
xylitol, caustic alkalis, nitrates, petroleum
products, mineral acids
SACCM, Ch 77
Decrease Toxin Absorption:
Adsorbents
Activated Charcoal
Dose = 1 to 4 grams/kg PO (recc 1-2 gm/kg)
Offer PO, mix with food.
Syringe feed (carefully!!)
Orogastric tube (anesthetized, intubated)
Most effective soon after ingestion.
First dose w/ sorbitol…
Risks: Aspiration
Unprotected airway, seizures patient, too sedate
Hypernatremia
SACCM, Ch 77
Abstract presentation
15 mg/kg of oral carprofen
2 g/kg activated charcoal (AC) 30 minutes after carprofen administration
Apomorphine-induced emesis at 30 minutes followed by 2 g/kg activated charcoal (EAC) administration at 60 minutes,
No treatment (control group).
activated charcoal alone is as effective as emesis followed by activated charcoal in dogs following carprofen overdose in this model
120 mg/kg of carprofen PO
a single 2 g/kg activated charcoal administration 1 hour following carprofen ingestion (AC)
2 g/kg activated charcoal with 3.84 g/kg sorbitol 1 hour following carprofen ingestion (ACS);
2 g/kg activated charcoal 1 hour after carprofen ingestion and repeated every 6 hours for a total of 4 doses (MD)
no treatment (control)
AC and ACS with are as effective as MD in reducing serum carprofen concentrations following experimental overdose in dog
Food with charcoal?
Food decreased adsorptive capacity
Unlikely to be clinically significant (but study invitro)
Decrease Toxin Absorption
Reduce enterohepatic recirculation
Repeated activated charcoal administration
WITHOUT sorbitol
Urinary bladder wall reabsorption
Urinary catheter placement or frequent walks
Methylxanthines and metabolites
SACCM, Ch 77, Sm Anim Toxicol p850
Enhance Toxin Elimination
Enhance GI Elimination: Cathartics
Accelerate expulsion of toxins from the GI tract
Saccharide (i.e. sorbitol)
Commonly available in some activated charcoal
preparations
Use Caution:
May cause dehydration, hypernatremia
Saline cathartics: Mg, phosphate may be absorbed
Caution in animals with renal disease, CHF, dehydration
SACCM, Ch 77
Enhance Toxin Elimination
Enhance Renal Excretion
IV fluids to promote diuresis
For renally excreted toxins
Risk of volume overload
Alter urine pH
i.e. ascorbic acid
Some products may cause systemic acidosis/alkalosis
Hemodialysis
An additional option for toxin removal
ethylene glycol
$$$, limited availabilitySACCM, Ch 77
Lipid rescue therapy
Intralipid 20% ($30/250 ml)
Mechanism of action:
???
Improved myocardial performance?
Lipid sink?
Dose?
1.5 ml/kg bolus over 1-3 min followed by 0.25-0.5 ml/kg/min x 30-60 min
Can repeat as long as serum is no longer lipemic
Potential complications
Minimal reported, no safety studies
Bacterial contamination (aseptic technique
required)
Hypersensitivity reaction
Pancreatitis?
ARDS
Pulmonary lipid emboli
General Supportive Therapy
IV Fluids
Antiemetics
Sedation, etc
Monitoring
ECG, TPR, BP, Mentation
Specific Toxicants
ADME
Absorption
Distribution
Metabolism
Excretion
Mechanism of Action/Toxicity
Diagnosis
Treatment
Hot off the press
Has it finally been solved??
Is it Tartaric acid?
Maybe???
Letter to the editor is lowest quality of evidence
Posses a hypothesis that we need to further investigate
Ethylene Glycol
Minimum lethal dose:
Dogs: 4.4 to 6.6 ml/kg Cats: 1.5 ml/kg
Mortality rate 59-70% in dogs, likely worse in cats.
A/D:
Rapidly absorbed after PO exposure→ distributed to all body tissues
Peak blood level at 3h, high concentration until ~12h, may be
undetectable by 48h
M/E:
Primarily metabolized in the liver
Alcohol dehydrogenase*
Variable amt excreted unchanged in urine
SACCM Ch 78, Sm Anim Toxicol Ch 45, Image: fixacar.net
SACCM Ch 78
Ethylene Glycol
Systemic Effects
Stage 1 (30 min – 12h):
CNS Depression
Due to glycoaldehyde, EG, hyperosmolality, metabolic acidosis
Depression, ataxia, somnolence, seizure, coma
CNS signs may improve ~12h after intoxication
GI Signs: Vomiting
Direct gastric mucosal irritation
CRTZ (increased serum osmolality)
PU/PD
Osmotic diuresis
SACCM Ch 78, Sm Anim Toxicol Ch 45
Ethylene Glycol
Systemic Effects
Stage 2 (12-24h):
CNS Depression Improves
Dogs appear improved/recovered
Cats remain depressed
Dehydration, tachycardia, tachypnea
SACCM Ch 78, Sm Anim Toxicol Ch 45
Ethylene Glycol
Systemic Effects
Stage 3
Acute Renal Failure
24-72h after ingestion in dogs
Earlier (12-24h) in cats
Mechanism of acute tubular necrosis
Incompletely understood
Calcium oxalate crystal deposition in renal tubules
Direct renal tubular epithelial cytotoxicity
Frequently oliguric/anuric, 72-96h post-ingestion
SACCM Ch 78, Sm Anim Toxicol Ch 45
Ethylene Glycol
Diagnostic Tests
CBC – +/- echinocytes, usually unremarkable
Serum Chemistry
Early:
Metabolic acidosis (↓HCO3-)
Elevated anion gap
Glycolic acid and other acid metabolite accumulation
+/- Hyperphosphatemia
Phosphate rust inhibitors
Late:
Renal failure:
Azotemia, hyperphosphatemia
Hyperkalemia (with oliguria, anuria)
Hypocalcemia (50% of cases)
Chelation of calcium by oxalic acid
SACCM Ch 78, Sm Anim Toxicol Ch 45
( ( Na+ + K + ) – ( Cl - + HCO3- ) )
Ethylene Glycol
Diagnostic Tests
Urinalysis
Isosthenuria (within 3h)
Osmotic diuresis → renal dysfunction
Calcium oxalate monohydrate crystalluria
As early as 3-6h
Other findings may include:
Hematuria, proteinuria, glucosuria, casts
SACCM Ch 78, Sm Anim Toxicol Ch 45
Ethylene Glycol
Diagnostic Tests
Confirmatory Tests
Ethylene Glycol Test Kit
Estimates blood levels ≥50 mg/dl
Cats can suffer intoxication below this level
False positive (propylene glycol, glycerol)
Activated charcoal, diazepam, semimoist diets
SACCM Ch 78, Sm Anim Toxicol Ch 45, Image: prnpharmacal.com/egtkit
Osm
+
2.8
Ethylene Glycol
Diagnostic Tests
Other supportive tests/procedures
Examination of patient with Wood’s Lamp
Fluorescein present on face, paws, in urine (up to 6h)
Also assess vomitus
Abdominal Ultrasound
“Halo sign”
Hyperechoic cortical/medullary regions with hypoechoic
corticomedullary junction and central medullary tissue
Supportive, not pathognomonic
SACCM Ch 78, Sm Anim Toxicol Ch 45, Image: prnpharmacal.com/egtkit
Ethylene Glycol
Treatment
Emesis (within 2h of ingestion)
(Activated charcoal = questionable benefit)
Competitive Inhibition of Alcohol Dehydrogenase
Ethanol (IV bolus or CRI)
CNS Depression, hyperosmolality, osmotic diuresis
4-Methylpyrazole (4-MP)
Higher dose (6x) required in cats
ADH has greater affinity for 4-MP > ethanol
Safer than ethanol
SACCM Ch 78, Sm Anim Toxicol Ch 45
Ethylene Glycol
Treatment
Supportive Therapy
IV Fluids
Tx (if necessary) for metabolic acidosis, hypocalcemia
Antiemetics
Hemodialysis
Prognosis
Variable/good if treated (EtOH/4-MP) within 8h
Grave prognosis: anuric acute renal failure
20% with hemodialysis
SACCM Ch 78, Sm Anim Toxicol Ch 45
Acetaminophen
Toxic Dose
Dogs: 200-600 mg/kg (as low as 75-100 mg/kg)
Cats: 50-100 mg/kg (as low as 10 mg/kg)
A/D
Rapidly absorbed after PO exposure
Peak blood levels in 30-60 minutes
M/E under NORMAL Conditions (at low doses)
90% undergoes hepatic metabolism - conjugation with:
Sulfate
Glucuronide
5% excreted unchanged in urine
5% metabolized to NAPQI (N-acetyl-p-benzoquinoneimine, TOXIC)
Normally conjugated with glutathione → nontoxic cysteine/mercapturicacid conjugates
SACCM Ch 79, Sm Anim Toxicol Ch 28, Image: amazon.com
Non-toxic metabolites
Acetaminophen
Metabolism
Image: sailingsimplicity.com/non-toxic-lifestyle-choices/
Acetaminophen
Low Dose
SulfationGlucoronidati
oncP450
Unchanged
in Urine
GS
H
Acetaminophen
TOXIC Dose
= NAPQI
Cats: low levels of glucoronyl
transferase
Acetaminophen
Systemic Effects
NAPQI
Reactive Oxygen Species
Binds to cellular proteins → oxidative injury
Cats
Methemoglobinemia, Hz bodies, Hemolytic Anemia
Feline RBC more susceptible (Hb contains 8 sulfhydryl groups)
Brown mucous membranes, respiratory distress, face/paw edema, depression, hypothermia, vomiting
Hepatotoxicity at higher doses and in males
Dogs
Hepatocellular Injury/Necrosis
Secondary vomiting, diarrhea, HE
Methemoglobinemia at higher doses
SACCM Ch 79, Sm Anim Toxicol Ch 28, Image: amazon.com, illustratedmedicine.blogspot.com/2010/09/methemoglobinemia.html
Fe2+→ Fe3+
Ferrous Ferric
Acetaminophen
Diagnostic Tests
Minimum Database
Brown tinge to whole blood (MetHb)
+/- Heinz bodies, hemolytic anemia (anemia, Hb-emia,
Hb-uria, ↑Tbili)
↑ALT, AST
↓Hepatic function (↓BUN, albumin, cholesterol)
Confirmatory Tests
Measurement of acetaminophen conc (?)
Co-oximetry (measure % methemoglobin)
SACCM Ch 79, Sm Anim Toxicol (Peterson) Ch 28, Sm Anim Toxicol (Osweiler), Image: amazon.com
Acetaminophen
Treatment
Decontamination:
Emesis, activated charcoal x 1 dose (recent exposure)
Additional doses AC not indicated, may bind antidote
Antidote
N-acetylcysteine
Increased synthesis/availability of GSH (precursor)
Direct binding/detoxification of NAPQI
Supplies substrate for sulfation (↑% nontoxic metabolites)
140 mg/kg IV loading, 70 mg/kg IV or PO q6h x 72h.
Side effects: nausea, vomiting, anaphylaxis (if PO given IV)
SACCM Ch 79, Sm Anim Toxicol (Peterson) Ch 28, Sm Anim Toxicol (Osweiler ), Image: amazon.com
Acetaminophen
Treatment
Adjunctive Therapy
Ascorbic acid (vitamin C)
30 mg/kg PO q6h x 6. → To reduce methemoglobin to hemoglobin
SAMe
Important for PL and glutathione production
Cats: protective against development of erythrocyte oxidative injury.
Cimetidine
Inhibitor of cP450, reduce metabolism to NAPQI
Methylene blue
MB + NAC had little advantage vs NAC
Worsen Hz body anemia
SACCM Ch 79, Sm Anim Toxicol (Peterson) Ch 28, Sm Anim Toxicol (Osweiler), Image: amazon.com
Rodenticides
Three Main Categories
Anticoagulant
Cholecalciferol
Bromethalin
Also..
Phosphide
Strychnine
Image: http://blommi.com
Anticoagulant Rodenticides
Examples:
Brodifacoum
Bromadiolone
Diphacinone
Chlorophacinone
Warfarin
NOT Bromethalin
SACCM Ch 82
Anticoagulant Rodenticides
LD50 and T1/2 varies by chemical
Categorized by generation
First Generation: 4-6 days
Second Generation: 2-4 weeks
Absorption:
Peak plasma conc in minutes to 1h after exposure
Clinical signs: ≥36h after ingestion
SACCM Ch 82, Peterson Sm Anim Toxicol
Anticoagulant Rodenticides
Mechanism of Toxicity
Vitamin K1 is required for synthesis of clotting factors:
Factors must be able to bind Ca++ to be activated
Dicarboxylic acid groups on clotting factors
Initial synthesis – single carboxylic acid group
Vitamin K1 required for addition of second carboxylic acid group
(post-translational modification)
SACCM Ch 82, Peterson Sm Anim Toxicol
Anticoagulant Rodenticides
Mechanism of Toxicity
Do these rodenticides remove Vitamin K1
from the body?
MOA: Inhibition of Vitamin K Epoxide Reductase
SACCM Ch 82
Anticoagulant Rodenticides
Mechanism of Toxicity
Coagulopathy:
1) Depletion of active Vitamin K1
2) Depletion of clotting factors
T1/2 of clotting factors
Which coagulation test becomes abnormal first?
Coag factors reduced by 24-64h after exposure
Bleeding generally does not occur until 3-5d after
ingestion
SACCM Ch 82, Peterson Sm Anim Toxicol
VII 6.2h
IX 13.9h
X 16.5h
Extrinsic
Intrinsic
Common
Anticoagulant Rodenticides
Systemic Effects No clinical signs (if acute presentation)
Hemorrhage
Anemia, tachycardia, tachypnea, hypotension, lethargy
Dyspnea, other specific signs of bleeding
What are typical sites of hemorrhage? Body cavities
Hemothorax
Hemoabdomen
Hemopericardium
Hemarthrosis
Other
Hematuria, hemoptysis, hematomas,etc.
SACCM Ch 82, , Peterson Sm Anim Toxicol
Anticoagulant Rodenticides
Diagnostic Tests
MDB: Anemia, hypoproteinemia, thrombocytopenia
(consumption)
Coag testing: Prolongation of PT > PTT/ACT
PIVKA (send-out)
Detects inactive precursor proteins to II, VII, IX, X, C/S.
Abnormal results are not specific to anticoagulant rodenticides
Anticoagulant rodenticide screen (3-5d for results)
Generally not necessary, proves exposure
SACCM Ch 82, , Peterson Sm Anim Toxicol
Anticoagulant Rodenticides
Approach to Treatment
1) Acute ingestion, asymptomatic, no previous exposure
Emesis, activated charcoal (repeated dosing)
Vitamin K1 PO
Or recheck PT at 24-36h, 96h after exposure and Rx if ↑
2) Acute ingestion, asymptomatic, possible previous exposure
Check PT. If not prolonged, treat same as above
If prolonged, avoid emesis +/- charcoal.
Administer Vitamin K1 (PO if eating) and monitor overnight for
bleeding
Ensure availability of plasma if needed
SACCM Ch 82, , Peterson Sm Anim Toxicol
Anticoagulant Rodenticides
Approach to Treatment
3) Symptomatic (bleeding) patient
Emesis / Activated Charcoal Contraindicated
Plasma Transfusion
+/- pRBC (or whole blood)
Other Supportive Care
Thoracocentesis (If symptomatic)
IV Fluids
Vitamin K1
No direct effect on coagulation
Requires 6-12h for clinically significant synthesis of new clotting factors
Still MUST be administered
PO at any point when the animal is eating (well absorbed)
SQ if not eating. NOT IV – risk of anaphylaxis,
SACCM Ch 82, , Peterson Sm Anim Toxicol
Anticoagulant Rodenticides
Approach to Treatment
Plasma
Can use: FFP, FP, Cryo-poor Plasma, FWB
How much?
To replace 1/3 of clotting factors? (15 ml/kg FFP)
6-10 ml/kg of plasma, 12-20 ml/kg FWB?
Every patient is different – assess efficacy / recheck PT
SACCM Ch 82, , Peterson Sm Anim Toxicol
Anticoagulant Rodenticides
Approach to Treatment
Vitamin K1
Dose:
2.5 mg/kg – 5 mg/kg PO daily (can be divided)
Duration of Vitamin K1 therapy
1st vs 2nd generation (1 wk or 2-4 wk)
Conservative approach: 4wk if toxin unknown
Recheck PT 48h after discontinuation of Vit K1
Other notes
Check patient environment for source of re-exposure
Prognosis: Good with appropriate supportive care
SACCM Ch 82, , Peterson Sm Anim Toxicol
Other Rodenticides
Cholecalciferol (Vitamin D3)
Severe hypercalcemia, hyperphosphatemia, ARF
Bromethalin
Uncoupling of oxidative-phosphorylation and decrease
in ATP production
Cerebral edema, ↑ ICP, CNS Depression, ataxia,
tremors.
SACCM Ch 82, Sm Anim Toxicol (Osweiler)
Other Rodenticides
Zinc Phosphide
Creates phosphine gas with exposure to gastric acid → free radicals, oxidative damage.
Vomiting, myocardial damage (arrhythmias, ↓ contractility), pulmonary edema, pleural effusion, metHb, Hz bodies, ataxia, seizures, increased ALT, AST, Tbili, etc,
Gas produced smells like rotten fish, acetylene, garlic
Strychnine
Prevents uptake of glycine at inhibitory synapses of Renshawcells in CNS → dis-inhibition (excitatory) effect.
Hyperextension of limbs, muscle (extensor) rigidity, seizures,
respiratory arrest.
SACCM Ch 82, Sm Anim Toxicol (Osweiler)
References
Bonagura JD, Twedt DC. 2009. Kirk’s Current Veterinary Therapy XIV. St Louis: Saunders Elsevier.
Mizutani et al. 1992. Efficacy of whole bowel irrigation using solutions with or without adsorbent in the removal of paraquat in dogs. Hum ExpToxicol 11(6):495-504.
Mount et al. 2003. Use of a test for proteins induced by vitamin K absence or antagonism in diagnosis of anticoagulant poisoning in dogs: 325 cases (1987–1997). J Amer Vet Med Assoc 222(2): 194-8.
Osweiler GD, et al. 2011. Blackwell’s five-minute veterinary consult clinical companion: Small animal toxicology. Ames, IA: Wiley-Blackwell.
Peterson ME, Talcott PA. 2006. Small Animal Toxicology, 2nd Edition. St. Louis: Saunders Elsevier.
Silverstein DC, Hopper K. 2009. Small Animal Critical Care Medicine. St. Louis: Saunders Elsevier.