management of the poisoned animal Flashcards

Question

tetanus diagnosis

Answer 1

* Clinical diagnosis: history and clinical signs * Spastic paralysis * No specific PM lesions * Confirmation: typically based on history and clinical presentation * Difficult to detect tetanolysin in plasma * PCR for C. tetani * Differential diagnoses: strychnine, tremorgenic mycotoxins * Meningitis, polioencephalomalacia

Answer 2

Bacillus anthracis * Anthrax toxin complex – 3 proteins * Spores are extremely environmentally resistant * Soil * Outbreaks associated with liberation of spores** in the environment * Flooding, excavation, contaminated feed * All species susceptible * Outbreaks most common in cattle and sheep

Answer 3

* Onset: Peracute/acute * Sudden death: animals found dead * Septicemia: febrile, tremors, respiratory difficulty, collapse, death * Edema * Terminal hemorrhage from orifices** – nostrils, mouth, anus, vulva * Bleeding due to breakdown of lymphatic tissues and blood vessels * Incomplete rigor mortis

Answer 4

* Pigs: subacute to chronic → swelling, fever, enlarged lymph nodes * Horses: acute → fever, depression, subcutaneous swelling, colic, signs of sepsis * Postmortem lesions * Dark, unclotted blood * Enlarged spleen * Swollen, congested, hemorrhagic lymph nodes

Answer 5

* Often cannot intervene fast enough to save a symptomatic animal * Antibiotics: penicillin * Quarantine: separate sick animals, remove from contaminated area * Field test kits available * Reportable disease**

Answer 6

* If anthrax is suspected, DO NOT NECROPSY * Inform lab of risk group 3 materials * Samples: blood, edema fluid * Microscopy, culture, PCR * PPE * DDx: water hemlock, urea, cyanide, nitrate, bracken fern, dicoumarol * Non-toxic: blackleg, redwater, grass tetany, lightning strike * Prevention: vaccination

Answer 7

* Not true bacteria, but not true algae either * Photosynthetic prokaryotic organisms * “Harmful Algal Blooms” (HAB) * Major public health and environmental health problem worldwide * Numerous species of BGA, multiple toxins * Not all BGA species are toxic * How do animals become exposed? * Consumption of contaminated water** * Common in dogs and livestock**

Answer 8

Warm, sunny weather (15-30 °C) – multiple consecutive days * Time of year: mid-summer to autumn * Shallow water bodies * Nutrient input / eutrophication * Nitrogen, phosphorous * Agricultural run-off, manure, etc

Answer 9

* Microcystis aeruginosa, many others * Clumped colonies * Global distribution * Prototypical toxin: microcystin-LR * “Fast death factor” * Many toxin congeners * Stable in the environment * Extremely toxic * Lethal dose: approx. 0.5 mg/kg

Answer 10

* Inhibition of protein phosphatases → disruption of cytoskeleton, oxidative damage, inhibition of glucose metabolism * Target organ: liver * Selective uptake into hepatocytes via organic anion transport polypeptides * Acute liver failure

Answer 11

* Onset: within 20 minutes to several hours post-ingestion * Acute liver failure * Vomiting, diarrhea with blood * Weakness, shock * Pale and/or icteric MM * Hepatic encephalopathy, seizures * Death within several hours * Hypovolemic shock secondary to intrahepatic hemorrhage or liver failure * Clinical pathology: elevated liver enzymes, indicators of liver failure, coagulopathy * Prognosis: poor to grave

Answer 12

-Dolichospermum spp., many others * Filamentous appearance * Less stable in environment * “Very Fast Death Factor” * Extremely toxic * Target organ: CNS * Cholinergic toxidrome – post-synaptic nAChR agonist and inhibitor of acetylcholinesterase

Answer 13

* Peracute neuroexcitation symptoms** * Rigidity and tremors that progress to seizures * Collapse * Abdominal breathing and dyspnea, cyanosis * Urination * Death within minutes to hours due to respiratory failure * Often found dead near water * No specific PM or histologic lesions

Answer 14

* No antidote available * Window for decontamination is narrow – often missed * Microcystin: aggressive symptomatic and supportive care * IVFT, colloids, dextrose, vitamin K1 (coagulopathy), hepatoprotectants, plasma/blood transfusions * Anatoxin-a: aggressive symptomatic and supportive care * Seizure control * Mechanical ventilation – can be several days to wee

Answer 15

Also known as relay toxicity * Carcass of a poisoned animal poisons the animal that consumes it** * Scavenging wildlife, dogs at the greatest risk * Some rodenticides have a very high risk* of secondary poisoning: * Strychnine * Fluoroacetate * Bromethalin * Second generation ACR

Answer 16

* Strychnos nux vomica – strychnine tree * Recently banned in Canada, for control of ground squirrels * Poisoning occurs by: * Consumption of strychnine-laced bait * Consumption of a strychnine poisoned animal * Malicious poisoning * All species susceptible → dogs most frequently poisoned * Target: CNS * Toxicity: extremely toxic * Dogs, horses, cattle: 0.5 mg/kg * Cats, pigs: 1.2 mg/k

Answer 17

* Glycine antagonist* at post-synaptic receptors in the spinal cord and medulla * Disinhibition of motor neurons * All skeletal muscles affected * Results in uncontrolled stimulation of motor neurons**

Answer 18

* Onset: within minutes – peracute * Behavioural: apprehension, anxiety, agitation * Neuromuscular: generalized muscle spasms * Severe extensor rigidity** * Tonic-clonic seizures** * Responsive to external stimuli** * Cyanosis * Dilated pupils * Sudden death possible * No specific PM or histologic lesion

Answer 19

No specific antidote: aggressive decontamination and supportive care * Asymptomatic: activated charcoal, can consider gastric lavage under GA * Seizure control: diazepam, general anesthesia * Respiration: intubation and mechanical ventilation * IV fluid diuresis * Manage of consequences of seizures: hyperthermia (DIC), rhabdomyolysis, hypoxia, acidosi

Answer 20

* Key clinical exam findings:** * Sudden onset of neurological signs * Extensor rigidity * Seizures that are responsive to external stimuli * Lack of GI signs * Presence of strychnine in stomach contents, vomitus, urine, liver, bait * Prognosis: poor to grave * If animal can survive 24-48 hours, the prognosis improve

Answer 21

-in home and garden stores, extremely to highly toxic * Dogs minimum toxic dose: 2.5 mg/kg BW (LD50: ~5 mg/kg BW) * Cats minimum toxic dose: 0.3 mg/kg BW - most sensitive species

Answer 22

* Two major mechanisms: * Uncouples oxidative phosphorylation in mitochondria → ↓ ATP production → impaired Na+K+ATPase → loss of oncotic control in the brain * Oxidative stress: cerebral lipid peroxidation * Culminates in cerebral edema** * Effect on the CNS: long nerve demyelination, accumulation of fluid within myelin sheath + increases in CSF pressure * Characteristic histologic lesion: intramyelinic edema**

Answer 23

* High dose exposures in dogs: convulsant syndrome** * Asymptomatic for a few hours (~2-12 hrs) → acute progression * Muscle tremors * Hyperesthesia * Agitation/hyperexcitability * Running fits * Seizures responsive to external stimuli * Obtundation * Death due to respiratory paralysis

Answer 24

* Lower dose exposures in dogs + any dose in cats: paralytic syndrome** * Delayed onset (one to several days post-exposure), progressive clinical course (2 days-2 weeks) * Hindlimb paresis, ataxia, decreased proprioception** * Cats: abdominal distension** * Progression to: * Loss of deep pain sensation * UMN bladder * CNS depression

Answer 25

* Clinical pathology * Few changes on bloodwork: mild hyperglycemia * May be hypernatremic * Increased CSF pressure * Normal CSF cytology – no inflammation, normal specific gravity and protein

Answer 26

B R O M E T H A L I N – M A N A G E M E N T * No antidote * Early gastrointestinal decontamination is key: * Activated charcoal + emesis * Hypernatremia** * Symptomatic patient * Management of cerebral edema * Seizure control * Supportive care

Answer 27

* Antemortem: history of exposure and compatible clinical signs * Consider in cases of progressive hindlimb paresis * Confirmation: detection of desmethylbromethalin in fat, serum, brain, kidney, liver * PM: characteristic histology * Diffuse white matter spongiosis / intramyelinic edema

Answer 28

* Sodium monofluoroacetate: Found in many plants * Use in Canada (Alberta): livestock anti-predator collars * 5 mg tablets * Collars: 10 mg/mL * Exposure scenarios * Stockpiled * Malicious poisoning * High risk of secondary poisoning + tertiary poisoning

Answer 29

* Inhibits key enzymes in the Krebs cycle * Converted to fluorocitrate--> shuts down citric acid cycle * Target organs: CNS, heart * Toxicity: extreme * Dogs are the most sensitive species

Answer 30

* Onset: within 30 minutes to multiple hours after ingestion * Sudden death without clinical signs possible * GI: vomiting, salivation, urination, defecation * CNS: hyperesthesia, frenzied, convulsions with extensor rigidity, running fits * Cats: vocalization * Cardiorespiratory: profound tachycardia, dyspnea, cyanosis, ventricular fibrillation possible * Death from cardiorespiratory failure PM: extensor rigidity, congestion and hemorrhage in several organs * Pulmonary hemorrhage

Answer 31

* Clinical pathology * Hyperglycemia, hyperammonemia * Metabolic acidosis, hyperlactatemia * Hypocalcemia * Elevated citrate (not routinely tested -no antidote * Supportive care: seizure management, fluids, correction of electrolyte derangements * Prognosis: poor to grave

Answer 32

-induce emesis if fully consious -gastric lavage and activated charcoal -fluid therapy

Answer 33

* Antemortem: history of exposure and compatible clinical signs * Confirmation: detection of fluoroacetate in bait, stomach contents, vomitus, urine * Nonspecific PM/histo lesions * Congestion and hemorrhage * Myocardial necrosis has been reported in sheep * DDx: same for strychnine + bromethalin

Answer 34

* First generation: warfarin, diphacinone, chlorophacinone * Multiple ingestions required * Second generation: brodifacoum, bromadiolone, difethialone, difenacoum * “Superwarfarins” * Developed because of warfarin resistant rodents * One ingestion can kill*** * Longer half-life

Answer 35

* Defect in secondary hemostasis * Inhibition of vitamin K epoxide reductase * Prevents recycling of vitamin K → depletion and inability to synthesis clotting factors 2, 7, 9, 10 (“1972”) * Relative vitamin K deficiency * First to be depleted: factor 7 → PT prolonged first

Answer 36

* Onset: delayed by 3-5 days post-ingestion * Anorexia * Lethargic, exercise intolerance, weakness * Pale MM * Dyspnea, tachycardia * Petechiae, ecchymoses, hematomas * Bleeding into any body cavity possible – affects the clinical presentation * Brain * Anterior chamber * Thorax * Abdomen/GIT * Joints

Answer 37

* Asymptomatic * Decontamination: induce emesis, A/C * Bloodwork: PCV/TP, (a)PT/(a)PTT * Antidote: Vitamin K1 (phytonadione)** * Give with fatty meal * Option 1: start Vit K1 treatment** * Duration: 21-28 days for SGARs * Check PT 48-72 hrs after last dose * Asymptomatic animal * Option 2: unsure if animal was exposed * Baseline PT → re-check in 48-72 hours * If normal after 72 hours: no treatment required * Start Vit K1 if PT is prolonged

Answer 38

* Symptomatic animal * Decontamination contraindicated * Immediate goal: stabilize animal * Hemorrhage ± anemia**: FP, FFP contains clotting factors * Whole blood – cross match * Autotransfusion * Oxygen Once stabilized → give antidote * Treatment duration: 28 days for SGAR * Imaging depending on location of bleeding * Fluids, supplemental O2 * Bloodwork: PCV/TP, PT/PTT * Close monitoring q 6-12 hr until normal

Answer 39

* Diagnosis usually made clinically * History of exposure, compatible clinical signs, prolonged PT/PTT*** * PT: extrinsic + common pathways (includes factor 7) * PTT: intrinsic + common pathways (includes factors 2, 10 Differential diagnosis * Prolonged PT/PTT: severe liver failure, DIC, vitamin K deficiency

Answer 40

* Toxicity: oral LD50: 20-40 mg/kg BW for most species * Contact with stomach acid** → release of phosphine gas * Differences * ZP: pH <4 * AP, MP: neutral pH * Phosphine gas: * Extremely irritating * Oxidative damage to multiple organ systems * Liver, kidney, lungs, heart, brain

Answer 41

* Onset: as soon as 15 minutes post-ingestion * Severe GI distress: vomiting, diarrhea ± hematemesis, hematochezia * Animals that cannot vomit are at higher risk** * Horses: colic signs** * Shock, pale MM → cardiovascular collapse, arrythmias * Profuse sweating * CNS: lethargy or hyperexcitation (tremors, seizures) * Pulmonary edema – tachypnea, dyspnea, cyanosis * Death within 3-48 hours

Answer 42

* Delayed onset kidney or liver failure is possible** * Characteristic odour: rotten fish or garlic (acetylene) * Human health risk * Clinical pathology * Dehydration * Elevated liver enzymes * Azotemia * Metabolic acidosis

Answer 43

* No specific antidote * Decontamination: well-ventilated area** * ZP: neutralize stomach pH** * Carbonate antacids * Dilute sodium bicarbonate * Tremor and seizure control * Monitoring: CBC/chem, blood gas, thoracic rads if PE suspected, liver chemistry including PT/PTT

Answer 44

* History of exposure and compatible clinical signs * PM lesions * Hemorrhagic GIT * Pulmonary edema * Hepatocellular necrosis and steatosis * Confirmation: detection of phosphine gas in stomach contents, vomitus, liver, kidney * Prognosis: symptomatic patients that survive 24 hours have a better prognosis

Answer 45

Phosphine gas is toxic to humans** * US EPA: highly toxic via inhalation * Hazardous at 0.3 ppm; death at 7 ppm * Tubing a horse, vomiting animal in clinic, etc * Symptoms in humans * Dizziness, lethargy * Nausea, vomiting * Cough, dyspnea * Liver failure symptoms: jaundice, delirium * Coma

Answer 46

Toxicity: acute lethal oral dose >2 mg/kg (dogs) * Clinical signs >0.1 mg/kg * >0.5 mg/kg → metastatic calcification * Disruption of calcium and phosphorous homeostasis * Hypercalcemia → dystrophic mineralization and multi-organ damage** * Relevant toxicokinetics: * Lipophilic * Long elimination half-life * EHC

Answer 47

Calcitriol actions: acts in liver/ kidney * Increased intestinal absorption * Increased tubular reabsorption * Increased bone resorption Hypercalcemia, hyperphosphatemia

Answer 48

* Onset: 12+ hours post-ingestion * Weakness, lethargy, anorexia * Vomiting, diarrhea (± blood) * PU/PD * Clinical pathological changes: hyperphosphatemia**, hypercalcemia**, azotemia, iso/hyposthenuria * 12, 24, 72 hours post-ingestion, respectively * Ca*P > 60 mg/dL: metastatic calcification** -kidney injury and renal failure

Answer 49

* Decontamination if not contraindicated Contraindicated: * Ca-containing fluids (LRS) * Thiazide diuretics * Dose-dependent treatment * 0.1-0.5 mg/kg: SC fluids, outpatient monitoring (tCa/iCa, P, PCV/TP, BUN, creatinine, electrolytes, UA) * >0.5 mg/kg: IVFT, baseline bloodwork and monitoring q24 hrs, cholestyramine * Clinically affected: * Hypercalcemia: IVFT, prednisone, furosemide * Hypercalcemic gastritis: GI protectants * CV monitoring: ECG, blood pressure

Answer 50

* History, bloodwork (R/O other causes of hypercalcemia) : Serum 25-hydroxyvitamin D * DDx: hypercalcemia → neoplasia, hyperparathyroidism (primary or secondary), kidney disease * Prognosis: * Good with early decontamination and supportive therapy * Guarded to poor with development of renal failure * Considerations: * Prolonged clinical signs * Chronic consequences of tissue mineralizatio

Answer 51

* PM lesions: soft tissue mineralization: kidneys, GIT, aorta, striated muscle * Histologic lesions: * Degeneration and necrosis of renal tubules * Calcium accumulation * Von kossa stain

management of the poisoned animal Flashcards

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