Final - Equine Tox

6 basic steps of Tx'g horse tox

1. Stabilise the patient when necessary2. Develop a clinical evaluation of the patient3. Decontaminate the patient if appropriate4. Enhance elimination of absorbed toxin if needed5. Administer an antidote if available and appropriate6. Provide symptomatic and supportive care as needed

Describe stabilization of the horse

- Keep the animal alive to be able to make a diagnosis- Address immediately life-threatening conditions- Procedures involved are basic medicine

4 things that need to be determined during your clinical eval of horse tox

a) Determine what is wrong with the patientb) the severity of the conditionc) treatment requirementsd) how aggressive treatment should be

5 things clinical eval is based on

a) History (which questions to ask the owner?)b) Physical examinationc) Basic diagnostic test as indicatedd) Dosage calculation if the amount of toxin is knowne) Occasionally environmental investigations will be necessary

Describe decontamination

- Decrease the amount of toxin absorbed into the body- Only indicated when unabsorbed toxin is still present in or on the body, or in the GI tract- Oral, dermal or gastrointestinal decontamination

3 contraindications of gastric lavages

a) Caustic or corrosiveb) A volatile petroleum hydrocarbonc) Increased risk of gastric perforation

3 complications of gastric lavages

a) Aspirationb) Trauma to nasal passages, oesophagus or stomachc) Inappropriate placement of the nasogastric tube into the lungs

Tx of corrosive or caustic substance tox

- Immediate dilution: "dilution is the solution"- Admin water or very moist foods- Chemical neutralisation (such as vinegar for alkalis and bicarbonate for acids) is discouraged- Activated charcoal is NOT useful for acid or alkali ingestion- Sucralfate can be used to protect oesophageal and gastric erosions- Stabilisation includes signs such as respiratory distress

3 contraindications of activated charcoal

a) Perforated GI tractb) Severe dehydration or electrolyte imbalancesc) Caustic or corrosive agents

3 complications of activated charcoal admin

a) Osmolarity changes and possibly hypernatremiab) Constipation (uncommon)c) Aspiration

What is a cathartic

substance that accelerates defication

5 contraindications of cathartics admin

a) Already has diarrhea or is likely to get diarrheab) Is likely to develop colic from the toxinc) Has a GI obstruction or blockaged) Is dehydrated or has electrolyte imbalancese) If the toxin is osmotically active

3 complications of cathartic admin

a) Colic, excessive diarrhoeab) Dehydration and electrolyte imbalancesc) Magnesium intoxication (b/c many are Mg based)

When is enhanced elimination indicated?4 ways this is this done?

Indicated when systemically absorbed toxin remains in the bodya) Diuresisb) Repeated doses of activated charcoal (b/c enterohepatic circ)c) Ion trapping (alter urinary pH)d) Chelation (altering the diffusion gradient for metal or metalloid toxins)

What is the antidote for the following toxins:a) amitrazb) anticoag't rodenticidec) benzodiazepinesd) black widow bitee) botulism

a) amitraz = yohimbineb) anticoag't rodenticide = whole blood, plasma or serum, Vit Kc) benzodiazepines = flumazenild) black widow bite = latrodectus (this is the scientific name according to Fernandez???)e) botulism = antitoxin

What is the antidote for the following toxins:a) bracken fernb) carbamatesc) cholecalciferold) cyanidee) digitalis

a) bracken fern = thiamineb) carbamates = atropinec) cholecalciferol = bisphosphonates or calcitonind) cyanide = Na nitrite or Na thiosulfatee) digitalis = digoxin immune Fab

What is the antidote for the following toxins:a) ethylene glycolb) Fec) metalsd) NSAIDse) opiods

a) ethylene glycol = ethanolb) Fe = deferoxaminec) metals = chelators (BAL, Ca EDTA)d) NSAIDs = misoprostole) opiods = naloxne

What is the antidote for the following toxins:a) organophosphatesb) scorpian bitesc) coral snake bited) rattlesnake bitee) tetanusf) xylazine

a) organophosphates = atropine and 2-PAM (pralidoxime)b) scorpian bites = centruroidesc) coral snake bite = micruroides (again, Fernandez says there isn't one)d) rattlesnake bite = antivenome) tetanus = antitoxinf) xylazine = yohimbine, atipamezole

Describe the pathophys of ionophore tox

- Ionophores bind to cations > Disruption of transmembrane ion gradients and electrical potentials- Especially detrimental in excitable cells (eg. nervous tissue, cardiac & skeletal mm)- Although main effects are on cardiac and skeletal muscles, neurologic or neuromuscular dysfctn is often observed

MOA of ionophore tox

bind to sarcolemnal membranes > influx Na and efflux of K > increased Ca influx > excessive uptake of Ca by mitochondria > mitochondrial damage > decreased cellular energy > mm necrosis (esp myocardium)

What is seen on neuro exam w/ ionophore tox?

- Normal mm tone, mentation, responses to pain,anal and tail tones- No cranial nerve deficits and interact reflexes- Unable to attain sternal recumbency

What is seen on clin path w/ ionophore tox?

- Leukocytosis with neutrophilia- Hyperglycemia- Increased CK and AP

What is seen on necropsy w/ ionophore tox

severe neuronal vacuolisation

Where are blister beetles found?What is the toxic agent?

- found on alfalfa (July - Sept)- contain cantharidin

CSs of blister beetle tox

- abd pain and colic- Depression and often submerges muzzle in water- Congested membranes- Increased heart rate, sweating- Bloody diarrhoea, potential hematuria

What is seen on clin path w/ blister beetle tox

- Increased PCV and hypoproteinemia- Neutrophilic leukocytosis- Increased blood urea nitrogen (BUN)

Describe the effects of cantharidin tox

- Causes GIT and UT blisters. - Direct effects on cardiac muscles (myocardial necrosis)- The exact mechanism of action is unknown- Cantharidin does cause an increased mitotic rate in epithelial cell cultures- Acantholysis and vesicle formation occur as a result of disruption of cell membranes through interference with oxidative enzymes

7 other toxicities assoc w/ hay

a) Red cloverb) Alsike cloverc) Botulismd) Mouldse) Rough maturef) Tall fescueg) Rye grass staggers

CSs of seasonal pasture myopathy (atypical myopathy)

- muscle weakness, stiffness, trembling- dark urine- periods of recumbency- colic-like signs

Pathophys of seasonal pasture myopathy

- Ingestion of box elder seeds (occurs in fall)- Degeneration and necrosis of mainly type 1 muscle fibres- Increased lipid in the muscle fibres- Deficiency of several mitochondrial acyl-CoA dehydrogenases (MADD) that utilise flavin adenine dinucleotide as cofactor

Describe MADD (multiple acyl-CoA dehydrogenase deficiency)

- involved in Beta-oxidation, AA and choline metabolism- Inhibited by a toxin named hypoglycin A (found in the box elder trees in the US and the sycamore maple tree in Europe)- Rapidly metabolised into active metabolite

Dx of MADD

- Hx and CSs- lab findings

What is seen on clin path w/ MADD?

- elevated muscle enzymes (CK most prominent)- decreased arterial blood oxygen (associated with deterioration of clinical signs and death)- Most important findings: elevated concentrations of acyl-carnitines in serum and abnormal organic acids in urine

Tx of MADD

- IVF- mulit-Vit injections- antioxidants- anti-inflammatories- restore Ca balance- Carb admin (oral)(Note: resp distress assoc w/ poor outcome)