1
Q
DAMNIT
A
- Degenerative, Developmental, Dementia
- Anomalous, Anatomic, Allergic, Autoimmune
- Metabolic, Mechanical
- Neoplastic, nutritional
- Inflammatory, infectious, immune medated, idiopathic, Ischemic
- Toxic, Trauma
2
Q
5 Steps to Emergency Stabilization
A
- Assess & Maintain Adequate Respiration
- Assess & Maintain Adequate Cardiovascular Function
- Control CNS Stimulation
- Control CNS / Respiratory Depression
- Control Temp
3
Q
How to Assess & Maintain Adequate Respiration
A
Resp. rate, depth, pattern, noises
Place patent airway
• endotracheal tube or tracheotomy
Adequate ventilation complications
• Ventilatory failure of patient
• Hypoxia due to interference w/ O2 absorption
• Bronchospasm or bronchoconstriction
Prevent Aspiration
• use cuffed endotracheal tube
4
Q
How to Assess & Maintain Cardiovascular Function
A
4 Step Fluid Resuscitation Plan • Hypotension / Hypertension • Acid base / Electrolyte / Elemental disturbances • Cardiac disturbances (ECG) • Reassess
5
Q
How to Control CNS Stimulation
A
o Control or minimize tremors & seizures
o Can be life threatening
o Use anticonvulsants, sedatives, or anesthetics
o Diazepam or Midazolam – first choice, tremors & seizures
o Methocarbamol – multiple routes, good for tremors, used for Pyrethrin toxicity
o Acepromazine – good to lower BP & control hyperactivity, monitor HR & BP
6
Q
How to Control CNS & Respiratory Depression & Temperature Change
A
Control CNS / Respiratory Depression
o Naloxone – reverse opioid overdose (Can give orally)
o Atipamezole - reverse Alpha 2
Control Temp
o Correct cause of temp change first
o SLOWLY cool patients to 102.5-103.5
7
Q
6 Goals in a Toxicology Case
A
o Emergency Stabilization / Life Support o Plan of Attack (Working Dagnosis) o Decontamination o Symptomatic & supportive care o Facilitate removal after absorption o Client education
8
Q
Normal TPR for Dogs
A
Temperature:
• 99.5-102.5
heart rate/pulse:
• 60-120 bpm
Respiratory rate:
• 10-30 rpm
9
Q
Dangerous pH’s
A
< 3
> 11
10
Q
Normal TPR for Cats
A
Temperature:
• 100-102.5
Resting heart rate/pulse:
• 110-130 bpm
Respiratory rate:
• 20-30 rpm
11
Q
Safety Factor for Toxicity
A
o for animals that toxicity was not studied
o Reduce LD50 by 10 for toxic dose
12
Q
Topical Decontamination
A
Dry
• Brush, vacuum, shave THEN bathe
Liquid H2O Soluble
• Bathe w/ warm H2O & mild detergent
Fat Soluble
• Use “hand-degreaser” -> bathe w/ mild detergent -> rinse
13
Q
Ocular & Inhalation Decontamination
A
Ocular Exposure
o Flush for 15-20 mins
o Monitor for symptoms
Inhalation Exposure
o Remove animal from environment
14
Q
Options to decontaminate oral exposure
A
Dilution
• Dilutie w/ milk, water, or egg whites
• Flush rostrally
Emetics
• Emetic -> after ~45 mins give an anti-emetic or pro-kinetic -> give activated charcoal
• Don’t use on rodents, rabbits, horses, ruminants
15
Q
Situations not to give an emetic in
A
- Corrosive agents
- Hydrocarbons-volatile
- Symptomatic or soon to be
- Already vomited or GI empty
- Brachycephalic breeds
- Medical conditions: megaesophagus, laryngeal paralysis, risk of aspiration pneumonia, recent surgery
- Toxicant/drug has anti-emetic properties
16
Q
Choices of Emetics for Dogs
A
- Apomorphine hydrochloride
- Ropinirole ophthalmic solution
- Hydrogen peroxide 3%
Do not use
o Syrup of ipecac
o Salt
17
Q
Apomorphine hydrochloride
A
o Triggers dopaminergic receptors o IV o Immediate & short duration o Only give 1 dose o Side Effects: persistent Vs & nausea, resp & CNS depression
18
Q
Ropinirole ophthalmic solution
A
o Triggers dopaminergic receptors
o Can give 2nd dose 20 mins later
o Side Effects: prolonged Vs & nausea, tachycardia
19
Q
Hydrogen peroxide 3% as Emetic
A
o At home use not clinic
o Don’t use in cats (necrosuppurative hemorrhagic gastritis)
o Onset 5-15 mins
o Duration: 30-45mins
o 1mL/lb
o Stimulates gastric mucosal sensory receptors -> vomiting center
o Side Effects: Ds, prolonged Vs, lethargy
o Can cause esophagitis & hemorrhagic gastroenteritis
20
Q
How to get cats to vomit
A
o Xylazine IM o Dexmedetomadine IM o Hydromorphone SQ o Onset: 2-20 mins o Side effects: sedation
21
Q
Gastric Lavage
A
- Orogastric tube -> oral fluids -> aspiration of content
- Instill fluids & THEN before tube removal, instill activated charcoal
- Use when emetics are unproductive or contraindicated
- Only material same or less than diameter of tube will come out
22
Q
Enemas & Whole Bowel Irrigation
A
Enemas
• Remove toxin from distal GI
• Not common or useful in many tox cases
• Avoid hypertonic sodium phosphate enemas
Whole Bowel Irrigation
• Clean the entire bowel
• Not common
• Takes a long time & sedation
23
Q
Surgical Endoscopy
A
- Foreign bodies
- Persistent material
- Consider stability of patient, cost, etc
24
Q
Activated Charcoal
A
- Binds non-specifically & prevents absorption
- 1g/Kg
- Combine w/ cathartic
- Can give multiple doses
- Rapid admin = V so administer over 1-2hrs
- Patient should be well hydrated
- Can cause hypernatremia, hypermagnesemia, hyperosmolality
- Don’t combine w/ oral drugs (inhibit absorbtion of med)
25
Basics of Cathartics
* give w/ 1st dose of activated charcoal
* accelerate the expulsion from the GIT
* osmotic induced fluid retention
* fluid volume causes stimulation of GI motility
* make sure patient is well hydrated
* saccharide (sorbitol)
* saline cathartics (bad choice)
26
Side Effects of Cathartics
* Volume depletion
* Hypotension
* Electrolyte imbalances (saline cathartics)
* Diarrhea
* Renal
* CNS depression
27
Cholestyramine
* binds weak acidic compounds
* binds to bile acids in intestine and forms an insoluble complex excreted in feces used for compounds that undergo enterohepatic recirculation or are trapped in bile
* use unflavored, no xylitol
28
Intravenous lipid therapy/emulsion/rescue
* efficacy not well documented. Lots of case reports
* no controlled studies
* Last resort
* May enhance lipid-soluble toxin absorption from GIT
29
Facilitate Removal After Absorption by Altering Metabolism
o Ethylene glycol (Pase 1 & 2)
o treat w/ ethanol or fomepazole
o inhibitors of alcohol dehydrogenase
30
Facilitate Removal After Absorption by Enhancing Excretion Rate
Diuresis
• Works on toxin in plasma, non-protein bound, non-lipohilic
```
Ion trapping in urine
• Usually don’t use
• Can cause worse acid/base disturbance
• Acidify w/ ammonium chloride
• Alkanize w/ sodium bicarbonate
```
31
Facilitate Removal After Absorption by Direct Removal
o Chelation therapy
| o hemodialysis
32
Cotton Plant
* Cotton plant – Gossypium
* Is very good protein, nutrient, fat, fiber, & energy
* Protein = 26-40%
33
Gossypol Basics & Toxicity
o Most abundant pigment in cottonseeds roots & stems
o Different strains vary
Toxicity
• “historical”
• cardiac toxin
• free unprocessed seed – potentially toxic
• processed - not toxic
• acute toxicosis – rare
• more likely to be due to accumulation / chronic
34
Gossypol; Animals Affected & Mechanism of Action
Animals Affected
• Immature ruminants
• Monogastrics
• Mature ruminants are pretty resistant
Mechanism of Action
• Lipid soluble
• In bile & feces as gossypol-iron complex
• Disruption of intra & extracellular K+ -> decrease K -> impair cardiac function\
35
Gossypol; Clinical Signs & Lesions
```
Clinical Signs
• Abrupt appearance
• Sudden death
• Heart failure
• Drop in production
• Anemia
• Effusion, edema
• Decrease male & female fertility
```
```
Lesions
• Icterus – liver & hemolysis
• Anemia
• Hemoglobinemia/uria
• Abomasitis
```
36
Gossypol Diagnosis
* Access to cottonseed
* Heart failure
* Analyses of free gossypol in diet
* Tissue testing
37
Gossypol Treatment
Acute
o Decontaminate
Chronic
o Remove source or dilute
o Treat for heart failure
o Supplement w/ vitamins, iron, protein
38
3 Ice Melts & Toxic Effects
Potassium chloride
o Increase K ->
o Weakness & cardiac issues
Magnesium Chloride
o Increase Mg ->
o Hypotension, cardiac issues, weakness, neuromuscular issues, low Phosphorous
Sodium Chloride
o Increase Na ->
o Tremors, PU/PD, seizures, vomiting
39
Basics of Ionophores;most common drugs
* Can be found in food additives
* Most commonly Monensin or Lasalocid
* Affects cows, sheep, poultry, goats, swine
* Used to alter microflora, increase feed efficiency, decrease lactic acidosis, & as a coccidiostat
40
Reasons for Ionophore Toxicosis
o Access to ionophores by non-target/susceptible species like horse, dog (acute)
o Mixing / math errors (acute; subacute: few days)
o Almost always history of recent feed change, 12-72 hrs
o macrolide antibiotics can make toxicosis 4 fold
41
Ionophores Mechanism of Action; part effected in each species
o Lipid soluble – limited but rapid absorption
o Metabolized by liver -> bile -> feces
o Small amounts go systemically – POTENT
o no long- term sequestration in tissues
o Cardiac muscle: cow, horse, poultry, camelids
o Skeletal muscle: swine, sheep, dog, cat, poultry, camelids
o Punches hole that allows Na+ & Ca++ in & K+ out, -> decrease oxidative phosphorylation -> myofiber necrosis
42
Ionophore Toxicosis Clinical Signs Initially & Later (specific drugs)
Initial
• GIT (12-72 hr)
• Partial to complete feed aversion/anorexia within 24 hrs
• diarrhea
• Weakness, ataxia, depression occurs up to days or later
Later
• Heart: drop dead / left and right heart failure
• Paresis / paralysis
• dyspnea, respiratory failure
• Salinomycin & Lasalocid affect nervous system depression
43
Ionophore Toxicosis Clin Path
```
o Non-specific or non-consistent
o Increase bilirubin
o Increase CK, LDH
o Increase troponin
o Myoglobinemia/uria (not common)
```
44
Ionophore Toxicosis Lesions & Diagnosis
```
Lesions
o None or subtle
o L/R heart failure
o Pale streaking of skeletal muscle
o Acute tubular necrosis of kidney
o Centrolobular necrosis (liver)
o Axonal degeneration of nerves/spinal cord
```
```
Diagnosis
o Recent feed change
o Appropriate signs
o Feed analysis
o Tissue samples (specifically heart in horses)
```
45
Ionophore Toxicosis Treatment & Prognosis for Asymptomatic & Symptomatic Patients
o Remove source
```
Asymptomatic:
• Decontaminate:
• SA: emesis, AC+ cathartic, gastric lavage, Vit E + Se, IV lipid rescue
• LA: mineral oil and AC, Vit E + Se
• Monitor daily for 5-7 days at least
```
Symptomatic:
• treat symptoms
• most likely to die if heart failure
• more likely to survive if only muscle damage
46
Basics of Macadamia Nuts
* unknown toxic principal, mechanism, or system affected
* only nut is toxic
* one kernel weighs 2.5-5g
* excellent prognosis
* recovery in 24-48hrs
47
Macadamia Nuts Toxic Dose & Treatment
Toxic Dose
o Unsure
o Go by the rule 1 nut/kg of BW
```
Treatment
o Decontamination thru Emesis AC
and cathartic?
o Monitor temp and hydration
o Monitor for pancreatitis
o Methocarbamol if tremors
o Bulk diet to encourage motility
```
48
Grapes Toxicosis basics; potential toxins
* All grape types & seeds toxic
* Cooked/processed is controversial
* Jelly or wine not toxic
* Affects DOGS, cats, ferrets
* Any dose is toxic
* Causes renal dz
* Variable whether dog will succumb or not
* potential toxin = tartaric acid & potassium bitartrate (also in cream of tarter & tamarinds)
49
Grape Toxicosis Clinical Signs, Pathology, & Lesions
```
Clinical Signs
o Non-specific
o w/in 16-24hrs of ingestion
o Vomit w/in 2hrs -> most likely develop renal dz if not treated
o Diarrhea
o Anorexia, lethargy, abdominal pain
```
```
Pathology
o Azotemia
o Hyper-electrolytes
o Polyuria first then anuria (if there is pee there is hope!)
o No crystals
```
Lesions
o Proximal tubule degeneration & necrosis
50
Grape Toxicosis Treatment for Asymptomatic & Symptomatic Animals
Asymptomatic
• Decontaminate w/ emesis, AC, & cathartic
• Fluid therapy
• Diurese to enhance renal excretion & GFR
• Monitor
• Prognosis is great if caught early!
```
Symptomatic
• Fluid therapy
• Phosphate binders
• Monitor
• Dialysis or transplant
• Many will recover over time but expensive
```
51
Basics of Vitamin D Toxicosis & What forms an animal may get ahold of
* Toxic to small animals
* Can affect large animals but not common
* Young animals more susceptible
* Need to know exact name/form due to different T1/2, onset of action
Cholecalciferol (Vit D3) rodenticide
o D-con
o Could have anti-coagulant or not
Human meds
o Calcitrol
o Dovonex
o Vitamin supplements
Feed/math mixing errors
52
Mechanism of Action for Cholecalciferol & Vit D Meds
```
Mechanism of Action Cholecalciferol
o Deposits in fat tissue ->
o Can stay in fat for ~2mo ->
o Absorbed in small intestine ->
o Liver ->
o Kidney
o Can take 12hrs - 5 days to see toxicosis
o Dose dependent
```
Mechanism of Action Vit D meds
o Onset < 3-6hrs
o Dose dependent
53
Clinical Signs Due to Vit D Toxicosis
Acute & persistently elevated Ca & P
• Due to increased Ca & P absorption from GI
• Increased osteoclastic activity in bone
• Increased Ca reabsorption by distal renal tubules
```
First signs (due to increased Ca)
• GI, Nervous system, Anorexia, increased urination
```
Later (due to mineralization)
• Increased GI & Nervous system issues
• Dyspnea, exercise intolerance
• Renal issues, abdominal pain, PU/PD
54
Clinical Pathology of Vit D Toxicosis
o Occur before symptoms
o Hypercalcemia
o Hyperphosphatemia
o Ca x P > 60-70 mg/dl
Later
• Azotemia, acidosis, hyperkalemia
• Hyposthenuria, proteinuria, casts, glucouria
• Medullary washout, nephrogenic diabete insipidus
55
Gross & Microscopic Lesions of Vit D Toxicosis
Gross
• Mineralized tissue (kidney, lung, arteries)
• Often not apparent
Microscopic
• Mineralization / degeneration & necrosis
• Hypertrophy & hyperplasia of parfollicular cells of thyroid
56
Six Parts of a Signalment
* species,
* breed,
* age,
* sex,
* weight,
* reproductive status
57
Normal TPR Horse
Temp
• 99 to 100.5
Pulse
• 28-40
Resp
• 8-16
58
Normal TPR Cow
Temp
• 100-102.5
Pulse
• 40-80
Resp
• 10-30
59
How to Assess Hydration Status
Base
• Packed Cell Volume, Total Protein
Other
• BUN, Creatinine
• Lactate, Glucose
• USG, Urine Output, BW
60
Essential Equipment for Necropsy
```
o gloves
o sharp knife, and equipment to keep it sharp (stone/steel)
o tissue forceps and scissors
o saw (or hatchet, ax or cleaver)
o shears
o fixative and containers
o sterile syringes, needles, whirl packs
o pen
o camera
```
61
Gastric Lavage Technique
* tube length = tip of nose to 9th intercostal space
* place speculum to prevent chewing on tube ->
* insert tube w/ head in normal position ->
* lower head ->
* instill fluid & AC at 5-10ml/kg
* allow fluid to flow out or suction out
* repeat 8-10 times
62
How many lbs in Kg
1kg = 2.2lb
63
PPM or Parts per Million
PPM = mg/kg = 1 mg/L
64
gallon to quarts to pints to cups
1 gallon = 4 quarts = 8 pints = 16 cups
65
Cups to oz
1 cup = 8 ounces
66
tsp & tbsp to ml
1 tsp = 5 mL
| 1 tbsp = 15 mL
67
oz to g or ml
1 ounce = 28 g or 29 ml
68
tons to lbs
1 ton = 2000 pounds
69
liters to quarts
1 liter = 1 quart;
70
GOSHDARNIT
```
Causes of hypercalcemia
o Granulomatous
o Osteolytic
o Spurious
o Humoral hypercalcemia of malignancy, Hyperparathyroidism, Hyperthyroidism
o Vitamin D toxicity
o Addison’s disease (hypoadrenocorticism
o Renal failure
o Neoplasia, Nutritional
o Idiopathic
o Tumor
```
71
Vit D Toxicosis Diagnosis
o History
o Hypercalcemia and/or hyperphosphatemia
o Hypercalcemic panel!
72
Vit D Toxicosis Treatment
Asymptomatic (normal Ca & P)
• Decontaminate: emetic, AC, cathartic
• May use cholestyramine instead of AC
• Monitor Ca, P, BUN, Cr, USG, PCV, TP every 12-24hrs for 4d
Symptomatic
• Lower Ca and/or P w/ Bisphosphonates (can take 2-4d)
• Fluid therapy 2-3x maintenance w/ physiologic saline, plasmalyte, or Norm R
• Prednisone/Prednisolone to promote calciuresis
• Low Ca/P diet
• GI protectant (sulcralfate) in necessary
• Oral P binders (aluminum hydroxide)
• Monitor every 3-6hrs until patient seems normal
73
Types of Ethylene Glycol & Crystals Produced
* Antifreeze
* Propylene glycol
* Methanol
* Diethylene glycol
* Calcium oxylate monohydrate crystals
74
Basics of Ethylene Glycol Toxicity & Pharmacodynamics
Toxicity
o All species susceptible
o Difficult to diagnose
o Need to intervene in cats w/in 3hrs dogs in 6-8hrs
Pharmacodynamics
o Rapid absorption (1-4hrs) -> decontamination difficult
o T ½ = 2-10hrs
o Metabolites are bad
o All gone in 16-24hrs
o >50% EG excreted in urine unchanged (osmotic diuretic)
75
Effects of Ethylene Glycol & it's Metabolites
Ethylene glycol, glycoaldehyde, glycolic acid
• CNS depression -> coma -> death
Metabolites (glycolic acid)
• Severe metabolic acidosis
All Metabolites
• Cytotoxic to renal tubular cells
Calcium oxalate monohydrate crystals
• mechanical obstruction
76
Chemical Path of Ethylene Glycol Metabolism
o Ethylene glycol ->
o Rate limiting step ->
o Glycoaldehyde (more toxic & short T ½) ->
o Glycolic acid (long T ½)
o Rate limiting step ->
o Glyoxylic acid (most toxic & short T1/2) ->
o Benzoic acid, oxalic acid, formic acid ->
o Hippuric acid, calcium oxalate monohydrate
77
Clinical Signs of Ethylene Glycol Tocicity
```
Stage 1
• 1-3 (or 12) hours
• CNS depression
• V, lethargy, ataxia, PU/PD
• Uncommonly death
```
```
Stage 2
• 6-12hrs
• Metabolic acidosis
• Worsen/lessen CNS depression
• Tachypnea
• PU/PD
```
Stage 3
• 6-24hrs or longer
• Oliguria/anuria
• Renal dz/failure
78
Clinical Pathology & Lesions of Ethylene Glycol Tocicity
```
Clin Path
o Not specific but consistent
o Most happen btwn 6-8hrs
o Monitor CBC/UA every 3hrs for 9hrs
o Increase osmolality
o Increase anion gap
o Metabolic aciocis
o Crystalluria
o Azotemia
o Hyperkalemia
o Hyperphosphotemia
o Isosthenuria
```
Lesions
o Proximal tubule degeneration & necrosis
79
PEACE PAIN
```
o Reasons for Hypocalcemia
o Phosphate enema
o Eclampsia
o Albumin is low
o Chronic renal disease
o Ethylene glycol toxicity
o Parathyroid deficiency
o Acute pancreatitis
o Intestinal malabsorption
o Nutritional (deficiency in vitamin D)
```
80
Diagnosis of Ethylene Glycol Toxicity
o Exposure history
o CBC, chem, UA, acid-base panel
Chemical analysis kit
• Often false (+) & (-)
• Use in 1st 12hrs
• Only shows exposure
o Put substance in freezer to see if it freezes
o CNS depression!
81
Treatment for Ethylene Glycol Toxicity
o Maybe decontaminate if VERY early exposure
Fluid therapy
• Diurese
• Help dehydration
• Support kidneys
o Monitor Chem, UA, electrolytes every 3-9hrs for 12-24hrs then daily for 3d
o Check for hypocalcemia every 4-6hrs for 24hrs
o Give ethanol or fomepazole
o Correct acidosis
o Correct Ca
o Get them to eat
82
Why treat Ethylene Glycol Toxicity w/ Ethanol or Fomepazole
```
o No metabolism of EG ->
o excreted unchanged in the urine –>
o no toxic metabolites
o Don’t use if in stage 3/when EG no longer around
o Do not combine
```
Ethanol
• competitive inhibitor of ADH
• Cheap / effective
• Few Side effects
fomepazole
• direct inhibitor of ADH
• More expensive
• More effective / fewer side effects
83
Propylene Glycol Basics, clinical signs, toxic dose, treatment
o “safer” antifreeze
o Fatalities rare!
o False positive on EG kit
```
Clinical Signs
• CNS depression
• Ataxia, incoordination, vomiting, PU/PD
• Acidosis (metabolized to lactate)
• Hyperosmolality
• No kidney problem!
• Heinz body anemia in cats (some dogs)
```
Toxic dose:
• 3-4× EG
Treatment
• hemodialysis if severe
84
Diethylene glycol, Methanol, & Ethanol
Diethylene Glycol
o No crystals
o Rare toxicosis in vet med
Methanol
o Only stage 1 & 2
o No renal component
o Treat w/ fluids & correct symptoms
Ethanol
o Only stage 1 & 2
o No renal component
o Treat w/ fluids & correct symptoms
85
Issue w/ fermented dough & Symptoms
o Yeast creates ethanol & CO2
o Can cause alchohol poisoning
Symptoms
• vomiting ataxia, incoordination, CNS depression, urinary incontinence, hypothermia,
• looks like stage 1 of EG
86
fermented dough risks & treatment
Risks
• Ethanol depression
• Bloat
Treatment
• Fast absorption -> decontamination not really a thing
• Cold water lavage with stomach tube – ice chips
• sometimes you might need to surgically remove
• Monitor for hypothermia
• Prevent aspiration – maintain airway –
ventilation
• IV fluids – maintenance, dilution, diuresis
Toxicology
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