Case overviews

Question 1

Acetaminophen toxicity

Answer 1

50mg/kg is toxic to cats, but dogs can safely get doses up to 150mg/kg.

Toxicity from the lethal synthesis of acetaminophen metabolite alters glutathione concentrations in hepatic and red blood cells.

Clinical signs: methemoglobinemia
Cats: anorexia, vomiting, salivation, lethargy, weakness, dyspnea, chocolate-colored urine and blood, facial and paw edema. Death occurs 18-36 hours.

Lab findings: methemoglobinemia, Heinz body anemia, increased ALT, ALKP and bilirubin. Metabolic acidosis

Prognosis is guarded to poor in cats

Question 2

Amitraz

Answer 2

alpha-1 and alpha 2 adrenergic agonist in tick/flea collars.

Clinical signs: CNS sedation, bradycardia, polyuria, pale MM, hypothermia, vomiting and respiratory depression.

Lab findings: hyperglycemia
Anticholinergics contraindicated in treatment of bradycardia.

Prognosis: fair

Question 3

Anticoagulant rodenticides

Answer 3

Antagonize vitamin K epoxide reductase. Depletion of factors II, VII, IX, X results in coagulopathy and hemorrhage.

Clinical signs: lethargy, vomiting, weakness, pallor, melena, epistaxis, hematemesis, hematuria, gingival bleeding, prolonged bleeding, dyspnea, sclerotic and conjunctival hemorrhage, lameness, joint swelling, bruising and hematomas. Acute death from hemorrhage in pleural cavity, abdomen, pericardial sac or mediastinum.

Lab findings: PT/PTT

Prognosis in non-clinical with rapid decontamination patients is excellent

Question 4

Avermectin

Answer 4

antiparasitic agents
MOA: GABA agonism

clinical signs: ataxia, behavioral disturbances, depression, hypersalivation, seizures, mydriasis, muscle tremors, recumbency, coma and death.

diagnosis made on history of exposure and clinical signs.

Treatment: decontamination, ILE therapy

Prognosis: guarded with prolonged recovery

Question 5

Bleach/household cleaners

Answer 5

Emesis and gastric lavage contraindicated.

Clinical signs: hypersalivation, vomiting and abdominal pain.

Treatment: milk or water

Question 6

Bromethalin

Answer 6

Pesticide that causes acute toxicity
MOA: uncoupling of oxidative phosphorylation in the CNS and liver mitochondria–> Increase ATP production–> Na/K ATPase activity –> loss in osmotic gradients and membrane potential in cells. This results in sodium influx into brain cells, resulting in cerebral edema.

Clinical signs: muscle tremors, hyperthermia, seizures, forelimb extensor rigidity (Schiff-Sherrington-like posture), ataxia, vomiting, respiratory paralysis, and death.

Diagnosis is made by history and clinical signs.

Treatment: early treatment to decontaminate. Once onset of symptoms, treatment is primarily supportive - manage seizures, elevate head 30 degrees and avoid compression of neck and jugular veins. ILE proposed - studies pending.

Prognosis: guarded to grave

Question 7

chocolate and methylxanthines

Answer 7

methylxanthines include caffeine, theobromine and theophylline. Half life up to 72 hours.
MOA: adenosine receptor blockages and increases cyclic adenosine monophosphate (cAMP), resulting in increase calcium concentrations in cells which increases muscular contractility.

Clinical signs include vomiting, diarrhea, hyperactivity, restlessness, ataxia, muscle tremors, cardiac arrhythmias, hyperthermia, seizures, coma and sudden death.

Treatment: decontamination with activated charcoal administration. Injectable beta blockers such as esmolol or propranolol for SVT, lidocaine to control ventricular arrhythmias. Consider U-cath because methylxanthines can be reabsorbed from the bladder and perpetuate toxicity. ILE has been successful in treatment of caffeine toxicosis.

Monitor: ECG, HR & BP

Question 7

Cholecalciferol

Answer 7

In numerous rodenticides.

MOA: Converted in kidneys to active vitamin D3, which promotes retention of calcium. Overdose leads to hypercalcemia, mineralization of blood vessels, kidneys (renal tubular injury), heart, and lungs.

Clinical signs: PU/PD, anorexia, V/D, hypertension, seizures

Lab work: hypercalcemia, hyperphosphatemia and azotemia

Diagnosis based on history, clinical signs and chemistry

Treatment: decontamination with activated charcoal, IVF to maintain renal perfusion, hydration and promote calciuresis. ILE may be effective
furosemide will produce rapid calciuresis
calcitonin, bisphosphate, clodronate.

Monitor: electrolytes, BUN/creatinine
Diet: low calcium
Guarded prognosis

Question 8

Ethylene glycol

Answer 8

Toxic dose in dogs: 4ml/kg, cats: 1.5ml/kg

MoA: EG is metabolized by the liver to glycoaldehyde, glycolic acid, glyoxalic acid, and oxalic acid. Oxalic acid forms insoluble calcium oxalate crystals which precipitates in renal tubules resulting in acute kidney failure.

Clinical signs depend on phase:
Initial phase (up to 12 hours post ingestion)- mild depression, ataxia, PU/PD, vomiting, anorexia, hypothermia and potential seizure
Second phase (12-24 hours post ingestion) - cardiorespiratory signs, tachycardia, tachypnea, severe depression, vomiting, azotemia, isosthenuria and AKI with oliguria by 24-72 hours post ingestion.

Lab findings: metabolic acidosis with severely increased anion gap. Increased osmolality. hyperglycemia, hypocalcemia, hyperphosphatemia and azotemia. U/A - glucosuria, renal tubular casts, isosthenuria, calcium oxalate crystalluria

Treatment: Fomepizole or 4-methylprazole or ethanol - alcohol dehydrogenase inhibitor directly competes with EG for alcohol hydrogenase –> prevents EG metabolism and allows it to be excreted unchanged. Hemodialysis can also be used if available. ILE considered because EG is highly lipophilic.

Prognosis: poor if already developed clinical signs. If cats are treated within three hours and dogs within 6 hours of ingestion, prognosis is guarded.

Question 9

Lead

Answer 9

MOA: nervous tissue demyelination and interference with GABA, cholinergic functions and heme synthesis

clinical signs: GIT and nervous system
vomiting, abdominal pain, diarrhea, anorexia and constipation. Neurologic (often as a result of cerebral edema): anxiety, odd behavior changes, seizures, ataxia, head pressing, polyneuropathy, opisthotonos, mydriasis and blindness

Diagnosis based on history and clinical signs

Lab findings: a large number of nucleated red blood cells, with evidence of severe anemia, anisocytosis, polychromasia, poikilocytosis, target cells, hyperchromasia, and potentially basophilic stippling (highly suggestive of lead toxicity). Blood lead level of 0.3-0.5 ppm is suggestive, > 0.6ppm is diagnostic. Urine lead levels > 0.75ppm

Treatment: emesis or endoscopy if possible. Surgical intervention may be necessary. activated charcoal will no be beneficial
IVF, thiamine supplementation and chelating agent (EDTA, D-penicillamine, dimercaptosuccinic acid, dimercaprol, succimer.
Supportive therapies for seizures, cerebral edema and GIT

Prognosis favorable for those who undergo chelation

Question 10

Lilies

Answer 10

The exact MOA is unknown - but proximal convoluted tubular necrosis occurs.

clinical signs: first 1-2 hours - vomiting, lethargy, anorexia
Over 1-3 days: PU/PD, glucosuria, azotemia, hyperphosphatemia

Treatment: decontamination with activated charcoal. fluid diuresis

Monitor for oliguria or anuria, may require dialysis

Prognosis: if timely treatment prognosis is excellent.

Question 11

Metaldyhyde

Answer 11

molluscicide (snail/slug killer) that is highly palatable.

MOA: unknown but acts on decreasing brain GABA, serotonin and norepinephrine resulting in convulsions

Clinical signs: seizures, hypersalivaation, muscle fasciculations, metabolic acidosis and tahycardia (hyperthermia of >108 F). Highly sensitive to light and sound. As toxicity progresses - initial CNS stimulation becomes CNS depression, bradycardia, respiratory failure, liver injury 3-5 days following exposure.

Diagnosis: history and clinical signs. Odor of acetaldehyde resembling formaldehyde.

Treatment: decontamination with activated charcoal, IFV, supportive care, anticonvulsants/muscle relaxants, sedatives. hemodialysis and hemoperfusion. Metaldeyde is poorly lipophilic, so ILE not considered.

Prognosis with supportive care is good.

Question 12

naphthalene and paradichlorobenzene (mothballs and moth repellant)

Answer 12

MoA: causes acute oxidative hemolytic anemia, heinz bodies, and occasionally methemoglobinemia.

Clinical signs: “mothball” odor, GI upset, vomiting, lethargy, weakness, collapse, icterus, brown colors MM, seizures.

Treatment: emesis +activated charcoal, IVF for diuresis, GI signs treat supportively with antiemetics and GI protectants. Blood transfusions if anemia affecting DO2.

Question 13

NSAID: ibuprofen, aspirin, naproxen, carprofen, meloxicam, deracoxib, firocoxib, piroxicam

Answer 13

MOA: inhibit COX and thereby prostaglandin production. Inhibition of gastric prostaglandins results in gastroenteritis, GI ulcer, GI perforation. Inhibition of renal prostaglandin can result in AKI.

Clinical signs: 4-6 hours depression, anorexia, vomiting, hematemesis, melena, ataxia, seizures, coma. AKI to follow

Diagnosis: history, clinical signs

Serum chemistry: azotemia, increased hepatic enzymes. possibly Heinz bodies in cats, metabolic acidosis and prolonged bleeding times. Aspirin = increase anion gap.

Treatment: ILE is possible, surgery if GI perforation, anticonvulsants if seizures present. decontamination and activated charcoal if recent exposure. Cholestyramine or activated charcoal. IVF to rehydrate, induce diuresis and support organ perfusion.
prostaglandin agonists (misoprostol) to aid in preventing GI ulcers
Proton pump inhibitors, sucralfate and H2 blockers. dialysis may be considered.

Prognosis depends on the drug and half life, ranging from excellent to grave depending on progression.

Question 14

Misoprostol

Answer 14

prostaglandin agonists

Can be used in overdose of cox inhibition (i.e. NSAID toxicity) to prevent GI ulcers

Question 15

organophosphates

Answer 15

Readily absorbed in skin and GIT and can cause irreversible inhibition of acetylcholinesterase activity.

MoA: Acetylcholinesterase is responsible for the breakdown of acetylcholine (Ach). When not broken down and there is an abundance of AcH, it can interfere with autonomic nervous system function.
Clinical signs: parasympathomimetic effects (muscarinic stimulation) such as salivation, lacrimation, vomiting, diarrhea, miosis, and bradycardia. Progresses to have nicotinic stimulation and then nicotinic blockade –> muscle twitching, seizures, respiratory depression, coma, and death.

Diagnosis: history, clinical signs

Treatment: decontamination (bathing animal), activated charcoal if ingested. Atropine combat muscarinic signs of toxicity.

Phenothiazine derivatives are not recommended.

Prognosis varies depending on agent and quantity of exposure.

Question 16

pyrethrines/pyrethroids

Answer 16

plant derivative used in flea and tick control.

Cats and birds are sensitive to acute toxicity. Safe range for dogs.

MoA:
Pyrethrins - delaying sodium channel closing resulting in repetitive nerve firing.
Pyrethroid - act as antagonists of GABA and glutamic acid.

Clinical signs: muscle tremors, hyperexcitability, hyperesthesia, hyperthermia, hypersalivation and less commonly V/D, CNS depression, generalized seizures.

Treatment: decontamination +/- activated charcoal if ingested. IVF, methocarbamol not to exceed 330mg/kg/day ILE has been successful in treating permethrin toxicosis in cats.

Prognosis is generally good if treated appropriately.

Question 17

Raisins, grapes, currants

Answer 17

AKI in dogs
MOA unknown but proximal renal tubular necrosis occurs.

Diagnosis: history and clinical signs.

Treatment: emesis and charcoal. IVF and monitoring for azotemia.

Prognosis: early decontamination is excellent with only 8.5% of patients developing AKI.

Question 18

Strychnine

Answer 18

restricted-use pesticide

MoA: antagonizes glycine (neurotransmitter) resulting in CNS excitation including spinal reflexes and striated muscles.

Clinical signs are rapid onset and begin within minutes of consumption and progress over 1-2 hours. Signs include anxiousness, muscle tremors, collapse, seizures, extensor rigidity, apnea and death.

Diagnosis: history and clinical signs

Lab work can confirm by analyzing stomach contents, urine or liver.

Treatment: emesis but may result in increased seizure activity. Activated charcoal to prevent further absorption. ILE is considered because strychnine is lipophilic. Anticonvulsant and anesthesia may be necessary to control seizures. Methocarbamol may also help. Ion trapping with IV or oral ammonium chloride may acidify urine and enhance urinary strychnine excretion.

Nursing: Keep patient sedate in a quiet room.

mortality rate 60%.

Question 19

Xylitol

Answer 19

MoA: in dogs, xylitol toxicity results in secretion of insulin resulting in severe acute hypoglycemia, ataxia, collapse, seizures. Because insulin also drives potassium, hypokalemia can also be observed. Xylitol can cause delayed acute hepatic necrosis and failure in 72 hours after initial recovery. Dogs who do not present for hypoglycemia are still at risk for hepatic injury.

Lab: hypoglycemia, hypokalemia, increased ALT, hyperbilirubinemia.

Treatment: decontamination. activated charcoal is not necessary because it does not effectively bind to xylitol IVF, maximize hepatic perfusion. BG monitor every 4-6 hours and supplement with IV dextrose. Hypoglycemia usually resolves within 24-36 hours. Antioxidant therapy may benefit from minimizing hepatic injury . Liver enzymes should be re-evaluated 48-72 hours post-ingestion to evaluate for hepatic failure.

The prognosis is generally excellent if the patient receives appropriate care and does not progress to hepatic failure. If the patient is in hepatic failure, the prognosis is poor.

Question 20

Zinc phosphide

Answer 20

active ingredient in mole and gopher powder and pellent rodenticide. Rotten fish odor.

MoA: In moist conditions, zinc phosphide undergoes chemical reaction to become toxic phosphine gas. Phosphine gas results in systemic oxidative injury, targeting brain, liver, lungs, heart and kidneys. Lethal dose 20-40mg/kg. Recent ingestion will worsen toxicity because of increased gastric acid secretion.

Clinical signs: vomiting, hematemesis, lethargy, abdominal pain. Abdominal distension, dyspnea. Progressive toxicity can include neurological signs, ataxia, hyperesthesia, and seizures.

Lab values: hypoglycemia, elevated liver enzymes, azotemia and metabolic acidemia.

Diagnosis: history with fishy or acetylene smell.

Treatment caution: treating staff around the patient’s vomitus is at risk of inhaling phosphine gas.

Emesis in a well-ventilated area, gastric lavage (controversial), sodium bicarbonate to alkalinize stomach pH, treat with antioxidant.

The prognosis is excellent.

Question 21

Zinc

Answer 21

pennies after 1983 have 97.5% zinc. Toxicity >100mg/kg.

MoA: Zinc in acidic environment like the stomach releases free zinc which can cause zinc salts. Zinc salts are caustic to GI tract and have corrosive effect. Zinc salts can lead to RBC oxidative damage.

Clinical signs: V/D, anorexia, and can progress to intravascular hemolysis (icterus) and anemia, pancreatitis, kidney injury, hepatic failure (icterus), and CNS signs.

Lab diagnostics: inflammatory leukogram, regenerative anemia, spherocytosis, heinz body formation, hyperbilirubinemia, azotemia secondary to tubular injury by hemoglobinuria, elevated liver enzymes, coagulopathy increased levels of serum zinc. radiographs will show zinc.

Treatment: decontamination via emesis, endoscopy, or surgery. Supportive care: IVF, gastro protectants, blood transfusions, chelation is considered controversial.

Prognosis is favorable.

Question 22

Refeeding syndrome

Answer 22

uncommon but potentially serious complications in malnourished patients.

MoA: reintroduction of nutrition results in rapid increase in insulin levels and other metabolic changes that result in shift of potassium, phosphorus, magnesium into the intracellular space.

Lab work: hypophosphatemia, hypokalemia, hypomagnesemia. Hypoglycemia and hyperglycemia also have been reported.

Clinical effects: muscle fatigue, weakness, intravascular hemolysis and possible cardiac and respiratory failure.

Treatment: gradual return to full RER over several days.

Monitoring: electrolytes

Question 23

Chronic valvular heart disease

Answer 23

Progressive degeneration of AV valves (most commonly left mitral valve).

Mild to moderate may not be associated with clinical signs.

Progressive - pulmonary edema, tachypnea, and dyspnea. Clinical findings may also include syncope, jugular vein distension, and mild hypothermia. Auscultations: pulmonary wheezes and crackles at the end of inspiration. Systolic heart murmur over on left apex over the fourth intercostal space; with intensity the murmur may radiate over to the right side of thorax. MM: cyanotic or grayish. Seere with effusion = muffled heart sounds.

diagnostics: radiographs to rule out bronchial disease. Left atrial enlargement early and then left ventricular enlargement with progression of disease. ECHO to confirm diagnosis.

Question 24

Esophagitis

Answer 24

Acute or chronic inflammatory disorder of esophageal mucosa. If severe, can cause perforation. Can also result in stricture formation.

Usually caused by ingestion of corrosive agent, foreign body, thermal burns, persistent vomiting, gastroesophageal reflux, or medication exposure (doxycycline in cats).

Clinical signs: gagging, anorexia, ptyalism, regurgitation, exaggerated swallowing motion, occasionally aspiration pneumonia

Diagnosis: history, clinical signs and diagnostics that rule out other causes. Endoscopy is diagnostic.

Treatment: soft food or withhold food 24-48 hours. Sucralfate, proton pump inhibitors (omeprazole), and H2 receptor antagonists (famotidine, ranitidine) have fallen out of favor due to limited effectiveness. Balloon dilation if a stricture is present.

Prognosis: excellent

Question 25

Esophageal obstructions

Answer 25

FB in area of esophagus that is least distensible, specifically thoracic inlet, heart base and lower esophagus.

Clinical signs: regurgitation, dysphagia, retching, neck stretching, gagging, ptyalism or painful swallowing (odynophagia).

Diagnostics: thoracic radiographs to reveal possible esophageal perforation, pneumothorax and pneumomediastinum.

Treatment: endoscopic removal is preferred if there is no perforation. If perforation into the thoracic cavity, exploratory surgery and thoracotomy are indicated. Antibiotics are indicated only if there is a perforation.

Pain management indicated.

Question 26

Megaesophagus

Answer 26

regional or diffuse dilation of the esophagus with minimal or non-existent peristalsis. Congenital or acquired.

If acquired, can be secondary to other disorders that affect neuromuscular function (myasthenia gravis, hypothyroidism, lead toxicity, immune-mediated polyneuritis, polymyositis, hypoadrenocorticism, systemic lupus and dysautonomia) or can be idiopathic.

Clinical sign: regurgitation +/- aspiration pneumonia, +/- secondary aspiration pneumonitis

Diagnostics: radiographs. CBC/chem, /ua, and specific testing such as acetylcholine receptor antibody testing for myasthenia gravis, free T4, serum lead levels, baseline cortisol or ACTH stimulation, muscle or nerve biopsies.

Treatment: treat underlying cause, symptomatic therapy. If secondary esophagitis - sucralfate and GI protectants

Question 27

Gastric Dilation Volvulus

Answer 27

gastric distension followed by malrotation (usually clockwise) - will include vessesls and spleen resulting in compression of vena cava and affecting venous return to the heart. Decreased cardiac output, blood pressure, tissue perfusion, affecting all organs including the heart. Progression will result in gastric necrosis and ischemic injury.

Clinical signs: non-productive retching, drooling, panting, abdominal distension, anxiety and collapse.

Diagnostic: right lateral abdominal radiograph. Pylorus normally at cranial ventral aspect of abdomen. With GDV, the pylorus is a cranial dorsal aspect of the radiograph.

Monitoring: ECG, CBC/Chem, blood pressure, lactate and thoracic radiographs.

Treatment: Reducing stomach size alleviates pressure on the vena cava and portal vein and improves cardiac output and blood pressure. Must be fluidly resuscitated prior. If not, a sudden reduction in stomach size can cause relative hypovolemia to worsen blood pressure.

Once stabilized, surgery to fix problem with gastropexy. W/O gastropexy, recurrent rate is as high as 80%.

Monitor for ventricular arrhythmia, hypoproteinemia secondary to gastric inflammation, GI losses of protein, acute inflammation resulting in negative acute phase protein response. Decrease in plasma proteins may lead to decrease colloidal oncotic pressure and delay wound healing, proinflammatory mediators + endotoxins, bacteria and tissue hypoxia = susceptible to sepsis.

Antimetics, gastroprotectants