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Small Animal Medicine and Surgery: Ethylene Glycol Poisoning
Terms in this set (65)
When do peak plasma levels occur with EG?
occur 3 to 6 hours after ingestion and remain significantly elevated for at least 12 hours,
When are EG levels usually undetectable?
after 48 hours post ingestiion
What happens to most of the EG ingested?
metabolized by the liver
What causes the actual problems with toxicity?
the metabolites formed by the liver
What effects do EG have?
- CNS depression
- vomiting (direct gastric irritation)
- osmotic diuresis.
What do the metabolites cause regarding problems or damage?
- severe high anion gap metabolic acidosis
- toxic renal tubular epithelial damage.
What occurs at the renal tubules and tissues?
calcium may combine with oxalate to form calcium oxalate crystals that precipitate out, obstruct the renal tubules and lead to ARF
What are 3 stages of EG toxicity?
Stage I - CNS Signs
Stage II - Cardiopulmonary Signs
Stage III Renal Signs
When does stage 1 occur?
30 minutes to 12 hours after ingestion of EG
What kind of acid base imbalance occurs in the first few hours?
severe normochloremic metabolic acidosis with a high anion gap
What are the CS of stage 1?
- alcohol intoxication:
• Focal or generalized seizures
Why is V+ commonly seen in stage 1?
1. EG is a gastric irritant
2. also from hyperosmolarity
What CS is commonly seen in dogs but not cats in the first 1-2 hours of ingestion? Why?
marked and progressive polydipsia → in response to the increase in serum osmolality
Why does a severe polyuria occur in both dogs and cats in stage 1?
What does the polyuria contribute to?
- secondary to a marked osmotic diuresis
- dehydration and hypoperfusion
What do animals look like after stage 1?
like they have gotten better
When does stage 2 occur?
12 -24 hours after EG ingestion
What are common CS of stage 2?
Tachypnea and tachycardia
**pulmonary edema despite being a common finding on necropsy, does not cause clinical signs.
What marks the final stage of EG toxicity?
Establishment of oliguric renal failure
When does stage 3 occur in cats? in dogs?
1. 12 to 24 hrs (cats)
2. 48 to 72 hours (dogs)
following ingestion of EG.
Why do CS fo stage 3 seem to appear faster in cats then in dogs?
produce more oxalates than dogs as they metabolize EG more rapidly
When do we see most pets with EG toxicity?
What are CS of Stage 3?
Why may seizures occur?
• oliguria or anuria
• Renal pain maybe detectable
• seizures may occur secondary to uremia or hypocalcemia
What might be found on CBC?
Describe the serum biochemistry profile?
1. Metabolic acidosis characterized by a high anion gap.
2. Hypocalcemia is seen in about 50 % of affected dogs and cats.
6. Hyperglycemia ** common
How common is hyperglycemia?
very common, approx 70%
What are some reason why hyperglycemia may occur? 2
1. inhibition of glucose metabolism by aldehyde metabolites
2. from physiologic stress
What is a consistent finding on UA?
- Calcium oxalate crystalluria
- as early as 3 hours after ingestion in cats
- by 4-6 hours after ingestion in dogs.
What type of crystals are more common?
monohydrate crystals (picket fence or dumbbell shaped)
What does the presence of . Dihydrate crystals - "Envelope shaped" indicate in dogs and cats?
- can be normal in dogs and cats
- if there is support for ARF and large numbers are present ethylene glycol should be considered.
What USG may be observed?
Isosthenuria - may be observed as early as 3 hours after EG ingestion
What are other possible findings on a UA in addition to the USG and Crystals?
1. Glucosuria secondary to injury to the proximal tubules may be seen.
4. renal epithelial cells
5. cellular and granular cast
Why is early dx of toxicity challenging?
1. nonspecific signs
2. history of ingestion is often not available
****YOU MUST maintain a "healthy" high index of suspicion for this toxicity
What are some key features that may aid in a more rapid dx of EG poisoning?
1. clinical signs of:
• polyuria, polydipsia
2. in combination with a metabolic acidosis characterized by a high anion gap
4. calcium oxalate monohydrate or dihydrate crystalluria,
5. hyperosmolality (if available)
What should you minimum data base include?
- serum biochemistry
- ideally a venous blood gas determination with ionized calcium included.
What are some specific diagnostic aids?
1. Measurement of Serum Osmolality
2. Metabolic Acidosis
3. EG SERUM Detection
4. Renal Ultrasonography
5. Renal Biopsy
Describe the metabolic acidosis?
- characterized by a high anion gap due to the presence of unmeasured serum anions
- May not be evident early on but will be in the later stages.
What is the Glycol Test kit?
- EG SERUM Detection
- use in dogs and appears to accurately measure serum EG concentrations ≥ 50 mg/dl
- false-negative results in dogs, despite ingestion of lethal doses of EG, have been documented.
When is this test kit most useful?
- first 12 hours after ingestion
- but may help document exposure up to 24 hours after ingestion.
Can you use this test kit in cats?
not sensitive enough
If you plan to use the kit, when do you need to use in relation to possible treatments?
- c) Blood samples for testing should be drawn before treatment is initiated
When can false positives occur with the test kit?
- with an additive in activated charcoal
- some anticonvulsants (diazepam).
What might you find on renal US in early stages? later stages?
- Increased cortical echogenicity is an early finding (within 4-6 hours of ingestion)
- in the later stages a distinct corticomedullary "rim sign" or "halo sign" may be seen
Describe the use of a renal biopsy?
will be diagnostic (acute tubular necrosis with calcium oxalate crystals within the renal tubules) although it is rarely needed to establish a diagnosis.
What are your goals for tx?
1. Prevention of further Absorption
2. Increase Excretion
3. Preventing Additional Metabolism
4. Supportive Care
What can you do to prevent further absorption?
When can you do this?
1. Induce vomiting → apomorphine or hydrogen peroxide
- if an animal presents within 1-2 hours of ingestion
2. Activated charcoal → not very effective at absorbing EG
3. Owners can induce V+, if they call you and should seek vet care
When is inducing vomiting contraindicated?
depressed or stuporous
What is needed in order to increase exretion?
1. Aggressive IV fluid therapy → Diuresis will also increase renal perfusion and help promote excretion of EG and its metabolites
2. Alkalinizing the urine also promotes glycolate excretion.
What kind of Intensive supportive care and monitoring is required?
- thermal support if hypothermic
- eye lubrication
-a well-padded bed
-turn patient if recumbent q 4 hours
What are methods to prevent further metabolism?
Inhibition of the enzyme alcohol dehydrogenase (ADH) responsible for initiating metabolism of EG
***cornerstone of specific therapy for EG intoxication
What specific antidotes available for EG intoxication?
2. 4- methylpyrazole
What is the best option for metabolism inhibition in cats? Why?
- because they metabolize EG too quickly for the doses of 4MP used in dogs to be effective
What dose of 4MP would be effective in cats?
Higher doses of 4MP (125 mg/kg)
if given within the first few hours of EG ingestion
Explain how ethanol works?
competitive inhibitor of ADH, with a higher affinity for the enzyme than EG.
What do you need to do with patient care if you use ethanol? Why?
Because of the CNS depression, patients will require very intensive monitoring and support.
How is ethanol best given?
continuous rate of infusion (CRI) rather than bolus administration
Explain how 4 MP works?
- a strong inhibitor of alcohol dehydrogenase
- is safe and effective
Why might 4MP be a more desirable form of treatment?
1. duration of activity of 4-MP is longer than for ethanol → allowing for a more practical dosing schedule
2. Does not cause CNS depression
( but more expensive)
DOSING OF 4MP
Dose for Dogs: initial loading dose: 20 mg/kg IV over 20 minutes followed by 15 mg/kg IV at 12 and 24 hours, and 5 mg/kg IV at 36 hours
Expensive - costs $7.25/ml; cost to treat a 15 kg is $90
What supportive care may be needed?
1. tx of hypocalcemia induced seizures or tetany
2. Nutritional support
3. Combat vomiting and anorexia
How could you tx the seizures or tentany?
1. Calcium gluconate at a dose of 0.5-1.5 ml/kg, administered slow IV to effect
2. conventional anticonvulsants → If ionized Ca 2+ is normal treat seizures with
What should you montor if giving Calcium gluconate?
Monitor an ECG while administering
What is the PX for recovery?
What determines the Px?
- once ARF has developed is very poor.
- In one study involving 36 dogs with EG intoxication treated with 4MP, all dogs that were azotemic at the time of presentation (18/36 dogs) died
- If animals present within the first 3-5 hours and are treated aggressively, the prognosis is good
11. What are the 3 stages of Ethylene glycol toxicity? What clinical signs are associated with each stage?
Stage 1 CNS depression → 30 minutes to 12 hours, drunk, Vomiting, severe normochloremic metabolic acidosis with a high anion gap, polyuria, polydypsia (dogs)
Stage 2 Cardiopulmonary → Occurs 12 -24 hours after EG ingestion
Stage 3 renal → oliguric renal failure , 12 to 24 hrs (cats) and 48 to 72 hours (dogs) following ingestion of EG
12. What findings will help direct you to a diagnosis of ethylene glycol toxicity in the early and late stages for this toxicity?
- CS of CNS depression
- ataxia, polyuria, polydipsia
- metabolic acidosis characterized by a high anion gap
- calcium oxalate monohydrate or dihydrate crystalluria
- hyperosmolality ( if available)
- in dogs EG test kit
- anorexia, vomiting
- azotemia, and oliguria or anuria.
- Renal pain maybe detectable
- seizures may occur secondary to uremia or hypocalcemia
- US evidence
- Ca ox cx in urine
- Aciduria, hematuria, renal epithelial cells, and cellular and granular casts
13. How will you treat
a) dog and
b) a cat with suspected ethylene glycol toxicity?
What general prognosis will you give the client of a pet with ethylene glycol toxicity?
A) 4MP + supportive care + diuresis
B) Ethanol + supportive care + diuresis
- depends when you see them
- if they come in soon after injestion, then with aggressive therapy and tx then Px can good
- if you see them and stage 3 has set in, with evidence of azotemia, then Px for recovery is very poor
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