QUESTIONS

1. Ethylene glycol is metabolized similarly to _______________ thus it is not surprising that animals show ataxia & CNs depression approx. 30 min after ingestion.  (Vomiting & PU/PD are also commonly observed during this time.)
    
2. What % of ethylene glycol is excreted unchanged by the kidney?
   
   a)  <1%          b)  5-10%          c)  25-50%         d)  >50%
    
3. The enzyme which acts on ethylene glycol to initiate the metabolism into toxic products is _______________.
    
4. The primary toxic metabolite of ethylene glycol is _______________ which contributes to acidosis & is directly toxic to renal tubular epithelium.
    
5. Which is the more toxic metabolite of ethylene glycol:
   
   OXALIC ACID         OR        CALCIUM OXALATE?
    
6. Approximately how long after ingestion does oliguria show up?
    
7. How is osmolal gap useful in the diagnosis of ethylene glycol toxicity?
    
8. How is anion gap helpful in the diagnosis of ethylene glycol toxicity?
    
9. At what point can ethylene glycol be measured in urine by in-house test kit?
    
10. How is ethanol used in the treatment of ethylene glycol toxicity?
     
11. How is 4-methylpyrazole used in the treatment of ethylene glycol toxicity?  Why can't it be used in cats?
    
    
    
    
     

ANSWERS

1. Ethylene glycol is metabolized similarly to ETHANOL thus it is not surprising that animals show ataxia & CNs depression approx. 30 min after ingestion.  (Vomiting & PU/PD are also commonly observed during this time.)
   
   
   
   
    
2. Ethylene glycol is excreted >50% unchanged by the kidney.  Our treatment goal is to see that more like 90% is excreted unchanged as it is the metabolites that wreak havoc.  Ethylene glycol blood levels peak approx 1-3 hours post-ingestion so you gotta work fast.
   
   
   
   
    
3. The enzyme which acts on ethylene glycol to initiate the metabolism into toxic products is ALCOHOL DEHYDROGENASE.
   
   
   
   
    
4. Accordeing to CVT, the primary toxic metabolite of ethylene glycol is GLYCOLATE (GLYCOLIC ACID) which contributes to acidosis & is directly toxic to renal tubular epithelium.  You could certainly argue for glyoxalate, though.
   
   
   
   
    
5. Oxalic acid promotes renal damage & contributes to acidosis.  Calcium oxalate, which results from interactions of oxalic acid with serum calcium, is of diagnostic significance only.
   
   
   
   
    
6. Oliguria shows up 48-72 hours post-ingestion in the dog & 12-24 hours post -ingestion in the cat.
   
   
   
   
    
7. Osmolality can be calculated by the equation:
   
   mOsm/kg = 1.86(Na+ + K+) + Glucose  + BUN  +  9
    -------    ----
       18       2.8
   
   Normally this comes out pretty close to the actually measured osmolality (Normal osmolality = 280-310 mOsm/kg w/a gap of <10 mOsm/kg)
   
   Because of all the ethylene glycol contributing to osmolality, the gap will be more like 50-100 mOsm/kg for 12-18 hours post ingestion.
   
   
   
   
    
8. Severe metabolic acidosis results within 3 hours due to all the nasty toxic metabolites.  Hyperkalemia goes with acidosis.  Bicarb drops with acidosis.
   
   Anion gap = (Na+ + K+) - (HCO3-  + Cl-)
   
   Normally the gap is 10-15 MEQ/L.  Metabolic acidosis is classified by whether or not anion gap is normal.  Knowing whether anion gap is normal will help you form a differential list for the metabolic acidosis in question.
   
   
   
   
    
9. Urine ethylene glycol level peaks 6 hours post ingestion.  It is undetectable 72 hours post ingestion. (Isosthenuria occurs by 3 hours & oxalate crystals show up 3 hours post-ingestion in the cat & 6 hours post ingestion in the dog.)
   
   
   
   
    
10. Alcohol dehydrogenase considers ethanol the preferred substrate & will ignore ethylene glycol in the presence of ethanol.  The problem is that the patient will pass out due to the large amounts needed for tx (you need 40 proof booze, usually vodka mixed in IV fluids).  Pulmonary edema is a recognized complication in comatose patients.
    
    
    
    
     
11. 4-methylpyrazole will occupy the relevant binding sites on alcohol dehydrogenase thus accomplishing the same thing as ethanol without making the patient comatose. You can use it in the cat if you want but don't expect it to work.  It seems to only work in cats if given at the same time as the ethylene glycol.