Page 472 - Clinical Small Animal Internal Medicine

440 Section 5 Critical Care Medicine

exposure to EG since many formulations contain a fluo- ings at different time points following EG ingestion again
VetBooks.ir rescent dye. Unfortunately, since some formulations do demonstrate how important it is to establish a timeline
of possible exposure.
not contain added dye, Woods’ lamp evaluation cannot
The treatment of EG toxicity is similarly dependent on
be used as a sole diagnostic test. Diagnosis of EG toxicity
must therefore be made based on clinical suspicion and timing of exposure. Definitive treatment of EG ingestion
the presence of certain findings on any of the following revolves around preventing accumulation of toxic metab-
tests: osmole gap, anion gap, urinalysis (calcium oxalate olites. Metabolism of EG to glycolic acid by the enzyme
crystalluria), blood chemistry, or abdominal ultra- alcohol dehydrogenase (ADH) is the most important step
sonography. Ethylene glycol is an effective osmole, and in the development of EG toxicity. Veterinary patients
the presence of significant ethylene glycol levels in the have traditionally been treated with IV ethanol adminis-
blood can result in neurologic symptoms (e.g., ataxia tration. Ethanol is metabolized by ADH, and ADH has a
and stupor) due to hyperosmolality. higher affinity for ethanol than EG. Administration of
The presence of significant amounts of EG in the ethanol, therefore, can limit glycolic acid accumulation.
blood leads to an increase in the “osmole gap,” which is At the same time, high rates of IV fluids can be given to
the difference between measured blood osmolality and drive urinary excretion of unmetabolized EG molecules.
calculated blood osmolality (equation 1). Ethanol administration can be an effective treatment for

Osmole gap Measured osmolalityCalculated osmolality EG ingestion, but long courses of treatment are needed
and side‐effects (including hyperosmolality, CNS signs
(Eq. 1) such as sedation, and GI signs such as vomiting) are fre-
Osmolality can be estimated using equation 2. quently observed. ADH inhibitors such as 4‐methyl-
pyrazole (4‐MP, also known as fomepazole) prevent
186 Na K BUN/. Glu/ 18 /. metabolism of EG to toxic metabolites while offering less
.
2 8
0 93 (Eq. 2)
risk of side‐effects than ethanol. The primary drawbacks
The normal whole‐blood osmole gap has been reported to 4‐MP are limited availability and relatively high cost
as 3.49 mOsm and the normal plasma osmole gap as compared with ethanol. Cats require very high doses of
–2.01 mOsm. A significant increase in the osmole gap in 4‐MP compared with dogs, making cats more likely to
a patient who may have been exposed to EG or who is develop side‐effects such as CNS depression and ataxia
showing symptoms should raise clinical suspicion for EG following treatment with 4‐MP. Treatment of cats with
poisoning. ADH inhibition using ethanol or 4‐MP is typically inef-
Fatalities due to EG toxicity are caused by acute renal fective if not begun within three hours of ingestion,
failure as EG metabolism leads to accumulation of whereas treatment of dogs is typically successfully if
metabolic acids such as glycolic and oxalic acid. This accu- started within eight hours of ingestion.
mulation leads to a metabolic acidosis and an elevated Hemodialysis is a very effective treatment for removal
anion gap (AG) seen at approximately three hours after of EG and glycolic acid; 90–95% of circulating EG can be
ingestion, peaking at six hours, and lasting up to 48 hours. removed in a single hemodialysis session. Intermittent
AG can be determined using equation 3. hemodialysis may also effectively treat azotemia and
hyperkalemia in patients with acute kidney injury from
Anion gap Na K Cl HCO3 (Eq. 3) EG toxicity, allowing time to determine if recovery of

kidney function occurs over the span of several weeks.
Normal AG is 12–24 mEq/L in dogs and 13–27 mEq/L Regardless of the mode of treatment, prompt interven-
in cats. An elevated AG indicates accumulation of tion is of utmost importance due to the time‐dependent
unmeasured anions. An elevated AG is not specific to nature of this lethal toxin.
EG intoxication, but an elevated AG 3–6 hours or more
after possible exposure to EG may be considered a sign Uncertain Exposure to a Known Toxin
of EG exposure. The oxalic acid formed during metabo-
lism of EG binds calcium, resulting in calcium oxalate When treating a patient who may or may not have been
monohydrate crystalluria as early as three hours after exposed to a known toxic substance, the clinician must
ingestion in cats (six hours in dogs). formulate a diagnostic testing and treatment plan based
In some cases, EG toxicity may not be diagnosed on the presence or absence of clinical symptoms, the
prior to the development of oligoanuric renal failure. likelihood of clinical symptoms developing if toxic
Progressive azotemia may help establish a diagnosis of exposure did in fact occur, and the danger of the toxin
EG poisoning, but this finding almost always indicates a involved. The clinician should consider contacting an
grave prognosis. Diagnosis of EG toxicity must be made animal poison control center to obtain the most extensive
prior to the development of azotemia to allow the best and up‐to‐date information regarding the probability of
chance at survival. The different clinicopathologic find- toxicity from any possible exposure to the substance in