Page 690 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Alcohols and Glycols Chapter | 49 655

VetBooks.ir Prognosis failure. Carbamylated hemoglobin concentration has been
shown to be useful in making this differentiation (Vaden
EG has a very high potential for a lethal outcome, but with
et al., 1997b; Heiene et al., 2001). In addition, animals
early recognition of the syndrome and timely institution of
therapy, animals can be saved. The quantity of EG with chronic renal failure may be anemic and in poor
ingested, rate of absorption, and time interval prior to insti- body condition. A history of the duration of clinical signs
tution of therapy are variables that affect the prognosis. is also helpful. Continuing to increase the awareness of
The prognosis is excellent in dogs treated with fomepizole the toxicity of EG, as well as other alcohols and glycols,
will aid in preventing exposure and result in earlier treat-
within 5 h of ingesting EG. In a retrospective study of dogs
ment of animals.
with confirmed EG poisoning, all of the dogs that were
azotemic when initially treated died. Of the dogs that did
not have azotemia when initially treated, approximately REFERENCES
90% survived (Connally et al., 1996). The prognosis for
Adin, C.A., Cowgill, L.D., 2000. Treatment and outcome of dogs with
cats is reasonably good if treatment is instituted within 3 h
leptospirosis: 36 cases (1990 1998). J. Am. Vet. Med. Assoc. 216,
following ingestion (Dial et al., 1994b). In contrast, the
371 375.
prognosis in humans who survive the initial syndrome of Anonymous, 1930. Possible death from drinking ethylene glycol
severe acidosis is very good. Terminal renal failure in (“Prestone”): queries and minor notes. J. Am. Med. Assoc. 94, 1940.
humans is rare, and most human patients regain renal func- Ballentine, C., 1981. Sulfanilamide disaster. FDA Consumer magazine.
tion by 2 months following EG poisoning (Davis et al., Barceloux, D.G., Bond, G.R., Krenzelok, E.P., et al., 2002. American
1997) likely due to the effectiveness of hemodialysis ther- Academy of Clinical Toxicology practice guidelines on the treat-
apyinhumans (Christiansson et al., 1995). ment of methanol poisoning. Clin. Toxicol. 40, 415 446.
Barton, J., Oehme, F.J., 1981. The incidence and characteristics of ani-
mal poisonings seen at Kansas State University from 1975 to 1980.
CONCLUDING REMARKS AND FUTURE Vet. Hum. Toxicol. 23, 101 102.
Bauer, M.C., Weiss, D.J., Perman, V., 1992a. Hematologic alterations in
DIRECTIONS adult cats fed 6 or 12% propylene glycol. Am. J. Vet. Res. 53, 69 72.
Bauer, M.C., Weiss, D.J., Perman, V., 1992b. Hematological alterations
Ethanol, methanol, isopropanol, propylene glycol, and
in kittens induced by 6 and 12% dietary propylene glycol. Vet.
butylene glycol toxicosis can produce ataxia and other
Hum. Toxicol. 34, 127 131.
CNS signs similar to those seen in acute EG poisoning
Berger, J.R., Ayyar, D.R., 1981. Neurological complications of ethylene
but are much less common than EG toxicosis. These dis- glycol intoxication: report of a case. Arch. Neurol. 38, 724 726.
orders can be differentiated by the diagnostic laboratory Bischoff, K., 2006a. Methanol. In: Peterson, M., Talcott, P. (Eds.), Small
tests discussed previously. Other causes of an increased Animal Toxicology. Saunders, St. Louis, MO, pp. 840 844.
anion gap include diabetic ketoacidosis and lactic acido- Bischoff, K., 2006b. Propylene glycol. In: Peterson, M., Talcott, P.
sis; these disorders can also be differentiated by appropri- (Eds.), Small Animal Toxicology. Saunders, St. Louis, MO,
ate laboratory tests. Other causes of increased osmolality pp. 996 1001.
include ethanol, isopropanol, methanol, and propylene Bostrom, W.F., Li, T., 1980. Alcohol dehydrogenase enzyme.
glycol toxicosis. Ethanol, like EG, can also produce hypo- In: Jakoby, W.B. (Ed.), Enzyme Basis of Detoxification. Academic
Press, New York, pp. 231 248.
calcemia (Money et al., 1989). Other differentials for
Brown, S.A., Barsanti, J.A., Crowell, W.A., 1985. Gentamicin-associated
acute renal failure include leptospirosis, ibuprofen, and
acute renal failure in the dog. J. Am. Vet. Med. Assoc. 186,
other nonsteroidal antiinflammatory drug toxicosis, ami-
686 690.
noglycoside antibiotics, hemolyticuremic syndrome, cho-
Burkhart, K.K., Kulig, K.W., 1990. The other alcohols. Emerg. Med.
lecalciferol toxicosis, grape and raisin toxicosis in dogs, Clin. North Am. 8, 913 928.
and ingestion of oxalate-containing plants such as philo- Cavender, F.L., Sowinski, E.J., 1994. Glycols. In: Calayton, G.D.,
dendron and lily toxicosis in cats (Brown et al., 1985; Clayton, F.E. (Eds.), Patty’s Industrial Hygiene and Toxicology.
Gunther et al., 1988; Peterson et al., 1991; Holloway Vol. 2F: Toxicology, fourth rev. ed. Wiley, New York,
et al., 1993; Vaden et al., 1997a,b; Poortinga and pp. 4645 4719.
Hungerford, 1998; Forrester and Troy, 1999; Adin and Christiansson, L.K., Kaspersson, K.E., Kulling, P.E., et al., 1995.
Cowgill, 2000; Hovda, 2000; Rumbeiha et al., 2000; Treatment of severe ethylene glycol intoxication with continuous
arteriovenous hemofiltration dialysis. J. Toxicol. Clin. Toxicol. 33,
Langston, 2002; Tefft, 2004). The majority of dogs with
267 270.
grape and raisin toxicosis are hypercalcemic, as are ani-
Christopher, M.M., Perman, V., Eaton, J.W., 1989a. Contribution of pro-
mals with cholecalciferol toxicosis (Fooshee and
pylene glycol-induced Heinz body formation to anemia in cats.
Forrester, 1990; Gwaltney-Brant et al., 2001); hypercalce- J. Am. Vet. Med. Assoc. 194, 1045 1056.
mia is not associated with EG toxicosis (Thrall et al., Christopher, M.M., Perman, V., White, J.G., 1989b. Propylene glycol-
1984b; Connally et al., 1996). Acute renal failure must be induced Heinz body formation and d-lactic acidosis in cats. Prog.
differentiated from acutely decompensated chronic renal Clin. Biol. Res. 319, 69 87.