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12 December 1999
KEY FACTS ABSTRACT: Acute ethylene glycol (EG) intoxication is a rapidly progressive, life-threatening
emergency with a complex pathophysiology—the key features of which include hyperosmolali-
■ Measurement of serum ty, high anion gap metabolic acidosis, and acute oliguric renal failure. Rapid diagnosis is critical
and requires a strong index of suspicion and often repeat analyses. Antidotal therapy is based
osmolality and calculation of the
on preventing biotransformation of EG to its toxic metabolites; however, intensive physiologic
osmolal and anion gaps may aid
monitoring and aggressive use of intravenous fluids and sodium bicarbonate are also essential
in diagnosis. components of treatment. Despite advances in our understanding of the pathophysiology and
therapy of EG intoxication, most animals are presented already in oliguric renal failure and may
■ Ethanol therapy is associated require hemodialysis or peritoneal dialysis to survive the effects of this intoxication.
with central nervous system and
respiratory depression as well as
A
exacerbation of EG-induced cute ethylene glycol (EG) intoxication is a rapidly progressive medical
hyperosmolality and osmotic emergency characterized by hyperosmolality, profound high anion gap
diuresis. metabolic acidosis, and acute oliguric renal failure. Although EG itself
causes central nervous system (CNS) depression, serum hyperosmolality, and os-
■ 4-Methylpyrazole is the treatment motic diuresis, most of the toxic effects are caused by the products of its
of choice for dogs but not cats. metabolism after initial conversion by hepatic alcohol dehydrogenase (ADH;
Figure 1). Glycolate in particular has been shown to be primarily responsible for
■ Intensive monitoring and the severe metabolic acidosis that develops and is thought to be the most likely
aggressive use of intravenous major mediator of toxicity; however, the mechanism of renal tubular epithelial
fluids and sodium bicarbonate necrosis remains poorly understood. The pathophysiology, clinical stages, and
are essential in the management clinicopathologic findings of acute EG toxicosis were reviewed in Part I of this
of acute EG intoxication. two-part presentation. This article discusses the diagnosis, current treatment rec-
ommendations, prognosis, and prevention of this devastating intoxication.
■ The use of peritoneal dialysis
may allow cats and dogs to DIAGNOSIS
recover from acute renal failure Early, rapid diagnosis of EG intoxication is critical because the prognosis for recov-
secondary to EG intoxication. ery is inversely related to the time elapsed between ingestion and initiation of thera-
py.1 Clinicians must maintain a high index of suspicion because a history of inges-
*Part I of this two-part presentation appeared in the November 1999 (Vol. 21, No. 11)
issue of Compendium.
Compendium December 1999 20TH ANNIVERSARY Small Animal/Exotics
tion is often unavailable, and clinical signs are relatively Calculated osmolality (mOsm/kg) =
nonspecific and may mimic other disease syndromes. 2(Na+ + K+) + (BUN ÷ 2.8) + (Glucose ÷ 18)
There are, however, a few key features that may aid in There is a significant correlation between serum EG
more rapid diagnosis. As discussed in Part I, clinical signs concentrations and the osmolal gap,4,5 such that the
of depression, vomiting, ataxia, polyuria, polydipsia, and serum EG concentration in dogs may be estimated by
tachypnea in combination with hyperosmolality, metabol- multiplying the osmolal gap by a factor of 6.2.5 Clini-
ic acidosis with an elevated anion gap (AG), isosthenuria, cians must keep in mind that serum osmolality and the
and calcium oxalate monohydrate or dihydrate crystalluria osmolal gap may not be elevated if animals are present-
are early findings in dogs and cats with acute EG intoxica- ed later in the course of intoxication (after most or all
tion. EG intoxication must also be considered in any ani- of the serum EG has been metabolized) or if animals
mal presenting with signs of acute renal failure. Laboratory have ingested small quantities of EG.
testing should ideally include a complete serum chemistry Another useful diagnostic aid is determination of the
profile, urinalysis, arterial or venous blood gas determina- AG, which is used to help characterize clinical causes of
tions, and preferably determination of ionized calcium metabolic acidosis. The AG is calculated as follows:
concentrations. Because the time of appearance of certain
of these key features, such as calcium oxalate crystalluria, AG (mEq/L) = (Na+ + K+) – (Cl– + HCO3–)
may vary among individuals, the importance of repeat
analyses cannot be overemphasized. Because positive and negative charges in the blood
TABLE I
Suggested Protocols for Supportive Therapy of Ethylene Glycol Intoxication in Dogs and Catsa
Therapy Purpose Parameters Monitored
IV crystalloid fluids Restore deficits and perfusion; Hematocrit and total plasma solids;
supply fluid for maintenance and body weight; urine output; heart rate;
ongoing losses; maintain diuresis mucous membrane color, capillary refill
time; central venous pressures;
electrolytes
Sodium bicarbonate Correct metabolic acidosis Arterial and/or venous blood gases;
Amount needed (mEq) = 0.3 × serum bicarbonate concentrations;
weight (kg) × base deficit/L (1⁄4 total carbon dioxide; urine pH
to 1⁄3 given slow IV bolus, the
remainder as a CRI over 4–6 hr)
or
6.2 mEq/kg IV every 4–6 hr
10% Calcium gluconate Control seizure activity, tetany, Electrocardiogram/bradycardia;
0.5–1.5 ml/kg slow IV bolus twitching seizures, twitching; serum and/or
(+/– 5–15 mg/kg/hr CRI) ionized calcium concentrations
and/or
Diazepam
Warming, turning, ophthalmic Additional therapy as needed Arterial blood gases, hemoglobin
lubrication; oxygen, ventilation; saturation (pulse oximetry), end-tidal
colloids, pressors; gastrointestinal carbon dioxide; arterial blood pressure,
protectants; avoidance of electrocardiogram; mentation/level of
aspiration consciousness; body temperature
a
See text for details.
CRI = continuous-rate infusion; IV = intravenous.
ment of choice for EG-intoxicated humans in France considered relatively nontoxic, and have been used or
since 1990,39 it was not approved for human use in the evaluated for use as food additives.20 1,3-Butanediol has
United States until late 1997.39 been shown to be efficacious in the treatment of EG in-
Although 4-MP is currently the treatment of choice toxication in dogs4,41,42; however, to our knowledge, no
in dogs, its use in cats cannot be recommended because studies have been reported that evaluate the use of
it has been shown to be effective only if given concur- pyrazoles or 1,3-butanediol in cats. It is unlikely that
rent with EG.3 As evidenced by this and by the lower further studies will be performed because of the efficacy
minimum lethal dose of EG and the earlier develop- and commercial development of 4-MP. Ethanol, al-
ment of crystalluria and azotemia in cats,3 it is apparent though not optimal, remains the recommended therapy
that considerable species differences exist in the for EG intoxication in cats.
metabolism of EG and the efficacy of various ADH in-
hibitors. Postulated reasons include a more rapid rate of Supportive Therapy
EG metabolism in cats3 and differences in the substrate Intensive physiologic monitoring and frequent
specificity of ADH33 and/or the pathways of EG bio- reevaluation are necessary in the management of EG-
transformation.40 Another proposed explanation is that intoxicated animals; patient status can change rapidly
feline renal tubular epithelium may be more sensitive throughout the course of treatment. Animals that pre-
to the cytotoxic effects of EG metabolites.3 sent or become severely obtunded or comatose may re-
Other 4-substituted pyrazoles may be better in- quire endotracheal intubation and ventilation in addi-
hibitors of ADH in cats and could possibly be useful. tion to hemodynamic support. Aspiration is a serious
Alkyldiols, such as 1,3-butanediol and 1,2-propanediol risk in these patients and must be avoided. Recumbent
(propylene glycol), are also substrates for ADH, are animals may need periodic turning to prevent conges-
tion and may require ophthalmic lubrication; thermal with underlying cardiopulmonary disease or that are
support is usually necessary as well. becoming oliguric, is also recommended.
Aggressive intravenous (IV) crystalloid fluid therapy Early and aggressive use of sodium bicarbonate is an-
is essential in the treatment of EG intoxication (Table other essential component of therapy in EG intoxica-
I). High infusion rates are usually required to combat tion, especially to help fully correct the initial excess of
the severe dehydration and hypoperfusion secondary to acids, particularly glycolate.34,48,49 The dose of sodium
EG- (and ethanol-) induced osmotic diuresis and other bicarbonate is controversial and, if possible, should be
ongoing losses, such as vomiting. Improved tissue per- based on determination of serial serum bicarbonate
fusion will also help correct metabolic acidosis and help concentrations using the following formula50:
promote renal excretion of EG and its toxic metabo-
Amount of HCO3– needed (mEq) =
lites.1,3,43,44 If possible, maintaining the animal in a state
0.3 × Weight (kg) × Base deficit/L
of diuresis is important because renal excretion of un-
metabolized EG is a major route for its elimina- If determination of serum bicarbonate concentra-
tion4,40,43–45 and depends on free water excretion.46 tions is unavailable, one recommendation is to use
Aseptic placement and maintenance of an indwelling sodium bicarbonate at a dose of 6.2 mEq/kg every 4 to
urinary catheter attached to a closed sterile collection 6 hours based on the fact that the average serum bicar-
system is important for monitoring urine output. Early bonate concentration in intoxicated cats and dogs is 8.5
in the course of intoxication, this will help ensure con- mEq/L.1 Ideally, serum bicarbonate levels should be
tinued diuresis and delivery of adequate volumes of IV monitored every 4 to 6 hours; at least 30 minutes must
fluids. Careful monitoring of urine output will also aid elapse after an infusion of sodium bicarbonate is com-
in the detection and management of oliguria and will pleted before its clinical effect can be determined.51
determine the reduced volumes of IV fluids required Monitoring urine pH may also be helpful. The aim of
during this period of limited urine production. Olig- therapy should be to increase the animal’s pH to 7.2 to
uria is defined as a urine output of less than 1 to 2 reduce the risk of life-threatening hemodynamic com-
ml/kg/hour in a volume-expanded animal.47 Monitor- plications. Bicarbonate therapy may also enhance renal
ing central venous pressures, particularly in animals excretion of glycolate by “ion trapping.”49,52 Potential
complications of sodium bicarbonate therapy include
(1) volume overload and exacerbation of hyperosmolal-
ity due to administered sodium, (2) tetany from de-
Raise the Standard of Practice at Your Hospital with creased serum ionized calcium concentrations sec-
ondary to increased binding of calcium to plasma
STANDARDS of CARE
ENDIU
MP
proteins, (3) paradoxical CNS acidosis as hyperventila-
M
CO
’S •
I
•
RE
CA
DA
N
R D S of
I STANDARDS of CARE
C O M P E N D I U M ’ S
quired in EG-intoxicated animals; if so, 10% calcium
M
CO
’S •
RE
S TA
CA
DA
N
R D S of
H
epatic lipidosis (HL) is the most common cause of jaundice in cats
in North America. It develops primarily in obese cats that have
recently been anorectic. By definition, HL occurs when >50% of
• Poikilocytosis (i.e., irregular
RBC shapes) is common.
• A mild nonregenerative anemia
accompanies primary
Expert help fast in a graphic monitoring.53 To maintain calcium levels, sub-
hepatocytes accumulate excessive triglycerides (TGs), resulting in severe cell
1).31,43,49 Although often advocated in human EG intox- within 5 hours of EG ingestion have a good prognosis,
ication, their use is controversial because of a lack of ex- and most dogs will recover if treatment is begun by 8
perimental or clinical data supporting any beneficial ef- hours after ingestion.6 The prognosis for cats is good if
fects and the potential of pyridoxine to cause peripheral ethanol therapy is initiated within 3 hours of EG inges-
sensory neuropathies.20 Furthermore, therapy to reduce tion.3,26 Most animals, however, are presented after the
oxalate levels may not sufficiently block toxicity if other onset of oliguric renal failure,1,17,30,60 and for these dogs
metabolites, particularly glycolate, are responsible for and cats, the prognosis is grave.17,60 Most cats and dogs
the adverse effects of EG intoxication. that receive dialysis and survive the acute renal failure
For animals that are presented in oliguric renal fail- phase will eventually regain normal renal function, but
ure, although most of the EG will already have been it may take as long as 1 year to regain the ability to ade-
metabolized, there may still be some small benefit to quately concentrate urine; a few animals may remain
trying 4-MP or ethanol. More importantly, reestablish- isosthenuric.6,17,30
ment of diuresis should be attempted with the judi-
cious use of IV crystalloids, mannitol, furosemide, and PREVENTION
dopamine.47 (Interested readers are referred to this latter Continuing to increase public awareness about the
reference for an excellent review of therapy of acute re- dangers of EG will help prevent exposure and may
nal failure.) If adequate diuresis cannot be established, prompt earlier presentation of intoxicated cats and
hemodialysis or peritoneal dialysis should be consid- dogs. Despite the use of more prominent warning la-
ered. The presence of intact tubular basement mem- bels on antifreeze products,61 the incidence of EG in-
branes and evidence of tubular epithelial regeneration toxication appears to be increasing.62 Antifreeze manu-
on histologic examination of renal biopsy specimens in- facturers and others whose products contain EG should
dicating potential reversibility19,54,55 may assist clinicians be encouraged to advertise the dangers of their prod-
in selecting candidates for dialysis. ucts more widely and to provide methods for their dis-
Hemodialysis is commonly used in human EG intox- posal. The addition of bittering agents to antifreeze and
ication not only to treat acute renal failure but also ear- other EG-containing products is another means of
ly in the course of intoxication to rapidly and effectively minimizing accidental ingestion that is already prac-
remove both EG and glycolate from the blood.32,44,49,52,56 ticed in some countries.63 A few antifreeze products
Early use of this invasive and expensive procedure has now contain propylene glycol rather than EG; although
recently been questioned, however, because of the rapid no nephrotoxicity is associated with propylene glycol
improvement seen with 4-MP therapy.20,38,57 Hemodial- ingestion, it does cause CNS depression, hyperosmolal-
ysis has also been demonstrated to efficiently and rapid- ity and osmotic diuresis, D-lactic acidosis with an in-
ly remove EG and glycolate from the circulation of creased AG, and (particularly in cats) Heinz-body
dogs,58 but the availability of this procedure in veteri- hemolytic anemia.64,65 Continued research into safe, ef-
nary medicine is currently limited. fective antifreeze products must be encouraged.
Peritoneal dialysis is a reasonable alternative for in-
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When this paper was submitted for publication, Drs. Gay-
moved by hemodialysis. Acta Med Scand 216:409–416,
1984. nor and Dhupa were affiliated with the Department of Clin-
57. Jacobsen D, McMartin KE: Methanol and ethylene glycol ical Sciences, School of Veterinary Medicine, Tufts Uni-
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