Page 718 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Hemodialysis and Extracorporeal Blood Purification 705

metabolites entirely from the animal as quickly as possible should be continued for prolonged periods for toxins with
and to correct the accompanying fluid, electrolyte, and delayed toxicity (i.e., paraquat), low blood concentrations,
acid-base disturbances, and attending uremia. For or significant redistribution following treatment.
suspected poisonings amenable to extracorporeal elimi- Ethylene glycol (antifreeze poisoning) is a common
nation hemodialysis or hemodialysis/hemoperfusion intoxication in companion animal practice. 34–36,59,95,96,173
should be initiated immediately upon diagnosis to ensure Clinical signs develop within minutes and progress
rapid elimination of the toxin regardless of previous anti- variablyfromlethargy,nausea,vomiting,dehydration,agita-
dotal therapy or the absence of clinical signs. If the animal tion,anddepressiontoconvulsions,coma,anddeath.Severe
needs to be transported, appropriate antidotal therapy metabolic acidosis and hypocalcemia are seen with signifi-
should be administered in addition to general supportive cant exposure, and in later stages of the intoxication
therapies. (12 to 24 hours), hypertension, cardiopulmonary
For some toxins (such as ethylene glycol), it generally failure, and acute oliguric renal failure dominate the
is possible to eliminate 90% to 95% or more of the toxin clinical presentation. Ethylene glycol concentrations are
with a single intensive extracorporeal treatment. For highly variable and significantly higher in nonazotemic
intoxications other than ethylene glycol, experience is compared with azotemic dogs presented for antifreeze poi-
more anecdotal and recommendations for extracorporeal soning (Figure 29-13). 137 Serum ethylene glycol and
blood purification must be made with less evidence. glycolic acid concentrations may persist for days at toxic
Therapeutic decisions must be balance against the histor- concentrations in azotemic or anuric animals despite
ical consequences of the intoxication, the efficacy of alter- therapy with alcohol or 4-methylpyrazole. These inhibitors
native therapies, and the potential for adverse of alcohol dehydrogenase merely delay the enzymatic
consequences of the procedure. Hemoperfusion should
be considered for lipid soluble, highly protein-bound
toxins with molecular mass larger than the cutoff limits
of the dialysis membrane. Therapy is more efficacious P 0.05
when the volume of distribution is small (plasma volume 7000
or ECF volume [i.e., <0.5 L/kg]). The treatment goal 6000
for detoxification is 100% elimination of the toxin and
5000
toxic metabolites. This is often difficult to achieve when
4000
experience with a specific toxins is limited and detection
assays are unavailable during the procedure. For toxins 3000 NS
and drugs including amatoxins, fluoroquinolones, and 2000
NSAIDs where morbidity is certain and molecular 1000
characteristics are favorable, urgent decisions to initiate
combined hemodialysis/hemoperfusion must be ad hoc 0 Azotemic Nonazotemic Azotemic Nonazotemic
but are generally justified because of the low morbidity Concentration (ppm) A
of these procedures and the possibility to alter the clinical 4000
course and outcome. As evidence for outcome benefits is P 0.05
acquired, more definitive recommendations can be
justified. A precise definition of the window of opportu- 3000
nity for these therapeutic interventions is necessary for
realistic therapeutic recommendations. Many toxins, P 0.05
such as amatoxins, will have sharply delimited therapeutic 2000
window in which the toxin can be eliminated before the
clinical course is solidified and intervention is unjustified.
Hemodialysis is indicated for the treatment of poison- 1000
ing or drug overdose with ethylene glycol, methanol, eth-
anol, salicylate, lithium, phenobarbital, acetaminophen,
theophylline, aminoglycosides, tricyclic antidepressants, 0 Predialysis Postdialysis Predialysis Postdialysis
and possibly metaldehyde. 14,20,79,161,185 Hemodialysis B Ethylene glycol Glycolic acid
secondarily corrects the acid-base and electrolyte Figure 29-13 A, Box and whisker plots of the serum
abnormalities and the azotemia that accompany some concentrations for ethylene glycol (left) and glycolic acid (right)in
intoxications (e.g., ethylene glycol, salicylate). Hemodial- azotemic (light boxes;n ¼ 20) and nonazotemic (dark boxes;n ¼ 6)
ysis should be initiated once conventional treatments are dogs presenting for hemodialysis. B, Box and whisker plots of the
deemed ineffective and continued until the concentration change in serum ethylene glycol (left) and glycolic acid (right)
of the toxin has decreased to an acceptable level and the concentrations before and following hemodialysis in 26 azotemic
clinical toxicity has disappeared. Dialysis treatments and nonazotemic dogs poisoned with antifreeze. 123