Page 686 - Cote clinical veterinary advisor dogs and cats 4th
P. 686

314   Ethylene Glycol Intoxication




            Ethylene Glycol Intoxication
  VetBooks.ir


                                              •  Patient  gradually  shows  more  weakness,
            BASIC INFORMATION
                                                depression, ataxia, anorexia, and tachypnea/  prognosis is worse > 12-24 hours after ingestion,
                                                                                 when overt clinical signs are more prominent.
           Definition                           dyspnea as AKI and oliguria/anuria occur   A typical approach to diagnosis and treatment
           Ethylene glycol (EG) intoxication manifests as   24-72 hours after ingestion.  is outlined on p. 1416.
           peracute-onset, marked central nervous system
           (CNS) depression and progressive, dose-related   PHYSICAL EXAM FINDINGS  Differential Diagnosis
           metabolic acidosis and acute kidney injury   •  CNS  depression,  generalized  weakness,   •  Acute CNS depression, ataxia, acidosis, or
           (AKI).                               hyporeflexia, hypothermia, slow capillary   AKI: encephalitis, cranial trauma, intracranial
                                                refill time (CRT), tachycardia, vomiting  neoplasia, diabetic ketoacidosis; or intoxica-
           Synonyms                           •  Urinary bladder may be empty on palpation.  tion with barbiturates, aspirin, methanol,
           •  EG poisoning, radiator antifreeze poisoning  •  Patient may have already progressed beyond   ethanol, isopropanol, propylene glycol, glycol
           •  Ethylene glycol: 1,2-ethanediolmonoethylene   the initial drunken phase, potentially delay-  ethers, vitamin D 3 , Lilium and Hemerocallis
            glycol, glycol alcohol, CAS 107-21-1  ing or confusing the clinical picture.  spp  (cats),  nonsteroidal  antiinflammatory
                                                ○   Overt  signs  of  AKI  (oliguria/anuria,   drugs, grapes, or raisins
           Epidemiology                           anorexia, vomiting, renomegaly with signs   •  AKI (p. 23)
           SPECIES, AGE, SEX                      of renal pain) typically begin 24-72 hours
           •  All animals are susceptible.        after ingestion.               Initial Database
           •  Cats are extremely sensitive to EG intoxication.  •  In severe intoxications, seizures, nystagmus,   •  Kacey Diagnostics Ethylene Glycol Veterinary
           •  Dogs are more commonly exposed than cats.   and tremors may occur in the first few hours   Test  Strips  (www.kaceydiagnostics.com/
            Intact young male dogs may be more likely   after ingestion (grave prognosis).  Toxicology.html or 828-685-3569): quantita-
            to be involved.                                                        tive test for dogs and cats; false-positives for
                                              Etiology and Pathophysiology         alcohols, including methanol and xylitol
           RISK FACTORS                       •  Lethal dose of 95% ethylene glycol: 4.4 mL/  •  VetSpec Ethylene Glycol Qualitative Reagent
           •  Pets living outdoors or having access to EG   kg (dog), 1.4 mL/kg (cat)  Test Kit (www.catacheminc.com/brochures/
            sources (e.g., garages)           •  Rapid oral absorption of EG       Ethylene-Glycol-Flyer.pdf or 203-262-0330):
           •  Freezing  temperatures  provide  increased   ○   Blood levels detectable in < 30 minutes  qualitative test for dogs and cats; false-positives
            opportunity, especially when water sources   ○   Initial CNS depression and narcosis,   for propylene glycol, glycerol, diethylene glycol
            are limited (frozen), and antifreeze remains   vasodilation, and hypotension with reflex   (or other cis-1,2 diols), and sorbitol
            in the liquid state because of its low freezing   tachycardia, diuretic effect  •  Serum biochemistry panel and electrolytes
                                                                                                  2+
                                                                                             2+
                                                                                                     +
            point.                            •  Metabolism involves hepatic alcohol dehy-  (especially  Ca , Mg ,  K ,  and  P):  azote-
           •  In hot climates, cars may overheat and leak   drogenase oxidation of EG to the aldehyde   mia, hyperphosphatemia, hyperkalemia
            engine coolant (i.e., antifreeze).  (glycoaldehyde),  a  saturable,  rate-limiting   with oliguria/anuria,  ± hypocalcemia,  ±
           •  Engine leak is the most common source of   step.                     hyperglycemia
            exposure in pets, and a home garage is the   ○   Metabolic progression can be interrupted   •  Acid-base:  blood  pH,  PCO 2 ,  PO 2 , serum
            most common exposure location.        at this point with fomepizole or ethanol.  bicarbonate; metabolic acidosis common ±
           •  Malicious  poisoning  is  encountered  on   •  Glycoaldehyde  is  very  toxic  but  quickly   compensatory respiratory alkalosis
            occasion.                           converts to glycolic acid.       •  Urinalysis: specific gravity, crystals, glucose,
                                              •  Glycolic  acid  (30%-45%  of  metabolite   cellular debris, granular casts
           GEOGRAPHY AND SEASONALITY            load) is fairly stable and further oxidizes to   ○   As for any cause of acute anuric kidney
           •  EG poisoning occurs year round; it is no   glyoxylic acid, which then converts to oxalic   injury, specific gravity is not necessarily
            longer a seasonal problem.          acid, glycine, formate, hippurate, CO 2 , and   isosthenuric
           •  Colder  climate  zones  are  overrepresented,   other compounds.     ○   Calcium oxalate monohydrate crystals
            but exposure can occur anywhere. Summer   •  Aldehyde and acid load create a high–anion-  (picket  fence  boards,  flattened  hexagon
            automobile radiator flushing is considered   gap metabolic acidosis.     shapes:      ) can be observed
            routine maintenance.              •  Metabolites inhibit the citric acid cycle and   3-18  hours  after  EG  ingestion  and  are
                                                substrate level phosphorylation, depress   much more specific for ethylene glycol
           Clinical Presentation                serotonin  and  pyruvate  metabolism,  and   intoxication than calcium oxalate dihy-
           HISTORY, CHIEF COMPLAINT             alter CNS amine levels.              drate  crystals  (Maltese  cross  or  square
           •  Indirect evidence of exposure   •  Secondary  lactate  accumulation,  hypo-  envelope appearance: ⊠), which can occur
            ○   Pet being near an automobile garage or   perfusion, and calcium oxalate crystal forma-  from nutritional or laboratory artifactual
              work area                         tion and precipitation in microvasculature   causes as well as EG intoxication; only
            ○   Roaming free in areas suspected or known   and renal tubules occur.  about 40% of cases have crystals.
              to have EG sources                                                 •  Fluids: measure total input and output; body
           •  Classic  “drunken  sailor”  behavior  (stupor,    DIAGNOSIS          weight
            narcosis, ataxia, falling, nausea) may be noted                      •  Optional Wood’s lamp examination (detects
            within 1-2 hours of ingestion.    Diagnostic Overview                  fluorescein dye in antifreeze); scan of muzzle,
           •  Stupor phase gradually subsides over several   A high index of suspicion should exist based   paws, vomitus, urine (excretes < 3-6 hours
            hours.                            on history alone (e.g., owner saw pet licking or   in humans) for fluorescence that subjectively
            ○   Stupor phase may go unnoticed, especially   in the same room as fluorescent green liquid).   supports exposure
              in outdoor pets                 Treatment must be implemented early—before
            ○   Owner may note the pet is “getting better.”  kidney injury and possibly before definitive   Advanced or Confirmatory Testing
            ○   Patient is quiet, depressed, polydipsic, and   diagnostic  confirmation  in  many  cases.  The   •  EG and glycolic acid levels (serum, urine);
              polyuric                        diagnosis is more straightforward, but the   requires STAT turnaround time to benefit

                                                     www.ExpertConsult.com
   681   682   683   684   685   686   687   688   689   690   691