Glycol Poisoning Research Articles

Studies on ethylene glycol poisoning: One patient – 154 admissions

Objective. Fomepizole is the antidote of choice in toxic alcohol poisonings. Potential side effects from frequent use of fomepizole were studied in a patient admitted 154 times with ethylene glycol (EG) poisoning. The intra-individual correlation between the serum-ethylene glycol (serum-EG) and the osmolal gap (OG) EG-kinetics, and other laboratory parameters were also studied. Methods. Combined pro- and retrospective collection of material from three different hospitals, and results from autopsy. Results. A 26-year-old female with a dissociative disorder was admitted with EG poisoning a total of 154 times. Her admission data revealed a median pH of 7.31 (range 6.87–7.49), pCO2: 4.2 kPa (1.2–6.7) (32 mmHg [9–50]), HCO–3: 15 mmol/L (4–26) (15 mEq/L [4–26]), base deficit (BD): 10 mmol/L (− 4 to 27) (10 mEq/L [–4 to 27]), serum-creatinine 65 μmol/L (40–133) (0.74 mg/dL [0.45–1.51]), OG 81 mOsm/kgH2O (25–132), and serum-EG 44 mmol/L (4–112) (250 mg/dL [25–700]). She was treated with fomepizole 99 times, ethanol 60 times (with a combination of both six times), and dialysis 73 times. The correlation between serum-EG and OG was good (r2 = 0.76). She was finally found dead outside hospital with an EG blood concentration of 81 mmol/L (506 mg/dL). An autopsy revealed calcium oxalate crystals in the kidneys, slight liver steatosis, and slight edema of the lungs. Discussion. The frequent use of fomepizole in this young patient was not associated with any detectable side effects; neither on clinical examination and lab screening, nor on the later autopsy. Regarding the sequelae from the repetitive EG-poisoning episodes, her kidney function seemed to normalize after each overdose. She was treated with buffer and antidote without hemodialysis 81 times without complications, supporting the safety of this approach in selected cases.

When is It appropriate to treat ethylene glycol intoxication with fomepizole alone without hemodialysis?

Seminars in DialysisVolume 24, Issue 4 p. 441-442 When is It appropriate to treat ethylene glycol intoxication with fomepizole alone without hemodialysis? Gregory K. Buller, Gregory K. Buller Department of Internal Medicine, Saint Mary’s Hospital, Waterbury, ConnecticutSearch for more papers by this authorCraig B. Moskowitz, Craig B. Moskowitz Department of Internal Medicine, Saint Mary’s Hospital, Waterbury, ConnecticutSearch for more papers by this author Gregory K. Buller, Gregory K. Buller Department of Internal Medicine, Saint Mary’s Hospital, Waterbury, ConnecticutSearch for more papers by this authorCraig B. Moskowitz, Craig B. Moskowitz Department of Internal Medicine, Saint Mary’s Hospital, Waterbury, ConnecticutSearch for more papers by this author First published: 31 July 2011 https://doi.org/10.1111/j.1525-139X.2011.00930.xCitations: 10 Address correspondence to: Gregory K. Buller, M.D., Saint Mary’s Hospital, 56 Franklin Street, Waterbury, CT 06706, Tel.: 203-709-6424, Fax: 203-709-3518, or e-mail: [email protected]. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume24, Issue4Special Issue: Curbside Consultations: Questions and Answers on DialysisJuly/August 2011Pages 441-442 RelatedInformation

Pseudorenal Insufficiency With Isopropyl Alcohol Ingestion

Isopropyl ingestion is usually a benign occurrence with little metabolic or renal abnormalities. We describe a case of a false elevation of serum creatinine due to laboratory interference in the setting of a toxic alcohol exposure that could have led to a misdiagnosis of ethylene glycol intoxication and a different treatment plan. Clinicians should be aware of this laboratory anomaly when treating suspected toxic alcohol ingestions.

Medication errors associated with the use of ethanol and fomepizole as antidotes for methanol and ethylene glycol poisoning

Introduction. Little is known about medication errors which occur with the antidotes ethanol and fomepizole, used for treatment of methanol and ethylene glycol poisoning. Study objectives were to describe and compare the frequency, type, outcome and underlying causes of medication errors associated with ethanol and fomepizole. Methods. Patients aged ≥13 years were included if they were hospitalized in 1996–2005 for methanol or ethylene glycol poisoning and treated with ethanol or fomepizole. Charts from 10 hospitals were separately reviewed by two abstracters who recorded case details. A consensus panel of clinicians used the abstracted data to identify medication errors and classify error outcome. Fisher's exact test determined significant differences in the proportion of ethanol and fomepizole-treated cases with medication error and univariate logistic regression identified risk factors associated with harmful dosage errors. Results. There were 145 ethanol- and 44 fomepizole-treated cases. There was ≥1 medication error in 113/145 (78%) ethanol- and 20/44 (45%) fomepizole-treated cases (p = 0.0001) with more ethanol-related errors involving excessive dose, inadequate monitoring and inappropriate antidote duration. Harmful errors occurred in 19% of ethanol- and 7% of fomepizole-treated cases (p = 0.06) and were largely due to excessive antidote dose or delayed antidote initiation. Occurrence of harmful dosage error was reduced in cases with Poison Control Centre consultation, odds ratio (95% confidence interval) 0.39 (0.17, 0.91), hemodialysis 0.37 (0.16, 0.88), or fomepizole versus ethanol 0.24 (0.06, 1.04). Conclusion. Fomepizole was less prone to medication error than ethanol. Error-related harm was most commonly due to excessive antidote dose or delayed antidote initiation.

4‐Methylpyrazole as a treatment in naturally occurring ethylene glycol intoxication in cats

To describe the clinical experience and therapeutic use of fomepizole (4-methylpyrazole [4-MP]) in 3 cats with naturally occurring ethylene glycol (EG) toxicity. All cats were documented to be EG positive by an ethylene glycol test kit. This report describes the dose of 4-MP used, available clinicopathological data, and clinical progression during hospitalization. All patients survived to discharge. IV use of 4-MP at 125 mg/kg as an initial dose and 31.25 mg/kg at 12, 24, and 36 hours is safe and effective for treatment of naturally occurring EG toxicity in cats. Increased HCO₃ concentrations were noted after IV use of 4-MP. This is the first report documenting the successful treatment of naturally occurring EG intoxication in cats with 4-MP.

생체시료에서 에틸렌 글리콜과 그 대사체 분석에 관한 연구

에틸렌 글리콜은 주로 자동차, 선박, 항공기 등의 부동액 성분으로 우리 실생활에 널리 쓰 이고 있으며 그 만큼 접근성이 용이하여 자살 목적이나 보관 사용 단계에서 의도적 혹은 실수로 인한 오용 사고가 끊이지 않고 있다. 에틸렌 글리콜 자체는 인체에 대한 독성이 그리 크지 않으나 생체 내에서 대사 과정을 거치면서 보다 독성이 높은 대사체를 생성하게 되며, 특히 글리콜산과 옥살산 대사체는 에틸렌 글리콜 중독의 주된 독성 발현체로서 대사성 산증 및 조직 손상 등을 유발하고 최종적으로 치사에 이르게 한다, 에틸렌 글리콜 중독으로 판정할 수 있는 가장 결정적인 데이터는 생체 시료 중 에틸렌 글리콜 농도가 되겠으나, 에틸렌 글리콜은 반감기가 3 ~ 5시간 정도로 매우 짧아 발견 당시 이미 상당 수준의 단계로 대사가 진행되어 있는 경우가 많고, 병원 등에서 위 세척 등 응급 치료 중 사망하기도 하며, 경우에 따라서는 매우 늦게 발견되어 시체가 부패되어 혈액을 채취할 수 없는 등, 에틸렌 글리콜 분석만으로 사인을 규명하기 어려운 때가 있으며, 이런 경우에 대사체의 분석이 필수적이다. 본 연구에서는 에틸렌 글리콜로 인하여 사망한 4건의 사례에서 혈액 및 조직 등 11점의 생체 시료에서 에틸렌 글리콜과 초기 대사체인 글리콜산 및 최종 대사체인 옥살산의 함량을 분석하고 그 분포에 대하여 살펴보았다. 에틸렌 글리콜 분석은 유도체화 후 가스크로마토그래프/질량분석법으로, 글리콜산과 옥살산 분석은 이온크로마토그래피로 수행하였으며, 혈액에서(3건)에서 에틸렌 글리콜 농도는 <TEX>$10\sim2,400\;{\mu}g/mL$</TEX> 글리콜산 농도는 <TEX>$224\sim1,164\;{\mu}g/mL$</TEX> 옥살산 농도는 불검출 <TEX>$\sim40\;{\mu}g/mL$</TEX> 이었다. 간, 신장, 담즙, 흉강 액의 시료(3건)에서는 에틸렌 글리콜 농도는 불검출 <TEX>$\sim55,000\;{\mu}g/mL$</TEX> 글리콜산 농도는 불검출 <TEX>$\sim1,124\;{\mu}g/mL$</TEX> 옥살산 농도는 불검출 <TEX>$\sim60\;{\mu}g/mL$</TEX> 이었다. 간 조직과 신장 조직에서는 치료 등에 따라 에틸렌 글리콜이 검출되지 않더라도 최종 대사체인 옥살산이 의미 있는 양으로 검출되어, 혈액과 더불어 유용한 생체 증거물 시료로서 권장되었다. Ethylene glycol (EG) is produced commercially in large amounts and is widely used as antifreeze or deicing solution for cars, boats, and aircraft. EG poisoning occurs in suicide attempts and infrequently, either intentionally through misuse or accidental as EG has a sweet taste. EG has in itself a low toxicity, but is in vivo broken down to higher toxic organic acids which are responsible for extensive cellular damage in various tissues caused principally by the metabolites glycolic acid and oxalic acid. The most conclusive analytical method of diagnosing EG poisoning is determination of EG concentration. However, victims are sometimes admitted at a late stage to hospitals or died during emergency treatment like a gastric lavage or found rotten dead, when blood EG concentrations are low or not detected. Therefore, in this study, the identification of EG was not only performed by gas chromatograpyc-mass spectrometry (GC-MS) following derivatization but also further toxicological analyses of metabolites, glycolic acid (GA) and oxalic acid (OA), were performed by ion chromatography in various biological specimens. A ranges of blood concentrations (3 cases) was <TEX>$10\sim2,400\;{\mu}g/mL$</TEX> for EG, <TEX>$224\sim1,164\;{\mu}g/mL$</TEX> for GA and ND <TEX>$\sim40\;{\mu}g/mL$</TEX> for OA, respectively, In other biological specimens (liver, kidney, bile and pleural fluid), a range of concentrations (3 cases) was ND <TEX>$\sim55,000\;{\mu}g/mL$</TEX> for EG, ND <TEX>$\sim1,124\;{\mu}g/mL$</TEX> for GA and ND <TEX>$\sim60\;{\mu}g/mL$</TEX> for OA, respectively. Liver and kidney tissues were recommended specimens including blood because OA, a final metabolite of EG, was identified large amounts in these despite no detectable EG caused by some therapy.

Calcium Oxalate Monohydrate Crystals: A Clue to Ethylene Glycol Poisoning

A 52-year old man presented to the emergency department in an obtunded state; no history was obtainable. Initial arterial blood gas showed pH 7.12; pCO2 11 mm Hg; and HCO3 4 mEq/L. The plasma anion gap was 21 mEq/L, and the plasma osmolal gap was 6 mOsm/Kg H2O. Initial serum creatinine was 2.33 mg/dL and blood urea nitrogen was 19 mg/dL. Urinalysis with microscopy showed numerous crystals, which resembled hippuric acid crystals (Figure 1). Under polarized light, the crystals showed strong positive birefringence, characteristic of calcium oxalate monohydrate crystals (Figure 2). Given the clinical, laboratory, and urine microscopy findings of calcium oxalate monohydrate crystals, a diagnosis of ethylene glycol poisoning was made (which was later confirmed by the patient once he regained consciousness). The patient was successfully treated with 8 hours of hemodialysis and fomepizole on the day of admission. He subsequently required 1 more session of hemodialysis for rising serum creatinine and uremia. Renal function subsequently stabilized, and at the time of follow-up 2 weeks later, his serum creatinine had decreased from 6.4 mg/dL to 2.5 mg/dL. Although the crystals were originally interpreted as hippuric acid crystals, urine microscopy was instrumental in making the diagnosis. Calcium oxalate monohydrate crystals, which resemble hippuric crystals and are highly specific for ethylene glycol poisoning, 1. Godolphln W. Meagher E.P. Sanders D. et al. Unusual calcium oxalate crystals in ethylene glycol poisoning. Clin Toxicol. 1980; 16: 479-486 Crossref PubMed Scopus (32) Google Scholar , 2. Huhn K.M. Rosenberg F.M. Critical clue to ethylene glycol poisoning. Can Med Assoc J. 1995; 152: 193-195 Google Scholar were identified by polarization showing strongly positive birefringent crystals. 3. Eder A.F. McGrath C.M. Dowdy Y.G. et al. Ethylene glycol poisoning: toxicokinetic and analytical factors affecting laboratory diagnosis. Clin Chem. 1998; 44: 168-177 PubMed Google Scholar This prompt recognition allowed the patient to receive life-saving treatment in a timely manner. The presence of calcium oxalate monohydrate crystals is very rare in either normal urine or in association with calcium oxalate calculi. Figure 2 View Large Image Figure Viewer

Deceased‐donor kidney transplant following ethylene glycol‐induced brain death

AbstractWe report on a deceased‐donor kidney transplant following ethylene glycol‐induced brain death. The donor was a 53‐year‐old man with a history of depression who presented to the emergency department after drinking a “cocktail amount” of windshield wiper fluid each day for the past 3 weeks. Upon presentation he became unresponsive and suffered a seizure. Fomepizole 1.2 g IV followed by emergent hemodialysis was initiated as indicated for acute treat‐ment of ethylene glycol poisoning. Unfortunately, the patient never regained consciousness and progressed to brain death. At the time of procurement his urine output was over 250 mL/h, and serum creatinine was 2.2 mg/dL. Renal biopsy following procurement revealed minimal tubule injury without evidence of intratubular oxalate crystals. The kidney recipient was a 76‐year‐old woman with end‐stage renal disease secondary to diabetes and hypertension. Cold ischemia time was 31 hours, 45 minutes. The only postoperative complication was delayed graft function and one episode of mild acute cellular rejection 7 weeks post transplant that resolved with IV methylprednisolone. Two years post transplant the patient continues to do well clinically with a baseline serum creatinine of 2.5 mg/dL.

The Role of Hemodialysis and Fomepizole in Ethylene Glycol Intoxication

Ethylene glycol is one of the most common toxic alcohol ingestions requiring hemodialysis for treatment. With the FDA approval in 1997 of fomepizole (4-methylpyrazole), the indications for hemodialysis in addition to fomepizole for ethylene glycol poisoning have been examined in recent articles and case reports. Fomepizole, a competitive inhibitor of alcohol dehydrogenase, binds to the same site on the enzyme as ethanol, however the pharmacokinetics of fomepizole are more predictable, and with fewer side effects compared to ethanol. Current guidelines cited in the literature for the use of hemodialysis in ethylene glycol poisoning include patients with severe metabolic acidosis (pH 7.3), serum ethylene glycol level 50 mg/dL, acute kidney injury, and deteriorating vital signs despite intensive care. This article is a review of the current literature with regard to the use of fomepizole as monotherapy for ethylene glycol poisoning, as well as the indications for hemodialysis in ethylene glycol poisoning.

Oxidation of methanol, ethylene glycol, and isopropanol with human alcohol dehydrogenases and the inhibition by ethanol and 4-methylpyrazole

Human alcohol dehydrogenases (ADHs) include multiple isozymes with broad substrate specificity and ethnic distinct allozymes. ADH catalyzes the rate-limiting step in metabolism of various primary and secondary aliphatic alcohols. The oxidation of common toxic alcohols, that is, methanol, ethylene glycol, and isopropanol by the human ADHs remains poorly understood. Kinetic studies were performed in 0.1 M sodium phosphate buffer, at pH 7.5 and 25 °C, containing 0.5 mM NAD + and varied concentrations of substrate. K M values for ethanol with recombinant human class I ADH1A, ADH1B1, ADH1B2, ADH1B3, ADH1C1, and ADH1C2, and class II ADH2 and class IV ADH4 were determined to be in the range of 0.12–57 mM, for methanol to be 2.0–3500 mM, for ethylene glycol to be 4.3–2600 mM, and for isopropanol to be 0.73–3400 mM. ADH1B3 appeared to be inactive toward ethylene glycol, and ADH2 and ADH4, inactive with methanol. The variations for V max for the toxic alcohols were much less than that of the K M across the ADH family. 4-Methylpyrazole (4MP) was a competitive inhibitor with respect to ethanol for ADH1A, ADH1B1, ADH1B2, ADH1C1 and ADH1C2, and a noncompetitive inhibitor for ADH1B3, ADH2 and ADH4, with the slope inhibition constants ( K is ) for the whole family being 0.062–960 μM and the intercept inhibition constants ( K ii ), 33–3000 μM. Computer simulation studies using inhibition equations in the presence of alternate substrate ethanol and of dead-end inhibitor 4MP with the determined corresponding kinetic parameters for ADH family, indicate that the oxidation of the toxic alcohols up to 50 mM are largely inhibited by 20 mM ethanol or by 50 μM 4MP with some exceptions. The above findings provide an enzymological basis for clinical treatment of methanol and ethylene glycol poisoning by 4MP or ethanol with pharmacogenetic perspectives.

Treatment of patients with ethylene glycol or methanol poisoning: focus on fomepizole.

Ethylene glycol (EG) and methanol are responsible for life-threatening poisonings. Fomepizole, a potent alcohol dehydrogenase (ADH) inhibitor, is an efficient and safe antidote that prevents or reduces toxic EG and methanol metabolism. Although no study has compared its efficacy with ethanol, fomepizole is recommended as a first-line antidote. Treatment should be started as soon as possible, based on history and initial findings including anion gap metabolic acidosis, while awaiting measurement of alcohol concentration. Administration is easy (15 mg/kg-loading dose, either intravenously or orally, independent of alcohol concentration, followed by intermittent 10 mg/kg-doses every 12 hours until alcohol concentrations are <30 mg/dL). There is no need to monitor fomepizole concentrations. Administered early, fomepizole prevents EG-related renal failure and methanol-related visual and neurological injuries. When administered prior to the onset of significant acidosis or organ injury, fomepizole may obviate the need for hemodialysis. When dialysis is indicated, 1 mg/kg/h-continuous infusion should be provided to compensate for its elimination. Side-effects are rarely serious and with a lower occurrence than ethanol. Fomepizole is contraindicated in case of allergy to pyrazoles. It is both efficacious and safe in the pediatric population, but is not recommended during pregnancy. In conclusion, fomepizole is an effective and safe first-line antidote for EG and methanol intoxications.

Delayed ethylene glycol poisoning presenting with abdominal pain and multiple cranial and peripheral neuropathies: a case report

IntroductionEthylene glycol poisoning may pose diagnostic difficulties if the history of ingestion is not volunteered, or if the presentation is delayed. This is because the biochemical features of high anion-gap metabolic acidosis and an osmolar gap resolve within 24 to 72 hours as the ethylene glycol is metabolized to toxic metabolites. This case illustrates the less well-known clinical features of delayed ethylene glycol poisoning, including multiple cranial and peripheral neuropathies, and the clinical findings which may point towards this diagnosis in the absence of a history of ingestion.Case presentationA 53-year-old Afro-Caribbean man presented with vomiting, abdominal pain and oliguria, and was found to have acute renal failure requiring emergency hemofiltration, and raised inflammatory markers. Computed tomography imaging of the abdomen revealed the appearance of bilateral pyelonephritis, however he failed to improve with broad-spectrum antibiotics, and subsequently developed multiple cranial neuropathies and increasing obtundation, necessitating intubation and ventilation. Computed tomography of the brain showed no focal lesions, and a lumbar puncture revealed a raised cerebrospinal fluid opening pressure and cyto-albuminological dissociation. Nerve conduction studies revealed a sensorimotor radiculoneuropathy mimicking a Guillain-Barre type lesion with an atypical distribution. It was only about two weeks after presentation that the history of ethylene glycol ingestion one week before presentation was confirmed. He had a slow recovery on the intensive care unit, requiring renal replacement therapy for eight weeks, and complicated by acute respiratory distress syndrome, neuropathic pain and a slow neurological recovery requiring prolonged rehabilitation.ConclusionsAlthough neuropathy as a result of ethylene glycol poisoning has been described in a few case reports, all of these were in the context of a known history of ingestion. As the diagnosis may well be obscured if the history of ingestion is not elucidated, it is important to be aware of this possibility especially if presentation is delayed.

Is the osmole gap a valuable indicator for the need of hemodialysis in severe ethanol intoxication?

Up-to-date no indicator for hemodialysis in severe ethanol intoxication is available. In these cases, the benefits have to outweigh the risks and costs of hemodialysis. In this case report, a suicidal patient had ingested 250 ml of 95% ethanol and was found in deep coma. In literature, some cases, especially of adolescents, are described with severe ethanol poisoning and blood ethanol levels above 740 mg/dL. Hemodialysis, if initiated, decreased ethanol levels significantly as compared to peritoneal dialysis, charcoal or gastric lavage and reduced also clinical costs. While recommendations exist for starting dialysis in ethylene glycol or methanol intoxications, no algorithm is available to determine the situations when hemodialysis is required in ethanol intoxication. The osmole gap may serve as an indicator to differentiate, which patients need haemodialysis - right now, the decision depends upon the physicians experience or preference.

Elevated lactate in ethylene glycol poisoning: True or false?

Abstract Background There have been an increasing number of reports on false increase of lactate in ethylene glycol poisoning. We recently encountered two cases of ethylene glycol poisoning with very high blood lactate concentrations on ABL blood gas analyzers. Methods Patient plasma lactate concentrations were measured on different chemistry instruments in addition to ABL analyzer. Serum ethylene glycol and glycolic acid were also determined. Lactate values were determined from samples spiked with various amounts of glycolic acid. Results In case 1, all the chemistry instruments produced similar lactate results compared to that by ABL analyzer whereas in case 2, the lactate on the ABL was dramatically elevated compared to that from all the chemistry analyzers. There was no glycolic acid detected in case 1 but high glycolic acid was obtained in case 2. Increased concentrations of glycolic acid resulted in a significant positive interference on lactate measurements on the ABL analyzer but none on other instruments. Conclusions False increase of blood lactate by blood gas analyzers may occur but true increase of lactate can also be observed in ethylene glycol poisoning. Elevated lactate concentrations on blood gas analyzers should be confirmed by a chemistry analyzer in the differential diagnosis of ethylene glycol poisoning.

Elevated lactate in ethylene glycol poisoning: True or false?

Background There have been an increasing number of reports on false increase of lactate in ethylene glycol poisoning. We recently encountered two cases of ethylene glycol poisoning with very high blood lactate concentrations on ABL blood gas analyzers. Methods Patient plasma lactate concentrations were measured on different chemistry instruments in addition to ABL analyzer. Serum ethylene glycol and glycolic acid were also determined. Lactate values were determined from samples spiked with various amounts of glycolic acid. Results In case 1, all the chemistry instruments produced similar lactate results compared to that by ABL analyzer whereas in case 2, the lactate on the ABL was dramatically elevated compared to that from all the chemistry analyzers. There was no glycolic acid detected in case 1 but high glycolic acid was obtained in case 2. Increased concentrations of glycolic acid resulted in a significant positive interference on lactate measurements on the ABL analyzer but none on other instruments. Conclusions False increase of blood lactate by blood gas analyzers may occur but true increase of lactate can also be observed in ethylene glycol poisoning. Elevated lactate concentrations on blood gas analyzers should be confirmed by a chemistry analyzer in the differential diagnosis of ethylene glycol poisoning.

Safety and efficacy of high-dose fomepizole compared with ethanol as therapy for ethylene glycol intoxication in cats

To determine the safety and efficacy of high-dose fomepizole compared with ethanol (EtOH) in cats with ethylene glycol (EG) toxicosis. Prospective study. University veterinary research laboratory. Thirteen cats. Two cats received injections of high-dose fomepizole (Study 1). Three cats received lethal doses of EG and fomepizole treatment was initiated 1, 2, or 3 hours later (Study 2). Eight cats received a lethal dose of EG and were treated with fomepizole or EtOH (Study 3). Cats treated with fomepizole received 125 mg/kg IV initially, then 31.25 mg/kg at 12, 24, and 36 hours. Cats treated with EtOH received 5 mL of 20% EtOH/kg IV initially, then every 6 hours for 5 treatments, then every 8 hours for 4 treatments. Cats also received fluids and supportive therapy as needed. Clinical signs were monitored and serial blood analyses performed. Cats receiving fomepizole experienced mild sedation but no biochemical evidence of toxicity. Cats receiving fomepizole for EG intoxication survived if therapy was initiated within 3 hours of EG ingestion. One of the 6 developed acute renal failure (ARF) but survived. Only 1 of the 3 cats treated with EtOH 3 hours following EG ingestion survived; 2 developed ARF and were euthanized. Cats treated 4 hours following EG ingestion developed ARF, whether treated with EtOH or fomepizole. Fomepizole is safe when administered to cats in high doses, prevents EG-induced fatal ARF when therapy is instituted within 3 hours of EG ingestion, and is more effective than treatment with EtOH.

The lactate gap revisited: variable interference with lactate analyses in ethylene glycol poisoning

(2010). The lactate gap revisited: variable interference with lactate analyses in ethylene glycol poisoning. British Journal of Biomedical Science: Vol. 67, No. 3, pp. 148-150.

Uncoventional Views on Certain Aspects of Toxin-Induced Metabolic Acidosis

This discussion will highlight the following 9 specific points that related to metabolic acidosis caused by various toxins. The current recommendation suggests that alcohol dehydrogenase inhibitor fomepizole is preferred to ethanol in treatment of methanol and ethylene glycol poisoning, but analysis of the enzyme kinetics indicates that ethanol is a better alternative. In the presence of a modest increase in serum osmolal gap (<30 mOsm/L), the starting dose of ethanol should be far less than the usual recommended dose. One can take advantage of the high vapor pressure of methanol in the treatment of methanol poisoning when hemodialysis is not readily available. Profuse sweating with increased water ingestion can be highly effective in reducing methanol levels. Impaired production of ammonia by the proximal tubule of the kidney plays a major role in the development of metabolic acidosis in pyroglutamic acidosis. Glycine, not oxalate, is the main final end product of ethylene glycol metabolism. Metabolism of ethylene glycol to oxalate, albeit important clinically, represents less than 1% of ethylene glycol disposal. Urine osmolal gap would be useful in the diagnosis of ethylene glycol poisoning, but not in methanol poisoning. Hemodialysis is important in the treatment of methanol poisoning and ethylene glycol poisoning with renal impairment, with or without fomepizole or ethanol treatment. Severe leucocytosis is a highly sensitive indicator of ethylene glycol poisoning. Uncoupling of oxidative phosphorylation by salicylate can explain most of the manifestations of salicylate poisoning.

Urinary Tract Lesions in Cats And Dogs: Epidemio-Pathological Study

The present study aimed to provide an epidemiological and pathological study on urinary tract diseases in dogs and cats, spontaneous cases, encountered in the Department of Pathology, Forensic Medicine, and Necropsy Diagnosis of FMV Cluj from 1st January 2008 to 1st March 2010. The biological material was represented by 49 cadavers, respectively 15 cats and 34 dogs which presented lesions of the urinary tract. The animals were brought to the Veterinary Pathology Department for the necropsy and histopathological exam. Necropsy was performed according to conventional necropsy technique. This was followed by collection of biological samples, inserted into the fixative agent (10% formalin, pH 7) for 24 hours then processed through the paraffin inclusion technique and examined microscopically for histopathological diagnosis. Histological analysis of samples was performed with an Olympus BX 41 optical microscope and image processing was performed using the software CellB. From the total of 768 animals (635 dogs and 133 cats) which were examined during the mentioned period, only 49 animals (6.38%) presented urinary tract lesions. A total of 11.27% of the investigated cats and 5.35% of the investigated dogs presented urinary tract disorders (table 1).Urinary tract pathology, respectively mainly renal pathology, is more important in cats than in dogs, and most significant lesions were represented by acute tubular necrosis (following ethylene-glycol intoxication), chronic fibrous and proliferative nephritis and lipid dystrophy. In dogs, the lesions that predominated were represented by acute and chronic renal infarcts, chronic nephritis (of fibrous and lympho-hystiocitic type), acute tubular necrosis and dystrophies (such as mineralization and hyalinization).

Alcohol-induced changes in the brain as assessed by MRI and CT

This review provides an overview of structural magnetic resonance imaging and computed tomography findings of direct and indirect alcohol-related toxic effects on the brain. In addition to ethanol-related changes to the brain, this article will also describe imaging findings in the acute setting of methanol and ethylene glycol poisoning. Alcohol will lead to brain atrophy, osmotic myelinolysis, Marchiafava-Bignami disease and, especially when related to malnutrition, may also cause Wernicke encephalopathy. Brain atrophy can be reversible if alcohol abuse is stopped. If not treated, Wernicke encephalopathy can lead to coma and death and an early diagnosis is important for immediate initiation of thiamine substitution. As clinical symptoms are often unspecific, the radiologist plays an important role in the detection of alcohol abuse and its related clinical conditions.