ISSN No. 1606-7754                   Vol.13 No.2  August 2005

Ethylene Glycol intoxication with and without simultaneous diabetic ketoacidosis: A report of nine cases and review of the literature
Juan Ybarra, Teresa Doñate, Josep Maria Pou, Zuhayr T Madhun
Servicio de Endocrinología y Nutrición, Hospital de San Pablo. Barcelona, Spain

Abstract

Objective: To describe the clinical and biochemical observations made on nine patients with ethylene glycol intoxication (EGI) of whom five presented with simultaneous diabetic ketoacidosis (DKA). Methods: A retrospective chart search for discharge diagnosis including the term ethylene glycol intoxication was conducted at University Hospitals of Cleveland Information Services (Cleveland, OH) from 1986 through 1998. Nine (N=9) patients were identified and subsequently divided into two Groups (A & B). Group A included 5 patients with both DKA and EGI. Group B included 4 patients with EGI without DKA. Clinical manifestations and laboratory tests are summarized for both Groups. Serum specimens for all patients were analyzed for ethylene glycol, propylene glycol, methanol, serum ketones, glucose, pH, electrolytes, liver and kidney function tests, lipase, amylase, cholesterol, triglycerides, C-peptide and glycosylated Hb. Results: Group A patients presented with more severe hyperglycaemia accompanied by increased insulin requirements, glucose toxicity, more severe osmotic diuresis induced severe dehydration, pre-renal azotemia, transient rhabdomyolysis and hypertriglyceridaemia. Their acute renal failure was fully reversible upon discharge. Finally, the length of hospital stay of patients in Group A was significantly longer than that of Group B patients, although mortality rate was reduced. Permanent and irreversible kidney damage requiring haemodialysis was seen in all Group B patients. Conclusions: severe DKA presenting with simultaneous high anion and osmolal gap should prompt suspicion to the hypothetical concomitant EGI, particularly in those patients with a history of alcoholism, depression and past suicidal attempts.

Key words: Ethylene glycol intoxication, diabetic ketoacidosis, anion gap, osmolal gap, haemodialysis

Introduction

Ethylene glycol is a colourless, odourless, water-soluble liquid with a sweet taste resembling some liqueurs, commonly found in radiator-antifreeze, detergent, paints, lacquers and solar collectors, among others. Intoxication is usually due to accidental ingestion, suicide attempt, or consumption as a substitute for ethanol.

Initial diagnosis is frequently delayed if history of ingestion is unavailable. Classical clinical presentation includes central nervous system symptoms (decreased mental status varying from lethargy to obtundation and coma), tachycardia, tachypnea, and acute renal failure.1-8 The biochemical profile is that of a high anion ([Na]-([Cl] + [HCO3]) and osmolal gap (measured plasma osmolality – calculated plasma osmolality) metabolic acidosis, acute renal failure and the presence of oxalate as well as hyppurate crystals in the urine.9-16 Haemodialysis, parenteral ethanol, 4-methylpyrazol and bicarbonate infusions have been shown to be useful in eliminating the toxin, blocking its hepatic metabolism and correcting the initial severe metabolic acidosis. Interestingly enough and to the best of our knowledge, the finding of simultaneous occurrence of true EGI and emerging diabetic ketoacidosis (DKA) has not been reported.

Material and Methods

A retrospective chart search of admissions at University Hospitals of Cleveland Information Services (Cleveland, OH) was conducted in a twelve year period from January 1986 to December 1998. Nine consecutive adult patients were found with the discharge diagnosis of EGI during that period. Their demographic characteristics are depicted in Table 1.

EGI was defined as classical clinical manifestations presenting with a history of ethylene-glycol containing product ingestion and serum concentrations higher than 3 mg/dl.

DKA was defined as a triad including hyperglycaemia-acidosis-ketosis, the primary cause of which is relative or absolute insulin deficiency. According to their biochemical profile on admission, patients were classified as:

Group A (N=5): presenting with DKA and EGI. Gender distribution was M4/F1. MeanSD age was 41.4±14.6 years. Four out of five were previously known diabetics while two out of five had a previous psychiatric diagnosis. Group B (N=4): presenting with EGI without DKA. Gender distribution was M2/F2. Mean±SD age was 46.3±8.3 years. Two out of four were previously known diabetics while 2 out of four had previous psychiatric diagnosis.

Serum electrolytes, complete blood count, amylase, lipase and other biochemical results were performed using a routine hospital serum multiple analyzer. Ethylene glycol determination was performed using a sensitive enzymatic assay GCMS from COBAS-BIO/Roche (Nurtely, NJ, USA, City/State) (17). The lower detection limit is 3 mg/dl and linearity is assured in the 3-200 mg/dl range (value of high standard). Interfering substances include: Glycerol, 1.2-Propane-diol, 2.3-Butane-diol, 1.4-Butane-diol, inositol, isopropanol, propylene glycol and sorbitol. The latter can produce falsely elevated results if present in the serum sample. Formulas for anion and osmolal gap calculation are the following: Anion gap= [Na] – ([Cl] + [HCO3]); NV=12  2 mEq/L. Osmolal gap= measured plasma osmolality – calculated plasma osmolality; NV= 10  2 mOsm/Kg. Calculated plasma osmolality=2 X [Na] + [Glucose]/18 + [BUN]/2.8 + [ethanol]/4.6.

Extracellular fluid markers of dehydration and plasma volume contraction and haemoconcentration in both Groups were defined as BUN, creatinine, albumin, uric acid and haematocrit.

Statistical methods: Data is expressed as mean ± standard deviation. Unpaired Student’s t-test and Chi square test were employed. Results displaying a P<0.05 were considered to be significant.

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