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Ethylene Glycol Poisoning J Postgrad Med J: first published as 10.1136/pgmj.52.611.598 on 1 September 1976. Downloaded from Postgraduate Medical Journal (September 1976) 52, 598-602 Ethylene glycol poisoning J. A. VALE B. WIDDOP M.B., M.R.C.P. B.Sc., Ph.D. N. H. BLUETT M.R.C.P., D.C.H. Poisons Unit and Paediatric Unit, Guy's Hospital, London SEI 9RT Summary ethylene glycol poisoning in a child who sub- Although an uncommon cause of death in Great sequently recovered, despite the development of Britain, ethylene glycol poisoning is potentially serious renal insufficiency, and describe the clinical presen- in that renal and cardiopulmonary failure and central tation and management ofethylene glycol poisoning. nervous system dysfunction can occur when doses of the order of 100 ml or more are ingested. A case is Case report described in which a child who swallowed approxi- A previously healthy child of 21 years ingested mately 100 ml of ethylene glycol was treated by pro- about 100 ml of ethylene glycol during the evening longed peritoneal dialysis. In addition, measures were of 12 March 1975. The child vomited but seemed taken to correct a marked acidosis. Substantial otherwise well when his parents put him to bed. The Protected by copyright. amounts of ethylene glycol were removed by the next morning, however, he was found unconcious in dialysis fluid and the child made a complete physical bed and taken to the local hospital. On arrival he and mental recovery. was collapsed, semi-concious, and hyperventilating. His pulse rate was 140/min, BP 30/0 mmHg and ETHYLENE glycol, (CH20H)2, is a colourless, scattered crepitations were present in both lung odourless, water-soluble liquid that has a variety of fields. He was given calcium gluconate intravenously; commercial applications. It is, however, most com- an infusion of ethyl alcohol was commenced and a monly used as an anti-freeze fluid to protect car diuresis was induced with frusemide. Subsequently, radiators. It has been suggested that its sweet taste the child had several haematemeses and his level of and its ready availability have contributed to its popu- consciousness deteriorated. In addition he was larity as a suicide agent and as a poor man's sub- oliguric (150 ml urine in 24 hr) and haematuria and stitute for alcohol (Parry and Wallach, 1974). albuminuria were noted. Further investigations Ethylene glycol came into widespread use in the revealed a haemoglobin of 10-8 g/100 ml, a leuco- 1920's and the first case of poisoning was described cytosis of 14-4 x 103/,d (72% neutrophils), a serum http://pmj.bmj.com/ in 1930 (JAMA, 1930). The toxicity of the glycols bicarbonate of 3-3 mmol/l (base excess -30), an was, however, not fully appreciated until 1937 when arterial pH of 6-87 and a urea of 12-36 mmol/l. He seventy-six people died following the use of elixir of was transferred to the Paediatric Renal Unit at sulphanilamide which contained 72% diethylene Guy's Hospital for peritoneal dialysis which was glycol (Geiling and Cannon, 1938). It is appalling commenced on 13 March 1975 and continued for 8 that in 1969 seven children died in Cape Town as a days. The next day the child had six convulsions; a result of the ingestion of an hypnotic also containing further five occurred on 15 March 1975 but all were this substance (Bowie and McKenzie, 1972). controlled by diazepam. The child was thereafter on September 26, 2021 by guest. Deaths from ethylene glycol poisoning are un- given phenobarbitone. He remained irritable, devel- common in Great Britain: there have only been oped a squint and had athetoid movements. By 16 twelve reported in a period of 29 years (1945-73). In March 1975 the urine output had increased to 2 contrast forty to sixty deaths occur each year in the 1/day and the level of consciousness had begun to U.S.A. (Haggerty, 1959). It is thought that the mini- improve. The child later developed a urinary tract mum lethal dose of ethylene glycol is about 100 ml infection but by 17 days after admission he had for an adult, although recovery has been reported made a complete physical and mental recovery. after the ingestion of 240 ml (Kahn, 1950) and 400 During the 8 days of dialysis (71-5 1) 26-9 g ethylene ml (Seeffet al., 1970). The pathogenesis ofthe clinical glycol (equivalent to 30 ml approximately) and 73 manifestations of this form of poisoning is now mg oxalate (between 10 and 40 mg oxalate are nor- better understood. We therefore report a case of mally excreted in the urine each day) were removed. Postgrad Med J: first published as 10.1136/pgmj.52.611.598 on 1 September 1976. Downloaded from Case reports 599 Methods Metabolism of ethylene glycol Ethylene glycol was measured in the dialysis fluid Ethylene glycol itself appears to be non-toxic. It by a gas chromatographic method. Aqueous stan- has no effect on respiration, the citric acid cycle or dards were prepared containing from 200 to 1,000 mg other biochemical pathways until metabolized (Bach- of ethylene glycol/l. To 1 ml of each of these stan- mann and Golberg, 1971). Metabolism takes place dards and the sample were added 1 ml aliquots of in the liver and kidney and proceeds as shown in propane 1,2-diol (1,000 mg/l in water) internal Fig. 1. The toxicity of ethylene glycol may be standard. After mixing thoroughly, 3 .d of the explained on the basis of the accumulation of three solution were injected on to a Poropak Q column metabolic products: operating isothermally at 180'C. The calibration (i) Aldehydes, which inhibit oxidative phos- curve derived by plotting concentration against the phorylation, respiration and glucose metabolism ratio peak area of ethylene glycol: peak area of pro- (Bachmann and Golberg, 1971; Kun, 1952; Lamothe, pane 1,2-diol was linear over the chosen range and Thuret and Laborit, 1971), protein synthesis (Kun, the concentration of ethylene glycol in the sample 1952), DNA replication and ribosomal RNA syn- was calculated by direct reference to this curve. thesis (Klamerth, 1968), central nervous system Oxalate concentration was measured by the fluori- respiration (Lamothe et al., 1971), serotonin metab- metric procedure of Zarembski and Hodgkinson olism (De Breyer, Ortiz and Soehring, 1970) and (1965). alter central nervous system amine levels (Laborit et al., 1971). The cerebral symptoms that occur 6-12 Comment hr after the ingestion of ethylene glycol (Table 1) This child illustrates many of the features of coincide with the maximum production ofaldehydes. ethylene glycol poisoning (Tables 1 & 2) including (ii) Oxalate, which may produce renal damage and vomiting, haematemesis, coma, convulsions, oph- acidosis. It is thought, however, that only about 1 % thalmoplegia, tachycardia, tachypnoea, pulmonary of ethylene glycol is converted to this compound Protected by copyright. oedema and acute renal damage. Investigations (McChesney et al., 1971). The production of oxalate demonstrated leucocytosis, acidosis, uraemia, haema- is also important in that it may chelate with calcium turia and albuminuria. Large amounts of ethylene ions forming relatively insoluble calcium oxalate glycol were removed by dialysis. crystals; hypocalcaemia may result. As well as renal intratubular obstruction, impairment of cerebral TABLE 1. Clinical features of ethylene glycol poisoning function follows deposition of calcium oxalate. Usual time (iii) Lactic acid, which is produced as a result of sequence after large amounts of nicotinamide adenine dinucleotide ingestion Clinical features being formed during the breakdown of ethylene gly- col (Oliva, 1970). In addition some of the conden- 30 min-12 hr Patient appears intoxicated with alcohol sation products of glyoxylate the (but no alcohol on the breath). metabolism inhibit Nausea, vomiting, haematemesis. citric acid cycle thereby increasing lactic acid pro- Coma and convulsions (often focal). duction (Fig. 1). Nystagmus, ophthalmoplegias, papilloe- http://pmj.bmj.com/ dema, optic atrophy, depressed reflexes, Clinical features myoclonic jerks, tetanic contractions. 12-24 hr Tachypnoea, tachycardia, mild hyper- Berman, Schreiner and Feys (1957) have suggested tension, and cyanosis. Pulmonary that the clinical syndrome of ethylene glycol poison- oedema, congestive cardiac failure. ing may manifest itself in three stages (Table 1). If 24-72 hr Flank pain and costovertebral angle the patient survives the initial 24-72 hr after inges- tenderness. Acute tubular necrosis. tion, when cerebral and cardiopulmonary symptoms are predominant, renal failure may become evident. TABLE 2. Typical laboratory investigations in ethylene glycol The severity of each stage and the progression from on September 26, 2021 by guest. poisoning one to the other depends very largely on the amount Investigation Abnormality of ethylene glycol ingested. Death may occur in any White cell count Raised (10-40 x 103/,Fj)-predomi- of the three stages. nantly neutrophils Serum bicarbonate Reduced (may be < 10 mEq/l) Diagnosis Serum calcium Reduced Ethylene glycol poisoning Serum potassium Raised should be strongly sus- Urinalysis Low specific gravity pected in the presence of: Proteinuria (i) An apparently inebriated patient with no alcohol Crystalluria (Ca oxalate) on the breath. Microscopic haematuria (ii) Coma associated with metabolic acidosis and a Cerebrospinal fluid Compatible with meningoencephalitis large anion gap. Postgrad Med J: first published as 10.1136/pgmj.52.611.598 on 1 September 1976. Downloaded from 600 Case reports - NADH- Lactic acid I / I II I / / I / I / / LDH LDH I . or or Ethylene ADH Glycooldehyde AO Glycolate GAO Glyoxylote AO Oxalate glycol GT| Glycine + Oxolomolote carbon a -Hydroxy -)i3- ketoodipote ADH = Alcohol dehydrogenose dioxide a-Hydroxy-a-ketoglutorate AO = Aldehyde oxidase Inhibition af GAO = Glycolic acid oxidase citric acid cycle GT = Glyoxylate transominose LDH = Lactic dehydrogenase t NADH = Nicotinamide adenine dinucleotide Lactic PRP = Pyridoxal phosphate FIG.
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