L.Symington, L.Jackson, B. Klaassen
Accident and Emergency, Ninewells Hospital, Dundee.
Correspondence to: Dr Linda Symington, Specialist Registrar, Accident and Emergency, Ninewells Hospital, Dundee. DD1 9SY Email: linda.r.symington@tuht.scot.nhs.uk)
SMJ 2005 50(3): 129-130
Abstract
Ethylene glycol is recognised as a potentially lethal poison if ingested. Approximately 100mls may be fatal in a 70kg adult. Current Toxbase guidelines are the accepted standard of treatment of such poisonings in the United Kingdom. These guidelines suggest that symptoms of significant poisoning are usually present within 30 minutes of ingestion i.e. ataxia, dysarthria, nystagmus, nausea and vomiting, haematemesis, coma and convulsions. In the absence of these symptoms, metabolic acidosis or ethylene glycol concentration more than 8mmol/l a single loading dose of ethanol and observation were the recommended course of management until recently. We report a case of a patient who remained relatively asymptomatic for almost 24 hours but then developed clinical symptoms with marked metabolic acidosis and renal impairment requiring intensive treatment including haemodialysis.
Key words: Ethylene glycol, poisoning, treatment
Case report
A 22-year-old female weighing 55kg attended the A&E department four hours post ingestion of four dihydrocodeine, two cans of cider, approximately 800mls of ethylene glycol and five mouthfuls of Domestos. She reported vomiting copious amounts of blue fluid immediately post ingestion. She vomited on arrival but this settled shortly thereafter. She denied any relevant past medical history, regular medication or allergies. She had no known previous psychiatric problems or episodes of self-harm.
On examination she was found to be alert and orientated, conversing normally. Pulse was 90bpm, BP 90/60, respiratory rate 14/min, oxygen saturation was 98% on room air. There was no evidence of ataxia, dysarthria or nystagmus. She was immediately given 150mls of 45% oral ethanol. Arterial blood gas analysis showed no evidence of metabolic acidosis (Tables I,II). Venous bloods were sent. It was not possible to get ethylene glycol levels acutely overnight in our hospital laboratory. Renal function and calcium levels were normal at this time.
The patient was discussed with the local poisons bureau. It was suggested that it was unlikely she had absorbed a dangerous amount of ethylene glycol in the absence of any significant clinical or biochemical findings. Advice was therefore to treat with the oral bolus of ethanol, as already given, and observe.
Progress
Repeat arterial blood gas at 8-9 hours post ingestion again showed no evidence of metabolic acidosis and the patient remained well and asymptomatic. The only biochemical abnormality at four hours had been a raised plasma osmolality. This had markedly improved at eight hours. On review 18 hours post ingestion this patient still showed no symptoms or signs of toxicity. She was tolerating oral intake and no intravenous fluids had been given. Pulse was 78bpm, BP 90/40, respiratory rate 18/ min. Venous bloods were repeated and ethylene glycol requested again on these and the admission samples. Urea and electrolytes and calcium were normal and osmolality was now 336mmol/l.
Acutely at 23-24 hours post ingestion this patient became agitated and ataxic. Pulse was now 120bpm, BP 138/84, respiratory rate 26/min. Repeat arterial blood gas showed a marked metabolic acidosis. Ethylene glycol levels were still unavailable at this time. A further oral dose of ethanol was given and intravenous ethanol was requested from pharmacy. Meanwhile intravenous fluids were started. At approximately 1530, almost 24 hours post ingestion ethylene glycol levels were notified to have been 84mmol/l at four hours and 34mmol/ l at 18 hours. Intravenous ethanol was being given. Urea and electrolytes now showed an elevated creatinine of 123.
Treatment continued with intravenous ethanol and fluids but over the next 12 hours the acidosis persisted and renal function worsened. Urine output was initially maintained but then became minimal. She was referred to the renal specialists and ICU and was haemodialysed. After a total of four haemodialysis sessions renal function began to improve and creatinine returned to 127 prior to discharge.
Discussion
This appears to be an unusual presentation and clinical course of a patient with a significant ethylene glycol poisoning.1,2 Although many of the metabolic changes are recognised to occur later, physical signs of ingestion are usually apparent in the early stages of significant poisoning. A medline search of ethylene glycol poisoning produced no case reports or clinical studies that indicated instances of a similar clinical course.
Toxbase guidelines at this time only advised continuous ethanol for patients who appeared severely poisoned i.e. unconscious, metabolic acidosis or a measured ethylene glycol concentration of more than 8mmol/l. It is known that prompt treatment of these patients can be very effective and the introduction of fomepizole gives a further, apparently effective, treatment.3
In this case severe poisoning has occurred in a patient who showed no marked early clinical or biochemical abnormalities except a raised osmolality. This highlighted the importance of rapid availability of the assay of toxic alcohol for such presentations. Following this case our department of Biochemical Medicine has changed practice to allow emergency testing at presentation. Assay availability has helped the management of patients presenting since this case. Toxbase now advises contacting the local poisons services or a biochemist in all cases of ethylene glycol ingestion as in many centres concentration assays are not readily available. We feel this case highlights the need to treat patients with a high index of suspicion until formal levels are available despite an absence of physical findings.
ACKNOWEDGEMENTS: We are grateful to Dr. Bateman at Scottish Poisons Information Bureau for his help and advice with this article.
REFERENCES
1 Hylander B, Kjellstand Cm. Prognostic factors and treatment of sever ethylene glycol intoxication. Intens Care Med 1996;22:546-552
2 Vale JA, Widdop B,Bluett NH. Ethylene glycol poisoning.Postgrad Med J 1976;52:598-602
3 Brent J, McMartin KE, Phillips S, et al. Fomepizole for the Treatment if Ethylene Glycol Poisoning. N Eng J Med 1999;340:832-838