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Toxicity of brake oil
  1. N Sharma,
  2. S Jain
  1. The Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India
  1. Correspondence to:
 Dr N Sharma, The Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India 160012;


Brake oil is an automobile transmission fluid composed of a mixture of toxic glycols and glycol ethers. Three cases of poisoning with toxic glycol based brake fluid are reported who presented with mild metabolic acidosis and acute renal failure. As all the cases had presented late, treatment with ethanol was not started. All of them were treated successfully with haemodialysis.

  • ethylene glycol
  • metabolic acidosis
  • brake fluid
  • renal failure

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A 30 year old man presented to the emergency room 72 hours after having consumed 100 ml of brake fluid after intake of 60 ml of whisky (40% proof). He had three vomits immediately after the consumption and a progressive decrease in his urine output the next day. At admission, the pulse was 92 per minute and blood pressure 164/100 mm Hg. The systemic examination was normal. Laboratory investigations revealed normal complete blood counts. The serum biochemistry values are given in table 1. The urine examination did not reveal any crystals of calcium oxalate; however, numerous red blood cells could be seen.

Table 1

Laboratory parameters of patients presenting with brake oil intoxication

The presence of renal failure necessitated immediate haemodialysis. Hypertension worsened requiring antihypertensive therapy with nifedipine and atenolol. The presence of prolonged oliguria raised suspicion of renal cortical necrosis but the renal biopsy showed only acute tubular necrosis. After receiving 15 haemodialyses over a period of five weeks he went into the diuretic phase of acute renal failure and was discharged soon thereafter in a satisfactory condition.


These were two brothers aged 40 years and 35 years. They presented to the emergency services 24 hours after having consumed approximately 40–60 ml of brake oil with 80 ml of rum. Both had many vomits over the next few hours followed by declining urinary outputs. At admission, the pulses and blood pressures of both were normal and systemic examination of both patients did not reveal any abnormality. Laboratory indices obtained showed normal complete blood counts. Serum biochemical values of both are presented in table 1. The urine examination of both patients showed a 2+ proteinuria, plenty of red blood cells but no crystals of calcium oxalate.

Both patients were taken up for immediate haemodialysis. The urine outputs of both remained in the oliguric range. After receiving six haemodialyses in one and eight in the other, both patients went into the diuretic phase of acute renal failure and were discharged a week later in a satisfactory condition.


Both ethylene glycol and diethylene glycol are colourless, odourless, sweet tasting compounds with widespread commercial use. Whereas ethylene glycol is used as antifreeze, coolant, and preservative, diethylene glycol has been used as a replacement for glycerine. The earliest reported toxicity of diethylene glycol dates back to 1937 when it was used as a vehicle for preparing sulfanilamide elixir.1 According to a document by Dow Chemical Company, a leading producer of automobile liquids, brake fluid is a transmission fluid composed of a mixture of several glycols like ethylene glycol, diethylene glycol, polyethylene glycol, polypropylene glycol and glycol ethers. To the best of our knowledge, so far there has been only one case report of poisoning resulting from the consumption of brake fluid.2

After ingestion of ethylene glycol, inebriation occurs but the typical smell of alcohol is lacking. Ethylene glycol is metabolised by the enzyme alcohol dehydrogenase to glycoaldehyde, glycolic acid and glyoxylic acid, which are responsible for most of the clinical effects of ethylene glycol poisoning.2 Cardiovascular toxicity of ethylene glycol usually appears after a period of 12–24 hours and is characterised by tachycardia, hypertension, and pulmonary oedema.2 In all the three cases, apart from nausea and vomiting, the other clinical features were not present. Acute renal failure usually occurs as a delayed manifestation after 24 hours of ingestion in 73%–84% of cases of ethylene glycol poisoning 2 and was present in all of our cases. The presence of proteinuria in all cases was consistent with acute tubular necrosis and was confirmed on biopsy of the kidney in case number 1. All of our cases also had microscopic haematuria.

For patients presenting early with ethylene glycol poisoning treatment with ethanol is preferred. Ethanol acts by competing with ethylene glycol for the enzyme alcohol dehydrogenase thus limiting the formation of toxic metabolites. All three patients had presented late (>24–72 hours) with established renal failure. As the elimination half life of ethylene glycol is three hours 2 and more than five times the elimination half life had elapsed, there would have been little ethylene glycol left in the body. Hence, treatment with ethanol would not have served any therapeutic purpose. The modality of treatment chosen was haemodialysis to facilitate removal of toxic metabolites of ethylene glycol and to combat uraemia.

Besides ethylene glycol, the other components of brake fluid may also have played some part in the manifestations of this unusual poisoning. Diethylene glycol has been incriminated earlier in a case report of five cases of acute renal failure complicating the use of diethylene glycol based silver sulfadiazene ointment.3 Recently, diethylene glycol has been implicated as the causative factor for renal failure in the paediatric population of Bangladesh, Haiti, and India.4–6 The mode of poisoning was from contamination of the available liquid peadiatric medications with diethylene glycol. In another case report, propylene glycol has also been suspected of having led to hyperosmolarity and cardiorespiratory arrest in an infant.7 All toxic glycols are metabolised by alcohol dehydrogenase resulting in profound metabolic acidosis attributable to the accumulation of organic acids. In all our cases, it is possible that the consumption of ethanol probably led to partial saturation of the enzyme alcohol dehydrogenase thereby limiting the formation of organic acids. The resultant metabolic acidosis was mild in all cases and significant toxicity on systems other than the kidneys was avoided.


Navneet Sharma was the treating physician who diagnosed, managed and treated the patients in the medical emergency. Sanjay Jain, a senior consultant in the emergency department, actively participated in the discussion of treatment modalities and review of this paper. Navneet Sharma is the guarantor of the paper.



  • Funding: none

  • Conflicts of interest: none