In relation to Ethylene glycol poisoning

Ethylene Glycol poisoning presents in three phases depending on timing: initially (30-60 minutes) after ingestion acute intoxication occurs. This may also result in excitatory symptoms, cerebral oedema, convulsions and coma. The second phase occurs at 12-18 hours with predominantly cardiovascular effects including dysrhythmias and cardiac failure. Profound metabolic acidosis often causes death during this phase. Phase three occurs at 2-3 days with predominantly renal failure and acute tubular necrosis due to calcium deposition. Finally, a delayed neurologic phase can occur 5-20 days post-ingestion, presenting with neurological effects including profound limb weakness, cranial nerve palsies and sensory disturbance. EG causes an increased anion gap acidosis. Other causes of a raised anion gap acidosis include lactate, toxins (ethanol, ethylene glycol, methanol, paraldehyde, aspirin, cyanide, iron, isoniazid), and ketoacidosis (diabetes, alcohol). Causes of a normal anion gap acidosis include gastrointestinal losses (diarrhea), renal loss of bicarbonate (proximal renal tubular acidosis), renal failure and hyperchloraemic acidosis. Renal replacement therapy is a very effective treatment for EG poisoning, as it corrects acid-base status and eliminates EG and some of the harmful metabolites. Fomepizole is a potent inhibitor of alcohol dehydrogenase preventing the production of toxic metabolites of EG. It is given as a loading dose 15mg/kg and then 10mg/kg every 12 hours for the next 48 hours. After which, the dose is increased to 15mg/kg 12hourly. It is continued until plasma EG levels are less than 20mg/dL.Reference: Glossop AJ, Bryden DC. Case repo: an unusual presentation of ethylene glycol poisoning. J Intensive Care Soc 2009; 10(2): 118-21