· Paraldehyde is a polymer of acetaldehyde and occurs as a colourless liquid with a pungent odour and disagreeable taste.
· It was previously popular as a hypnotic, but is today used only for the treatment of alcoholic withdrawal (deliriumtremens), or certain other psychotic states in hospitalisedpatients.
· Paraldehyde is irritating to the alimentary tract and hence is never given orally. Oral administration has produced severe corrosion of the stomach. Parenteral use is associated with serious problems (narrow safety margin on IV administration; skin sloughing, sciatic nerve damage, sterile abscess formation, etc. on IM injection). For these reasons, paraldehyde is usually only given rectally.
Proper storage of paraldehyde is essential—below 30° C— in small, light resistant, well filled, tightly covered containers, or else it is likely to depolymerise to acetaldehyde which then gradually metabolises to acetic acid. Severe poisonings and fatalities have been reported following administration of partially decomposed paraldehyde.
Metabolites in man have not been determined but based on animal studies, it is thought that up to 80% of paraldehyde is converted to acetaldehyde in the liver which is then converted to acetic acid. Acetic acid is thought to be further metabolised via the Krebs cycle to carbon dioxide and water. Approximately 28% is excreted by way of the lungs, and 3% is excreted unchanged in the urine.
Continued use of large doses of paraldehyde may cause visual and acoustic hallucinations, delusions, impairment of memory, intellect, and speech, unsteady gait, tremors, anorexia, and weight loss.
Signs and symptoms of poisoning include pungent odour on breath, irritation of mouth and throat, bleeding gastritis, muscular irritability, vertigo, hypotension, tachycardia, miosis (or mydriasis), pulmonary haemorrhages and oedema, dilata-tion of the right heart, oliguria, albuminuria, fatty changes in the liver and kidney with toxic hepatitis and nephrosis, azotaemia, and coma. A high anion-gap metabolic acidosis is characteristically encountered. Leucocytosis is also said to be a common finding. Cough is a common early symptom, and intense coughing for 2 to 5 minutes is often seen with IV administration of low doses.
Deaths have been reported with ingestion of as little as 25 ml of paraldehyde. Other deaths have been reported from ingestion of 31 to 120 ml, and rectal administration of 12 to 31 ml. Intravenous paraldehyde has been fatal at doses of 35 ml.
Treatment involves mainly supportive measures with particular emphasis on maintenance of airway, breathing, and circulation. Therapeutic levels of paraldehyde vary consider-ably due to individual susceptibility, but the estimated concen-tration to prevent convulsions is 100 to 200 mg/L. Check for possible acidosis. Correction of metabolic acidosis is impera-tive. Although hypotension is usually not severe, support with pressor drugs may be necessary. For acute lung injury, maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FiO2 is required to maintain adequate oxygenation, mechanical ventilation, and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 ml/kg) is preferred if ARDS develops.