differential diagnosis of coma

 confirmation of brain death

 monitoring of drug abuse

 investigation of suspected non-accidental poisoning (e.g. in children).

 Salicylate poisoning can result in severe metabolic acidosis, from which the patient may not recover. This common drug must be tested for if there is any likelihood that it has been taken. The treatment for salicylate poisoning is intravenous sodium bicarbonate, which both enhances excretion and helps correct the acidosis (Fig 60.2).

 Paracetamol (acetaminophen) poisoning causes serious hepatocellular damage and severely affected patients may die of liver failure. In cases of poisoning, the plasma paracetamol concentration, related to time of ingestion, is prognostic (Fig 60.3). A specific therapy, N-acetylcysteine, given intravenously, can prevent all of the hepatotoxic and nephrotoxic effects of paracetamol poisoning. Therapy should be started within 12 hours of ingestion, and hopefully before any clinical symptoms or biochemical changes develop. Patients who abuse alcohol are at particular risk from paracetamol poisoning.

 Slow release theophylline preparations in overdose can lead to late development of severe arrhythmias, hypokalaemia and death. In cases of suspected poisoning, the plasma theophylline concentration should be measured and its rise or fall monitored. Measures to aid elimination are of limited effect.

 Organophosphate and carbamate pesticides, in which cholinergic symptoms persist for some time. Cholinesterase should be monitored.

 Atropine, causing anticholinergic features, e.g. hallucinations with dry mouth, dry hot skin and dilated pupils. Cases occur most often from ingestion of herbal medicines.

 Opiates, where overdose leads to pin-point pupils that rapidly dilate on treatment with naloxone.

 Cardiac glycosides, both pharmaceutical and herbal, give rise to severe bradycardia.

 Methanol and ethylene glycol, poisoning is not uncommon, especially in alcoholics. These toxins are metabolized to formic acid and oxalic acid respectively. Patients develop a severe metabolic acidosis and, in the case of ethylene glycol, hypocalcaemia. Measuring the serum osmolality and calculating the osmolal gap can be useful here. Treatment is with intravenous ethanol to a plasma concentration of around 20 mmol/L. The ethanol is preferentially metabolized and the unchanged alcohols are gradually eliminated in the urine. An alternative is to block metabolism with fomepizole, but high costs limit its use.