Lithium salts are chemical salts of lithium used as mood stabilizing drugs, primarily in the treatment of bipolar disorder, depression, and mania; but also in treating schizophrenia. Usually lithium carbonate (Li2CO3), but sometimes the citrate salt, lithium citrate is used. The orotate salt, lithium orotate, may also be used. The salt is widely distributed in the central nervous system and interacts with a number of neurotransmitters and receptors, decreasing noradrenaline release and increasing serotonin synthesis.
The use of lithium salts was developed by the Australian psychiatrist John Cade, after an accidental discovery of their effects on animals led to trials on human patients.
Lithium treatment is used to sedate overactive and euphoric patients. Initially, lithium is often used in conjunction with antipsychotic drugs as it can take up to a week for lithium to have an effect. Lithium treatment is generally considered to be unsuitable for children.
Lithium toxicity and side effects
Those who use lithium should receive regular blood tests and should monitor the thyroid and kidney for toxic damage. As it is a salt, lithium can cause dehydration. Dehydration, which is compounded by heat, can result in increasing lithium levels.
High doses of haloperidol, fluphenazine, or flupenthixol may be hazardous when used with lithium; irreversible toxic encephalopathy has been reported.
Lithium salts, with the exception of lithium orotate, have a narrow therapeutic/toxic ratio and should therefore not be prescribed unless facilities for monitoring plasma concentrations are available. Patients should be carefully selected. Doses are adjusted to achieve plasma concentrations of 0.6 to 1.2mmol Li+/litre (lower end of the range for maintenance therapy and elderly patients) on samples taken 12 hours after the preceding dose. Overdosage, usually with plasma concentrations over 1.5mmol Li+/litre, may be fatal and toxic effects include tremor, ataxia, dysarthria, nystagmus, renal impairment, and convulsions. If these potentially hazardous signs occur, treatment should be stopped, plasma lithium concentrations redetermined, and steps taken to reverse lithium toxicity.
Lithium toxicity is compounded by sodium depletion. Concurrent use of diuretics that inhibit the uptake of sodium by the distal tubule (e.g. thiazides) is hazardous and should be avoided. In mild cases withdrawal of lithium and administration of generous amounts of sodium and fluid will reverse the toxicity. Plasma concentrations in excess of 2.5 mmol Li+/litre are usually associated with serious toxicity requiring emergency treatment. When toxic concentrations are reached there may be a delay of 1 or 2 days before maximum toxicity occurs.
In long-term use, therapeutic concentrations of lithium have been thought to cause histological and functional changes in the kidney. The significance of such changes is not clear but is of sufficient concern to discourage long-term use of lithium unless it is definitely indicated. An important consequence is the development of diabetes insipidus (inability to concentrate urine). Patients should therefore be maintained on lithium treatment after 3-5 years only if, on assessment, benefit persists. Conventional and sustained-release tablets are available but it should be noted that different preparations vary widely in bioavailability and a change in the formulation used requires the same precautions as initiation of treatment. There seem few if any reasons for preferring one or other of the simple salts of lithium; the carbonate has been the more widely used but the citrate is also available.
Signs that lithium levels within the body are too high include: confusion, diarrhea, lethargy, severe tremors, and/or an upset stomach.
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