Lithium salt

This article discusses the pharmacological uses of lithium salts: for information on the chemistry of individual lithium salts, see :Category:Lithium compounds

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 interferes with the regulation of sodium and water levels in the body, lithium can cause dehydration. Dehydration, which is compounded by heat, can result in increasing lithium levels.

Related Topics:
Blood - Thyroid - Kidney - Sodium - Dehydration - Heat

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High doses of haloperidol, fluphenazine, or flupenthixol may be hazardous when used with lithium; irreversible toxic encephalopathy has been reported.

Related Topics:
Haloperidol - Fluphenazine - Flupenthixol - Encephalopathy

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Lithium salts, with the possible exception of lithium orotate, have a narrow therapeutic/toxic ratio and should therefore not be

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prescribed unless facilities for monitoring plasma concentrations are

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available. Patients should be carefully selected. Doses are adjusted to achieve

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plasma concentrations of 0.6 to 1.2mmol Li+/litre (lower end of the

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range for maintenance therapy and elderly patients) on samples taken 12 hours

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after the preceding dose. Overdosage, usually with plasma concentrations over

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1.5mmol Li+/litre, may be fatal and toxic effects include

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tremor, ataxia, dysarthria, nystagmus, renal impairment, and

Related Topics:
Tremor - Ataxia - Dysarthria - Nystagmus

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convulsions. If these potentially hazardous signs occur, treatment should be

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stopped, plasma lithium concentrations redetermined, and steps taken to reverse lithium toxicity.

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Lithium toxicity is compounded by sodium depletion. Concurrent use of

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diuretics that inhibit the uptake of sodium by the distal tubule (e.g.

Related Topics:
Diuretic - Distal tubule

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thiazides) is hazardous and should be avoided. In mild cases withdrawal of

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lithium and administration of generous amounts of sodium and fluid will reverse

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the toxicity. Plasma concentrations in excess of 2.5 mmol Li+/litre

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are usually associated with serious toxicity requiring emergency treatment.

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When toxic concentrations are reached there may be a delay of 1 or 2 days

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before maximum toxicity occurs.

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In long-term use, therapeutic concentrations of lithium have been thought to

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cause histological and functional changes in the kidney. The significance of

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such changes is not clear but is of sufficient concern to discourage long-term

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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.

Related Topics:
Diabetes insipidus - Bioavailability

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