Lithicarb, lithium carbonate, priadel
- Treatment of bipolar disorder
PRESENTATION AND ADMINISTRATION:
Lithicarb FC 250 mg and 400 mg tablets (white)
Lithium carbonate capsules 250 mg (green / clear)
Controlled Release Tablets:
400 mg tablets (white)
250 mg – 1200 mg total per day
Give BD as divided doses (tablets and capsules) or OD as total dose (controlled release tablets)
Ongoing dosage is adjusted to levels
Note: no information is available on NG administration. Check with pharmacist if this is only route available
DOSAGE IN RENAL FAILURE AND RENAL REPLACEMENT THERAPY:
Avoid where possible if eGFR <50. If lithium must be used, reduce dosage and monitor plasma concentration carefully
DOSAGE IN PAEDIATRICS:
5-20 mg/kg total per day in divided doses (BD or TDS)
Do not use controlled release tablets in children
Lithium is an element of the alkali-metal group. Preclinical studies have shown that lithium alters sodium transport in nerve and muscle cells and effects a shift toward intraneuronal metabolism of catecholamines, but the specific biochemical mechanism of lithium action in mania is unknown.
- Significant renal or cardiovascular disease
- Severe dehydration
- Sodium depletion
- Patients receiving diuretics
Likelihood of toxicity increases with increasing serum lithium levels. Levels > 1.5 mEq/l carry a greater risk than lower levels. Some patients sensitive to lithium may exhibit toxic signs at serum levels below this. Diarrhoea, vomiting, drowsiness, muscular weakness and lack of coordination may be early signs of lithium toxicity, and can occur at lithium levels < 2.0 mEq/l. At higher levels, giddiness, ataxia, blurred vision, tinnitus and a large output of dilute urine may be seen. Serum lithium levels > 3.0 mEq/l may produce a complex clinical picture involving multiple organs and organ systems. Serum lithium levels should not be permitted to exceed 2.0 mEq/l during the acute treatment phase.
Nephrogenic diabetes insipidus
Chronic lithium therapy may be associated with diminution of renal concentrating ability, occasionally presenting as nephrogenic diabetes insipidus, with polyuria and polydipsia. Such patients should be carefully managed to avoid dehydration with resulting lithium retention and toxicity. This condition is usually reversible when lithium is discontinued.
Lithium decreases sodium reabsorption by the renal tubules which could lead to sodium depletion. In addition to sweating and diarrhoea, concomitant infection with elevated temperatures may also necessitate a temporary reduction or cessation of medication
Lithium levels should be checked in any patient on lithium admitted to ICU. Samples should be collected in a yellow top tube (SST) and should be taken 12 hours post-dose. The therapeutic range is 0.6 - 1.2 mmol/L
In the setting of acute overdose, peak levels > 5 mmol/L may be seen 4-8 hours after ingestion.
Drug/Laboratory Test Interactions:
IMPORTANT DRUG INTERACTIONS IN ICU:
Combined use of haloperidol and lithium
An encephalopathic syndrome (characterised by weakness, lethargy, fever, tremulousness and confusion, extrapyramidal symptoms, leucocytosis, elevated serum enzymes & urea followed by irreversible brain damage) has occurred in a few patients treated with lithium and haloperidol. A causal relationship between these events and the concomitant administration of lithium and haloperidol has not been established. However, patients receiving such combined therapy should be monitored closely for early evidence of neurological toxicity and treatment discontinued promptly if such signs appear.
Neuromuscular blocking drugs
Lithium may prolong the effects of neuromuscular blocking agents. Therefore, neuromuscular blocking agents should be given with caution to patients receiving lithium.
Caution should be used when lithium and diuretics or angiotensin converting enzyme (ACE) inhibitors are used concomitantly because sodium loss may reduce the renal clearance of lithium and increase serum lithium levels with risk of lithium toxicity.
Lithium levels should be closely monitored when patients initiate or discontinue NSAID use. In some cases, lithium toxicity has resulted from interactions between NSAIDs and lithium.
Tremor, muscle hyperirritability (fasciculations, twitching, clonic movements of whole limbs), ataxia, choreo-athetotic movements, hyperactive deep tendon reflexes
Central Nervous System:
Blackout spells, epileptiform seizures, slurred speech, dizziness, vertigo, incontinence of urine or faeces, somnolence, psychomotor retardation, restlessness, confusion, stupor, coma, acute dystonia, downbeat nystagmus
Cardiac arrhythmia, hypotension, peripheral circulatory collapse, sinus node dysfunction with severe bradycardia (which may result in syncope)
Cases of pseudotumour cerebri (increased intracranial pressure and papilloedema) have been reported with lithium use
Anorexia, nausea, vomiting, diarrhoea
Albuminuria, oliguria, polyuria, glycosuria
Drying and thinning of hair, anaesthesia of skin, chronic folliculitis, xerosis cutis, alopecia and exacerbation of psoriasis