The mechanism of action of lithium is unknown. It may include alterations in transmembrane ion flux and / or reduction in phosphatidylinositide turnover, which lead to mood stabilization.
- Gastro intestinal disturbance
- Fine tremor
- Blocking of ADH action and tubulointerstitial damage. This nephrogenic diabetes insipidus causes polydipsia and poyuria
- Weight gain and oedema
- Exacerbation of psoriasis
- Goitre (hypothyroidism more common than hyperthyroidism) and thyroid dysfunction
- Lithium intoxication (blurred vision, worsening gastrointestinal symptoms, drowsiness, ataxia, coarse tremor)
- Severe toxicity (hyper-reflexia, convulsions, psychosis, syncope, renal insufficiency)
- Extra-pyramidal side effects
- Renal impairment
It’s worth noting that Lithium's manufacturer states that side effects are usually related to serum lithium concentration and are less common in patients with plasma lithium concentrations below 1.0 mmol/l. Due to Lithium's narrow therapeutic/toxic ratio the patient should have serum levels checked regularly and aim for a level of 0.4-1mmol/L (or 0.8-1mmol/L if treating acute mania) 12 hours post dose.
Lithium patients should also have their renal function, BMI, thyroid function and cardiac function monitored intermittently also.
Patients should be counselled to maintain adequate fluid intake and avoid dietary changes which, might result in increased or decreased sodium intake. Patients with diarrhoea or vomiting should suspend their lithium. Patients should also be warned that lithium may impair performance of skilled tasks (e.g driving). 'Lithium cards' with advice are available for patients. Lithium should be withdrawn slowly.
Lithium is absorbed from the gastrointestinal tract and is excreted by the kidneys. It can take days to start to act. Lithium salts have a narrow therapeutic / toxic ratio - serum lithium concentration should be measured regularly.
