last updated 24-06-2024



Lithium is a monovalent cation and behaves much like like Na+ throughout the body. However, the understanding of its pharmacology and therapeutic use for psychiatric disorders continues to grow. It is believed that lithium works by interfering with the post-synaptic receptor response by modulating overactive phosphatidyl inositol metabolism and thereby modulating the activation of ion channels and various intracellular enzymes. Lithium can take up to 2 weeks to exert its therapeutic effects. Therefore therapy is often initiated with adjunctive agents which will help the acute symptoms. Before lithium is started baseline leucocytes, electrolytes, urea, creatinine, urine specific gravity, TSH and T4, an ECG and a pregnancy test (if indicated) should be obtained. Lithium doses are titrated to therapeutic serum concentrations and these levels are individualized based on the patient's age, weight, salt intake and renal clearance.

Drug interactions can be serious with lithium as they can result in wide fluctuations in lithium serum concentrations and CNS toxicity. ACE inhibitors, diuretics and NSAIDs are known to increase lithium levels, whereas acetazolamide, sodium containing products and theophylline are known to decrease lithium levels. CNS toxicity is known to occur with antipsychotics, carbamazepine, and methyldopa. If a patient presents with a sudden onset of a fine hand tremor or GI complaints such as nausea, diarrhea, polyuria, polydipsia or anorexia it is likely they are above the therapeutic range for lithium and experiencing toxicities. If doses are not adjusted, these can progress to lethargy, hyper-reflexia, confusion, stupor, and even seizures, cardiovascular collapse and death.


Lithium is eliminated by the:


Since lithium can cause stomach upset, a reasonable solution for administration would be to provide the patient with: