Lithium, an element in the alkali metal group, is approved for the treatment of acute mania and bipolar disorder and also as a long-term prophylaxis of bipolar disorders (1). Lithium act by substituting potassium ions, which affects the ratio of these ions inside and outside the cell. These changes may affect the release of certain neurotransmitters and their uptake. Lithium plays a neuroprotective role, increasing gray matter volume in several brain areas including the amygdalea, hippocampus and prefrontal cortex. At the cellular level lithium decreases excitatory and increases inhibitory neurotransmission. Lithium is available only for oral administration as lithium carbonate salt. It is almost completely absorbed from the gastrointestinal tract. Peak levels occur in 2-4 hours. The plasma elimination half-life of a single dose of lithium takes from 12 to 27 hours. Lithium is almost exclusively excreted by the kidneys and dosing must be adjusted to the renal function. Most filtered lithium is reabsorbed in the proximal tubule. Reabsorption of lithium is increased in patients who are hyponatremic or volume depleted, both of which are possible consequences of diuretic therapy. The therapeutic dose to obtain the desired therapeutic serum levels of 0.6-1.2 mEq/L is 300-2700 mg/d (2).

While it is effective drug for the treatment of bipolar disorders, lithium therapy is associated with risk of toxicity even when blood level is in narrow therapeutic window (2). Elderly patients may exhibit signs of toxicity at serum levels ordinarily tolerated by other patients. The central nervous system is the major system affected, although the renal, gastrointestinal, endocrine, and cardiovascular systems also may be involved (3). Lithium toxicity may be of an acute or chronic nature. Acute intoxication manifestations are predominantly gastrointestinal, but progression to neuromuscular signs may occur, acute-on-chronic both gastrointestinal and neurologic manifestations may be also present, whatever chronic manifestations are primarily neurologic. Acute toxicity occurs typically in the setting of accidental or intentional overdose. Diarrhea, vomiting, somnolence, muscular weakness and lack of coordination may be early signs of lithium toxicity, and can occur at lithium concentrations below 2.0 mEq/L. At higher concentrations, dizziness, ataxia, blurred vision, tinnitus and a large output of dilute urine may be seen. Serum lithium concentrations above 3.0 mEq/L may cause a complex clinical picture involving multiple organs and organ systems with coma, and eventually death. Chronic toxicity often manifests as gradual development of neurological symptoms similar to those of late phase of acute toxicity. Chronic lithium treatment may be associated with diminution of renal concentrating ability, occasionally presenting as nephrogenic diabetes insipidus, with polyuria and polydipsia. Lithium can cause hyponatremia by decreasing sodium reabsorption by the renal tubules, leading to sodium depletion. It can also cause chronic tubulointerstitial nephropathy. An encephalopathic syndrome, characterized by weakness, lethargy, fever, tremulousness and confusion and extrapyramidal symptoms has occurred in patients treated with lithium and an antipsychotic. Lithium can precipitate serotonin syndrome, a potentially life-threatening condition. Long-term lithium treatment is associated with persistent hyperparathyroidism and hypercalcemia. There have been reports of a possible association between treatment with lithium and the unmasking of Brugada syndrome. Brugada syndrome is a disorder characterized by abnormal electrocardiographic findings and a risk of sudden death. Pseudotumor cerebri characterized by increased intracranial pressure and papilledema have been reported with lithium use. The risk of lithium toxicity is especially high in patients with significant renal or cardiovascular disease, severe dehydration or sodium depletion, and in patients receiving medications that may affect kidney function, such as angiotensin converting enzyme inhibitors, diuretics loops and thiazides and nonsteroidal anti-inflammatory drugs (indomethacin, piroxicam, selective cyclooxygenase-2 (COX-2) inhibitors). Accurate lithium treated patient's evaluation requires both clinical and laboratory analysis. Before initiating treatment with lithium, renal function, serum electrolytes and thyroid function should be evaluated. There have been no adequate studies conducted to evaluate the mutagenic potential of lithium. Due to potential risk to the featus and neonate, lithium can not be recommended during pregnancy and breast-feeding (1). Lithium is contraindicated in patients with known hypersensitivity to any ingredient in the lithium carbonate tablet. No specific antidote for lithium poisoning is known. Early symptoms of toxicity can usually be treated by reduction or cessation of lithium. Treatment of lithium intoxication depends on the degree of toxicity. In cases of mild toxicity lithium discontinuation may be sufficient. Moderate toxic episodes require fluid infusion with saline diuresis. The most severe cases defined by extraordinarily high lithium levels above 4 mmol/l or marked clinical symptoms may require hemodialysis (4).