Lithium may cause anterograde amnesia, slightly slowed motor movement, and diminished creativity; however, those symptoms could be associated with bipolar disorder itself as opposed to lithium use. There are no suggested systematic treatment strategies for lithium-associated cognitive function. A first consideration should be to lower the lithium serum level since cognitive effects seem dose related. Second, a review of other psychotropic medications being prescribed and whether they might contribute to the side effect would be in order. Stimulants should be considered as well.
Sexual dysfunction from lithium has been relatively neglected as a topic of clinical inquiry; however, stable bipolar patients on lithium showed decreased libido and sexual satisfaction. Aspirin 240 mg daily has been shown to reduce overall sexual dysfunction and improve erectile dysfunction. Phosphodiesterase 5 inhibitors should also be considered for those with lithium-associated sexual difficulties.
In mild cases of acne caused by lithium use, dermatologic remedies should be considered. A trial found a positive effect of inositol 6 g daily in decreasing the severity of psoriatic lesions in lithium-treated patients.
Lithium toxicity has been divided into 3 patterns: acute, acute-on-chronic, and chronic. In mild lithium toxicity, symptoms include weakness, worsening tremor, mild ataxia, poor concentration, and diarrhea. With worsening toxicity, vomiting, the development of gross tremor, slurred speech, confusion, and lethargy emerge. In cases of mild toxicity, discontinuation of lithium may suffice. With moderate toxic episodes, fluid infusion with saline diuresis is recommended along with gastric lavage and whole bowel irrigation using polyethylene glycol. In the most severe of cases, hemodialysis should be instituted.
Lithium can cause severe renal damage in the kidneys, and general guidelines for minimizing the risk of renal damage include: monitor serum creatinine and eGFR regularly during lithium treatment at intervals of every 6 months to 1 year; avoid episodes of lithium toxicity, keep mean lithium levels within the low therapeutic range when possible, and consider once-daily dosing.
The prevalence of thyroid dysfunction in lithium-treated patients can be seen in cases of overt hypothyroidism, subclinical hypothyroidism, or goiter without reference to biochemical markers. Thyroid parameters should be checked before lithium is instituted and then monitored after 3-6 months initially and then every 6-12 months. A clinical rule to remember is that hypothyroidism never justified lithium discontinuation. Thyroid hormones should be prescribed to bring abnormal TSH values within the normal range.
Lithium also increases renal calcium reabsorption and independently stimulates parathyroid hormone release. Mild evaluations of hormone levels in asymptomatic patients can be monitored. With higher levels of the hormone, switching from lithium to a different mood stabilizer, calcimimetic therapy with cinacalcet or local or subtotal parathyroidectomy are the reasonable treatment options.
- Gitlin M. Lithium side effects and toxicity: prevalence and management strategies. Int J Bipolar Disord. 17 December 2016. DOI: 10.1186/s40345-016-0068-y