Sign Out
To maximize benefits, minimize the risks, and reduce as much as possible the adverse effects of lithium therapy, it is essential to provide proper information to patients and relatives about the treatment regimen and control procedures required during treatment, as well as an explanation of the expected benefits and the most commonly experienced immediate and long-term side effects. In most cases, appropriate written material should be provided to supplement verbal information.
Out-patients and their families should be warned that the patient must discontinue therapy and contact the physician if such clinical signs of lithium toxicity as diarrhea, vomiting, tremor, mild ataxia, drowsiness, or muscular weakness occur.
Occupational hazards: Further, since lithium may impair mental and/or physical abilities, patients should be cautioned about undertaking activities requiring alertness (e.g. operating vehicles or machinery).
Previously existing underlying thyroid disorders do not necessarily constitute a contraindication to lithium therapy; where hypothyroidism exists, careful monitoring of the thyroid function during lithium stabilization and maintenance allows for correction of changing thyroid parameters, if any. Where hypothyroidism occurs during lithium stabilization and maintenance, supplemental thyroid treatment may be used.
Lithium decreases sodium re-absorption by the renal tubules which would lead to sodium depletion. Therefore, it is essential for the patient to maintain a normal diet, including salt, and an adequate fluid intake (2 500 to 3 000 mL), at least during the initial stabilization period. Decreased tolerance to lithium has been reported to ensue from protracted sweating or diarrhea and, if such occur, supplemental fluid and salt should be administered. In addition to sweating and diarrhea, concomitant infection with elevated temperatures may also necessitate a temporary reduction or cessation of medication.
Parathyroid Disorders: Hypercalcemia with or without hyperparathyroidism has been reported in patients on lithium therapy. Screening of serum calcium level and if necessary serum parathormone level need to be considered.
Drug Interactions: Combined use of haloperidol and lithium: An encephalopathy resembling the malignant neuroleptic syndrome (characterized by weakness, lethargy, fever, tremulousness and confusion, extrapyramidal symptoms, leucocytosis, elevated serum enzymes, BUN and FBS) followed by irreversible brain damage has occurred in a few patients treated with lithium plus haloperidol. A causal relationship between these events and concomitant administration of lithium and haloperidol has not been clearly established; however, patients receiving such combined therapy should be monitored closely for early evidence of neurological toxicity such as rigidity and/or hyperpyrexia and treatment discontinued promptly if such signs appear.
Combined use of phenothiazines and lithium: Both pharmacokinetic interactions and clinical toxicity with the combined use of these agents have been described. Lithium-induced reductions in plasma chlorpromazine levels, phenothiazine-induced increases in red cell uptake of lithium and chlorpromazine-induced increases in renal lithium excretion have been reported. Clinically, occasional cases of neurotoxicity have been reported and may be more likely to occur with thioridazine than other phenothiazines, when combined with lithium. Therefore, the clinician should be alert for altered response to either drug when used in combination and when either drug is withdrawn.
The action of neuromuscular blocking agents may be prolonged in patients receiving lithium. Therefore, caution should be exercised when the combination is required. A temporary omission of a few doses of lithium can reduce the risks of this interaction. Indomethacin has been reported to increase steady state plasma lithium levels by 30 to 59%. There is also evidence that other nonsteroidal anti-inflammatory agents may have a similar effect. When such combinations are used, increased frequency of monitoring plasma lithium levels is recommended.
There are reports that concurrent use of methyldopa or tetracycline may increase the risk of lithium toxicity.
Concurrent use of lithium and carbamazepine or phenytoin might result in an increased risk of CNS toxicity. The administration of aminophylline or theophylline to patients on lithium therapy may require increased lithium doses to maintain the psychotropic effect. Patients stabilized on lithium therapy who receive a thiazide diuretic may require a reduction of lithium dosage to avoid accumulation and toxicity, since there is often a 20 to 40% reduction of renal lithium clearance. Furosemide appears to be less likely to affect lithium clearance.
