Lithium Carbonate Tablets, USP Rx Only Rev. 12/11

Lithium Carbonate Tablets, USP contain the following inactive ingredients: Magnesium Stearate, Microcrystalline Cellulose, Polyvinylpyrrolidone, Sodium Lauryl Sulfate, and Sodium Starch Glycolate. 

Lithium is an element of the alkali-metal group with atomic number 3, atomic weight 6.94, and an emission line at 671 nm on the flame photometer.

Lithium acts as an antimanic.

Lithium Carbonate is a white, light, alkaline powder with molecular formula Li₂CO₃ and molecular weight 73.89.

The ability to tolerate lithium is greater during the acute manic phase and decreases when manic symptoms subside (see DOSAGE AND ADMINISTRATION).

The distribution space of lithium approximates that of total body water. Lithium is primarily excreted in urine with insignificant excretion in feces. Renal excretion of lithium is proportional to its plasma concentration. The half-life of elimination of lithium is approximately 24 hours. Lithium decreases sodium reabsorption by the renal tubules which could lead to sodium depletion. Therefore, it is essential for the patient to maintain a normal diet, including salt, and an adequate fluid intake (2500-3000 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.

Previously existing underlying thyroid disorders do not necessarily constitute a contraindication to lithium treatment; where hypothyroidism exists, careful monitoring of 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.

A condition known as Brugada Syndrome may pre-exist and be unmasked by lithium therapy. Brugada Syndrome is a heart disorder characterized by abnormal electrocardiographic (ECG) findings and risk of sudden death. Patients should be advised to seek immediate emergency assistance if they experience fainting, lightheadedness, abnormal heart beats, or shortness of breath.

Outpatients and their families should be warned that the patient must discontinue lithium therapy and contact his physician if such clinical signs of lithium toxicity as diarrhea, vomiting, tremor, mild ataxia, drowsiness, or muscular weakness occur.

Lithium may impair mental and/or physical abilities. Caution patients about activities requiring alertness (e.g., operating vehicles or machinery).

Lithium is excreted in human milk. Nursing should not be undertaken during lithium therapy except in rare and unusual circumstances where, in the view of the physician, the potential benefits to the mother outweigh possible hazards to the child.

Since information regarding the safety and effectiveness of lithium in children under 12 years of age is not available, its use in such patients is not recommended at this time. There has been a report of a transient syndrome of acute dystonia and hyperreflexia occurring in a 15 kg child who ingested 300 mg of lithium carbonate.

The likelihood of toxicity increases with increasing serum lithium levels. Serum lithium levels greater than 1.5 mEq/L carry a greater risk than lower levels. However, patients sensitive to lithium may exhibit toxic signs at serum levels below 1.5 mEq/L.

Diarrhea, vomiting, drowsiness, muscular weakness and lack of coordination may be early signs of lithium toxicity, and can occur at lithium levels below 2.0 mEq/L. At higher levels, giddiness, ataxia, blurred vision, tinnitus and a large output of dilute urine may be seen. Serum lithium levels above 3.0 mEq/L may produce a complex clinical picture involving multiple organs and organ systems. Serum lithium levels should not be permitted to exceed 2.0 mEq/L during the acute treatment phase.

Fine hand tremor, polyuria and mild thirst may occur during initial therapy for the acute manic phase, and may persist throughout treatment. Transient and mild nausea and general discomfort may also appear during the first few days of lithium administration.

These side effects are an inconvenience rather than a disabling condition, and usually subside with continued treatment or a temporary reduction or cessation of dosage. If persistent, a cessation of dosage is indicated.

The following adverse reactions have been reported and do not appear to be directly related to serum lithium levels.

Tremor, muscle hyperirritability (fasciculations, twitching, clonic movements of whole limbs), ataxia, choreo-athetotic movements, hyperactive deep tendon reflexes.

Blackout spells, epileptiform seizures, slurred speech, dizziness, vertigo, incontinence of urine or feces, somnolence, psychomotor retardation, restlessness, confusion, stupor, coma, acute dystonia, downbeat nystagmus.

Cardiac arrhythmia, hypotension, peripheral circulatory collapse, sinus node dysfunction with severe bradycardia (which may result in syncope), unmasking of Brugada Syndrome (See WARNINGS: Unmasking of Brugada Syndromeand PRECAUTIONS: Information for the Patients).

Cases of pseudotumor cerebri (increased intracranial pressure and papilledema) have been reported with lithium use. If undetected, this condition may result in enlargement of the blind spot, constriction of visual fields and eventual blindness due to optic atrophy. Lithium should be discontinued, if clinically possible, if this syndrome occurs.

Anorexia, nausea, vomiting, diarrhea.

Albuminuria, oliguria, polyuria, glycosuria.

Drying and thinning of hair, anesthesia of skin, chronic folliculitis, xerosis cutis, alopecia and exacerbation of psoriasis.

Blurred vision, dry mouth.

Euthyroid goiter and/or hypothyroidism (including myxedema) accompanied by lower T3 and T4. Iodine 131 uptake may be elevated. (See PRECAUTIONS). Paradoxically, rare cases of hyperthyroidism have been reported.

Diffuse slowing, widening of frequency spectrum, potentiation and disorganization of background rhythm.

Reversible flattening, isoelectricity or inversion of T-waves.

Fatigue, lethargy, transient scotomata, dehydration, weight loss, tendency to sleep.

Transient electroencephalographic and electrocardiographic changes, leucocytosis, headache, diffuse non-toxic goiter with or without hypothyroidism, transient hyperglycemia, generalized pruritis with or without rash, cutaneous ulcers, albuminuria, worsening of organic brain syndromes, excessive weight gain, edematous swelling of ankles or wrists, and thirst or polyuria, sometimes resembling diabetes insipidus, and metallic taste.

A single report has been received of the development of painful discoloration of fingers and toes and coldness of the extremities within one day of the starting of treatment of lithium. The mechanism through which these symptoms (resembling Raynaud’s Syndrome) developed is not known. Recovery followed discontinuance.

To report SUSPECTED ADVERSE REACTIONS, contact West-ward Pharmaceutical Corp. at 1-877-233-2001 or the FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

No specific antidote for lithium poisoning is known. Early symptoms of lithium toxicity can usually be treated by reduction of cessation of dosage of the drug and resumption of the treatment at a lower dose after 24 to 48 hours. In severe cases of lithium poisoning, the first and foremost goal of treatment consists of elimination of this ion from the patient.

Treatment is essentially the same as that used in barbiturate poisoning: 1) gastric lavage, 2) correction of fluid and electrolyte imbalance and 3) regulation of kidney functioning. Urea, mannitol, and aminophylline all produce significant increases in lithium excretion. Hemodialysis is an effective and rapid means of removing the ion from the severely toxic patient. Infection prophylaxis, regular chest X-rays, and preservation of adequate respiration are essential.

Optimal patient response to Lithium Carbonate Tablets usually can be established and maintained with 600 mg t.i.d. Such doses will normally produce an effective serum lithium level ranging between 1 and 1.5 mEq/L. Dosage must be individualized according to serum levels and clinical response. Regular monitoring of the patient’s clinical state and of serum lithium levels is necessary. Serum levels should be determined twice per week during the acute phase, and until the serum level and clinical condition of the patient have been stabilized.

The desirable serum lithium levels are 0.6 to 1.2 mEq/L. Dosage will vary from one individual to another, but usually 300 mg of Lithium Carbonate t.i.d. or q.i.d. will maintain this level. Serum lithium levels in uncomplicated cases receiving maintenance therapy during remission should be monitored at least every two months.

Patients abnormally sensitive to lithium may exhibit toxic signs at serum levels of 1 to 1.5 mEq/L. Elderly patients often respond to reduced dosage, and may exhibit signs of toxicity at serum levels ordinarily tolerated by other patients.

Blood samples for serum lithium determination should be drawn immediately prior to the next dose when lithium concentrations are relatively stable (i.e., 8-12 hours after the previous dose). Total reliance must not be placed on serum levels alone. Accurate patient evaluation requires both clinical and laboratory analysis.