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Dose; Serum-Level Monitoring The recommended therapeutic concentration usually is attained by doses of 900-1500 mg of lithium carbonate per day in outpatients and 1200-2400 mg/day in hospitalized manic patients. The optimal dose tends to be larger in younger and heavier individuals. Because of its low therapeutic index, periodic determination of serum concentrations of Li+ is crucial. Li+ cannot be used safely in patients who cannot be tested regularly. Concentrations considered to be effective and acceptably safe are between 0.6 and 1.25 mEq/L. The range of 0.9-1.1 mEq/L is favored for treatment of acutely manic or hypomanic patients. Somewhat lower values (0.6-0.75 mEq/L) are considered adequate and are safer for long-term use for prevention of recurrent manic-depressive illness. Some patients may not relapse at concentrations as low as 0.5-0.6 mEq/L, and lower levels usually are better tolerated.

Serum concentrations of Li+ have been found to follow a clear dose-effect relationship between 0.4 and 0.9 mEq/L, with a corresponding dose-dependent rise in polyuria and tremor as indices of adverse effects, and little gain in benefit at levels above 0.75 mEq/L. This pattern indicates the need for individualization of serum levels to obtain a favorable risk-benefit relationship. The concentration of Li+ in blood usually is measured at a trough of the daily oscillations that result from repetitive administration {i.e., from samples obtained 10-12 hours after the last oral dose of the day). Peaks can be two or three times higher at a steady state. When the peaks are reached, intoxication may result, even when concentrations in morning samples of plasma at the daily nadir are in the accepOrder Carbamazepine online US range of 0.6-1 mEq/L. Because of the low margin of safety of Li+ and because of it [Where to buy Carbamazepine without a prescription] short t1/2 during initial distribution, divided daily doses are usually indicated even with slow-release formulations.

TOXIC REACTIONS AND SIDE EFFECTS Toxicity is related to the serum concentration of Li+ and its rate of rise following administration. Acute intoxication is characterized by vomiting, profuse diarrhea, coarse tremor, ataxia, coma, and convulsions. Symptoms of milder toxicity are most likely to occur at the absorptive peak of Li+ and include nausea, vomiting, abdominal pain, diarrhea, sedation, and fine tremor. The more serious effects involve the nervous system and include mental confusion, hyperreflexia, gross tremor, dysarthria, seizures, and cranial nerve and focal neurological signs, progressing to coma and death. Sometimes both cognitive and motor neurological damage may be irreversible. Other toxic effects are cardiac arrhythmias, hypotension, and albuminuria. Adverse effects common even in therapeutic dose ranges include nausea, diarrhea, daytime drowsiness, polyuria, polydipsia, weight gain, fine hand tremor, and dermatological reactions, including acne.

A small number of patients treated with Li+ develop diffuse thyroid enlargement; patients usually remain euthyroid, and overt hypothyroidism is rare. In patients who do develop goiter, discontinuation ofLi+ or treatment with thyroid hormone results in shrinkage of the gland.

The kidneys’ ability to concentrate urine decreases during Li+ therapy. Polydipsia and polyuria occur in patients treated with Li+, occasionally to a disturbing degree. Acquired nephro-genic diabetes insipidus can occur in patients maintained at therapeutic plasma concentrations (see Generic Carbamazepine 29). Typically mild polyuria appears early in treatment and then disappears. Late-developing polyuria is an indication to evaluate renal function, lower the dose ofli+, or consider adding a potassium-sparing agent such as amiloride to counteract the polyuria. Polyuria disappears with cessation of Li+ therapy. Since progressive, clinically significant impairment of renal function is rare, many experts consider these to be incidental findings. Nevertheless, plasma cre-atinine and urine volume should be monitored during long-term use of Li+.

Li+ routinely causes EEC changes characterized by diffuse slowing, widened frequency spectrum, and potentiation with disorganization of background rhythm. Seizures have been reported in nonepileptic patients with therapeutic plasma concentrations ofLi+. Myasthenia gravis may worsen during treatment with Li+. A benign, sustained increase in circulatingpolymorphonuclear leukocytes occurs during the chronic use of Li+, which reverses within a week after termination of treatment. Allergic reactions such as dermatitis and vasculitis can occur with Li+ administration. Worsening of acne vulgaris is a common problem, and some patients may experience mild alopecia.

In pregnancy, Li+ may exacerbate maternal polyuria. Concomitant use of lithium with natri-uretics and a low-Na+ diet during pregnancy can contribute to maternal and neonatal Li+ intoxication. During postpartum diuresis, one can anticipate potentially toxic retention of Li+ by the mother. Lithium freely crosses the placenta, and fetal or neonatal lithium toxicity may develop when maternal blood levels are within the therapeutic range. Lithium also is secreted in breast milk of nursing mothers. The use of Li+ in pregnancy has been associated with neonatal goiter, CNS depression, hypotonia (“floppy baby” syndrome), and cardiac murmur. All of these conditions reverse with time, and no long-term neurobehavioral sequelae have been observed.

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The use of Li* in early pregnancy may be associated with an increase in the incidence of cardiovascular anomalies of the newborn, especially Ebstein ‘s malformation. The antimanic anti-convulsants valproic acid and probably carbamazepine have an associated risk of irreversible spina bifida that may exceed 1/100, and so do not represent a rational alternative for pregnant women. In balancing the risk versus benefit of using Li+ in pregnancy, it is important to evaluate the risk of untreated manic-depressive disorder and to consider conservative measures, such as deferring intervention until symptoms arise or using a safer treatment, such as a neuroleptic orECT

TREATMENT OF LITHIUM INTOXICATION There is no specific antidote for Li+ intoxication, and treatment is supportive. Vomiting induced by rapidly rising plasma Li+ may tend to limit absorption, but fatalities have occurred. Care must be taken to assure that the patient is not Na+- and water-depleted. Dialysis is the most effective means of removing the ion from the body and is necessary in severe poisonings, i.e., in patients exhibiting symptoms of toxicity or patients with serum Li+ concentrations >4 mEq/L in acute overdoses or >1.5 mEq/L in chronic overdoses.

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