Non-fatal Lithium Intoxication with 5.5 mmol/L Serum Level

Introduction ▼ Since John Cade’s high dosage regimen in lithium therapy was established about 6 decades ago, lithium intoxication has become and continues to be a common clinical problem [1, 2]. From a clinical perspective, there are 2 categories of lithium intoxication: acute and chronic. Acute lithium intoxication includes accidental poisoning and suicide attempts in patients with or without lithium maintenance therapy. The chronic form is characterized, most notably, by volume loss leading to limitation of renal lithium excretion which involves elevation of lithium levels in patients under lithium medication. Concerning the symptomatology of acute and chronic intoxication, the different subtypes vary mainly due to lithium pharmacokinetics [3, 4]. Whereas acute lithium poisoning is ostensibly associated with gastrointestinal symptoms, cardiotoxic effects and late developing neurological signs, chronic intoxication primarily involves neurological alterations including confusion states, myoclonus, seizures and nephrological complications like nephrogenic diabetes insipidus [3]. Furthermore, after acute lithium intoxication, cases of persisting neurological deficits were also reported. The SILENT syndrome (syndrome of irreversible lithium effectuated neurotoxicity) is most often characterized by long-lasting cerebellar signs assumed to be caused by demyelinating effects [5]. In chronic lithium poisoning, severe neurotoxicity seems to occur more often in patients with defined risk factors (e. g., age > 50 years, limited renal function, nephrogenic diabetes insipidus and thyroid dysfunction) [6].