Abstract Lithium is an effective mood stabilizer but carries a narrow therapeutic index. Toxicity may develop with dehydration, renal impairment, or polypharmacy and can manifest as tremor, ataxia, or encephalopathy. Although most patients recover once lithium levels normalize, a subset experience persistent neurologic deficits, termed Syndrome of Irreversible Lithium-Effectuated Neurotoxicity (SILENT). This rare condition is often difficult to differentiate from catatonia, neuroleptic malignant syndrome (NMS), or metabolic encephalopathy. A 70-year-old woman with schizophrenia, chronic kidney disease stage 1, and osteoporosis was transferred from a skilled nursing facility for acute confusion and facial droop. Her medications included lithium ER 450 mg daily, divalproex 1 g BID, olanzapine 25 mg daily, and lurasidone 120 mg daily. She was afebrile and hemodynamically stable. CT and MRI of the brain showed simply chronic atrophy and small-vessel disease. Laboratory results revealed creatinine 1.9 mg/dL (baseline 0.8), calcium 11.1 mg/dL, and lithium 1.813 mmol/L. Psychotropic agents were held, and she was started on IV fluids. Despite correction of metabolic derangements, improvement in renal function and lithium normalization, her mental status worsened. On hospital day 4, she developed acute hypoxic respiratory failure requiring intubation. CTA chest showed dense right-lower-lobe consolidation without pulmonary embolism. She remained ventilator-dependent despite several extubation trials, requiring tracheostomy and PEG placement. EEG demonstrated diffuse slowing consistent with toxic-metabolic encephalopathy, without seizure activity. Lorazepam challenge yielded no improvement, and creatine kinase remained normal despite rigidity, arguing against catatonia or NMS. With continued coma despite normalized lithium, neurology and psychiatry diagnosed probable SILENT. She was transferred to a long-term acute care facility for ventilator weaning and neurorehabilitation on hospital day 24. This case highlights lithium toxicity complicated by prolonged encephalopathy and respiratory failure consistent with SILENT. The patient’s advanced age, renal impairment, and polypharmacy likely contributed to accumulation. SILENT is characterized by persistent cognitive dysfunction, rigidity, or ataxia after serum lithium normalizes, thought to reflect irreversible neuronal injury, particularly to cerebellar and basal ganglia circuits. Neuroimaging is typically nonspecific, and diagnosis remains clinical. Management is supportive, emphasizing airway protection, metabolic stability, and withdrawal of lithium. Recovery may be protracted or incomplete. Clinicians should monitor lithium closely in elderly or renally impaired patients and recognize that neurologic recovery may lag far behind biochemical resolution. This abstract is funded by: None
Thota et al. (Fri,) studied this question.