Lithium antidote12/29/2023 ![]() Nephrogenic DI often underrecognized until patient without free access to water. Symptoms: drowsiness, weakness, ataxia, tremor, dysarthria, blurred vision, nystagmus, tinnitus, hyperreflexia, choreoathetoid movements, clonus, confusion, stupor, seizure, coma.Ĭlinical scenarios: therapeutic use of lithium with new dehydration, worsening GFR, increased dose, hyponatremia, new drug introduced with interaction, salt restriction.ĭrugs that are known to significantly increase serum lithium levels: thiazide diuretics, loop diuretics, ACE inhibitors, NSAIDs. ![]() Patients taking lithium chronically with an acute overdose experience symptoms consistent with CNS penetration and toxicity earlier at lower serum lithium levels compared with lithium-naive patients. Lithium-naive patients have no whole body stores and experience less toxicity than patients taking lithium chronically. With time and increasing CNS penetration, symptoms may progress to include drowsiness, confusion, stupor, seizure, coma.Ĭlinical scenarios: intentional or unintentional overdose Symptoms: nausea, vomiting, diarrhea, EKG abnormalities (ST- and T-wave abnormalities, bradycardia, Brugada pattern, long QT). The goal of treating toxicity is to avoid CNS and renal effects, which prolong recovery and increase morbidity and mortality.Īdverse effects of chronic use include: nephrogenic DI, thyroid disorders, hyperparathyroidism, renal dysfunction of various types, including polyuria. ![]() Serum levels may not correlate with CNS (“target organ”) levels in toxicity. With therapeutic use, peak serum concentration occurs in 1 – 2 hrs after ingestion of normal preparations, and 2 – 6 hrs or more after sustained-release preparations. Lithium has complex and lengthy distribution and elimination phases, which are expected to be prolonged in overdose. Hyponatremia causes the kidney to retain lithium.Ĭhronic lithium therapy may cause polyuria and nephrogenic DI, increasing risk for toxicity. Lithium is a monovalent cation metal handled much like sodium by the kidneys. Chronic toxicity presents with neurologic symptoms. Acute toxicity presents with GI distress. It is an effective treatment for bipolar affective disorder with a complex and incompletely understood mechanism of action involving inositol depletion and possibly dopamine and serotonin.Īcute toxicity and chronic toxicity have different clinical features. Lithium is available in normal and extended-release preparations. Description of the problem What every clinician needs to know
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