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EM SAQsLithium poisoning

EM SAQs · Lithium poisoning

Management of chronic lithium toxicity

An ACEM-style short-answer question on chronic lithium toxicity precipitated by an NSAID and volume depletion, using EXTRIP 1D/2D indications rather than the circulating chronic-2.5 ladder.

10 marks10 min2 min readSource-verified ·

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Prompt
A 72-year-old woman on long-term lithium carbonate for bipolar affective disorder is brought to the emergency department by her daughter with a three-day history of a worsening coarse hand tremor, an unsteady wide-based gait, slurred speech, and progressive confusion. She started ibuprofen 400 mg three times daily for knee osteoarthritis one week ago, and has had diarrhoea and poor oral intake for two days. On examination she is afebrile, pulse 96, blood pressure 104/64, respiratory rate 18, oxygen saturation 97 per cent on room air, and she is drowsy and disoriented with a Glasgow Coma Scale of 13. She has a marked coarse tremor, dysmetria on finger-to-nose, and a wide-based ataxic gait. Investigations: serum lithium 2.9 mmol/L, creatinine 168 micromol/L (baseline 95 micromol/L), sodium 146 mmol/L. ECG is in sinus rhythm. Outline your diagnosis, precipitants, immediate management and the EXTRIP dialysis decision.

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This is chronic lithium poisoning: maintenance lithium plus a drug–drug interaction and volume depletion. Baird-Gunning: chronic is the most common pattern, usually unintentional, from intake exceeding elimination. The CNS is the primary target — tremor, ataxia, dysarthria, confusion and drowsiness fit EXTRIP’s mild-to-severe spectrum.[1][2]

Precipitants. Ibuprofen: NSAIDs raise serum lithium and diminish renal lithium clearance (Ragheb; ibuprofen and naproxen named). Diarrhoea and poor intake: EXTRIP names volume depletion (and thiazides) as conditions that increase proximal lithium reabsorption and raise [Li+]. Do not add ACE-inhibitor or loop-diuretic mechanisms as sourced EXTRIP facts — they are not in the papers fetched for this pass.[1][3]

Immediate management. Stop lithium and the NSAID. Give intravenous isotonic saline. Do not give activated charcoal — it does not bind lithium. Whole-bowel irrigation is not required in this chronic-accumulation presentation; EXTRIP notes there are no outcome data for any decontamination procedure, and no millilitre-per-hour irrigation recipe is sourced. Unsourced 1 L boluses, urine-output targets, QTc-surveillance recipes and benzodiazepine milligram lists are not taught here.[1]

EXTRIP indication already met. GCS 13 drowsiness is a decreased level of consciousness — extracorporeal treatment is recommended (1D) irrespective of the lithium concentration. Do not justify dialysis with a circulating “chronic above 2.5 mmol/L with neurotoxicity” ladder; those 2.5 figures appear in other sources EXTRIP tabulated, not as EXTRIP’s own 1D vote. The 4.0 mEq/L 1D rule is paired with impaired kidney function as EXTRIP defines it (CKD 3B–5 / eGFR below 45, KDIGO AKI stage 2 or 3, or no-baseline creatinine 176 micromol/L in adults) — creatinine 168 from 95 is not automatically that definition. Intermittent haemodialysis is preferred (1D); CRRT if intermittent HD is unavailable.[1]

After extracorporeal treatment. Stop when [Li+] is below 1.0 mEq/L or clinical improvement is apparent (1D); continue at least 6 hours if the level is not measurable. Then obtain serial [Li+] over 12 hours to decide further sessions. Redistribution rebound after high-efficiency dialysis is maximal at 6–12 hours (about 0.5–1.0 mEq/L) and is not typically associated with recurrent symptoms. The circulating “recheck at six hours and re-dialyse if above 1.0 with symptoms” rule is not EXTRIP.[1]

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References3ShowHide
  1. [1]Decker BS, Goldfarb DS, Dargan PI, et al. Extracorporeal Treatment for Lithium Poisoning: Systematic Review and Recommendations From the EXTRIP Workgroup. Clinical Journal of the American Society of Nephrology, 2015.PMID 25583292
  2. [2]Baird-Gunning J, Lea-Henry T, Hoegberg LCG, Gosselin S, Roberts DM. Lithium Poisoning. Journal of Intensive Care Medicine, 2017.PMID 27516079
  3. [3]Ragheb M. The clinical significance of lithium-nonsteroidal anti-inflammatory drug interactions. Journal of Clinical Psychopharmacology, 1990.PMID 2258452
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