Lithium toxicity — acute-on-chronic emergency (MEQ)

(i) Pattern and mechanisms. This is chronic or acute-on-chronic lithium toxicity: long-term therapeutic use with reduced clearance plus intercurrent illness, not a single naive overdose. Neurotoxicity dominates (coarse tremor, ataxia, dysarthria, confusion) at 2.6 mmol/L with AKI. Ibuprofen (NSAID) reduces renal prostaglandins and lithium clearance; ramipril (ACE inhibitor) can reduce GFR and promote lithium retention; vomiting/poor intake causes volume depletion, increasing proximal sodium-linked lithium reabsorption. Pattern-of-exposure literature links chronic/acute-on-chronic presentations to greater severity relative to serum numbers.^[5][3][4][2]

(ii) Immediate management. Stop lithium, stop NSAID, hold/review ACEI. ABCDE already partly reassuring but continue cardiac monitoring given ECG changes. Investigations: serial lithium levels timed from last dose, U&E/creatinine trend, sodium, calcium/TFT context, glucose already done, consider co-ingestants only if history suggests. Supportive care: IV isotonic saline to restore euvolemia and renal perfusion — cornerstone when volume depleted; avoid forced loop-diuretic diuresis as primary detox; activated charcoal does not bind lithium. Early toxicology and nephrology involvement.^[8][2]

(iii) EXTRIP. Lithium is dialyzable. Recommended ECTR if severe poisoning; or impaired kidney function with Li greater than 4.0 mEq/L; or decreased consciousness, seizures, or life-threatening dysrhythmias at any level. Suggested if Li greater than 5.0, significant confusion, or expected time to Li less than 1.0 exceeds 36 hours. This patient has impaired kidney function, significant confusion, and Li 2.6 — he may not yet hit the Li greater than 4.0 recommended band, but significant confusion is a suggested criterion, and expected clearance time with AKI may exceed 36 hours; escalate with nephrology now rather than waiting for coma. Preferred modality: haemodialysis; continuous RRT acceptable alternative. Continue until clinical improvement or Li less than 1.0 (minimum 6 hours if level not measurable). Recheck for rebound after dialysis.^[1]

(iv) Differentials. Cerebellar stroke, Wernicke encephalopathy, hyponatraemia-related encephalopathy, other toxidromes (serotonin toxicity, NMS if antipsychotics), seizure-related injury, primary psychiatric decompensation with incidental level rise. Discriminators: lithium history + level + renal precipitants + progressive neuro ladder.^[2][8]

(v) After recovery. Document precipitants; sick-day rules; medication reconciliation (avoid unsupervised NSAID/ACEI/thiazide combinations); timed 12-hour trough monitoring and renal–thyroid–calcium schedule if lithium restarts. Restart is a shared decision: lithium’s maintenance and anti-suicide value may still justify supervised reintroduction after renal recovery and education — not automatic same-dose restart into the same drug trap. Counsel on SILENT risk if deficits persist and arrange neurology/rehab early.^[7][6][3]