Lithium Level Interpreter
Lithium Level Interpreter
Band a 12-hour post-dose serum lithium from subtherapeutic to severe toxicity, and see why the number matters less than whether the exposure is acute or chronic.
Lithium level
1 input → mmol/LSerum lithium 0.9 mmol/L, sampled 12 hours after the last dose
How the level is read
1 mmol/L = 1 mEq/L, because lithium is monovalent
Therapeutic range 0.6 – 1.2 mmol/L
- 12-hour sample
- the range is defined on a trough sample 12 hours post-dose; a level taken at any other time cannot be compared with it
- mEq/L
- numerically identical to mmol/L for lithium, since a monovalent ion carries one equivalent per mole
- acute vs chronic
- the same number means something different in an acute overdose and in a chronically treated patient, because tissue distribution differs
Worked example
Serum lithium 0.9 mmol/L, sampled 12 hours after the last dose
0.90 mmol/L = 0.90 mEq/L, since lithium is monovalent
0.90 lies between 0.6 and 1.2 → therapeutic range
Interpretable only because the sample was taken 12 hours post-dose
Bands on a 12-hour post-dose sample
| Serum lithium (mmol/L) | Band | Typical features |
|---|---|---|
| < 0.6 | Below the therapeutic range | Check adherence and sample timing before increasing the dose |
| 0.6 – 1.2 | Therapeutic range | Routine monitoring of level, renal and thyroid function |
| 1.2 – 1.5 | Above the therapeutic range | Look for a precipitant; often asymptomatic |
| 1.5 – 2.5 | Mild toxicity | Tremor, nausea, diarrhoea, unsteadiness |
| 2.5 – 3.5 | Moderate toxicity | Confusion, ataxia, myoclonus, hyperreflexia |
| > 3.5 | Severe toxicity | Seizures, coma, cardiovascular instability |
What raises a lithium level
| Precipitant | Mechanism |
|---|---|
| Dehydration, vomiting, diarrhoea | Reduced renal clearance and increased proximal reabsorption |
| NSAIDs | Reduced renal prostaglandin synthesis and glomerular filtration |
| ACE inhibitors and ARBs | Reduced glomerular filtration and sodium depletion |
| Thiazide diuretics | Sodium depletion with increased proximal lithium reabsorption |
| Any fall in glomerular filtration | Lithium is cleared almost entirely by the kidney |
Why the level alone is a poor guide
The therapeutic range for lithium is 0.6 to 1.2 mmol/L on a sample taken 12 hours after the last dose, and that timing is not a detail. Lithium distributes slowly into tissue, so a level drawn 4 hours after a dose reflects a peak that has not yet equilibrated and cannot be compared with the published range at all. Millimoles per litre and milliequivalents per litre are numerically identical here, because lithium is monovalent and one mole carries one equivalent, so no conversion is needed between the two reports.
Symptoms correlate poorly with the number, and the reason is distribution. In an acute overdose in someone not previously taking lithium, a high serum level sits largely in the vascular compartment and has not yet entered the central nervous system, so the patient can look surprisingly well. In chronic therapy the tissue compartment is already loaded, and a modest rise produces serious neurotoxicity. A level of 2.0 mmol/L in a chronically treated patient can therefore represent a far sicker person than 3.0 mmol/L in an acute ingestion.
Most chronic toxicity is precipitated rather than spontaneous. Lithium is cleared almost entirely by the kidney and is handled like sodium in the proximal tubule, so dehydration, vomiting, diarrhoea, NSAIDs, ACE inhibitors, angiotensin receptor blockers, thiazide diuretics and any fall in glomerular filtration all raise the level in a patient whose dose has not changed. An intercurrent illness in hot weather is a classic trigger, and correcting volume state is often the single most effective intervention.
Decisions about extracorporeal removal follow the clinical picture and renal function rather than the number. EXTRIP recommends haemodialysis where renal function is impaired and the level is high, or where there is a depressed conscious state, seizures or life-threatening arrhythmia, and explicitly warns against treating a level in isolation. Lithium poisoning is time-critical and management should be guided by a poisons centre or clinical toxicology service; this interpreter supports that discussion and never replaces it.
Frequently asked questions
What is the therapeutic range for lithium?
0.6 to 1.2 mmol/L on a sample taken 12 hours after the last dose. A level drawn at any other time cannot be interpreted against that range, because lithium has not finished distributing into tissue.
Is mmol/L the same as mEq/L for lithium?
Yes. Lithium is monovalent, so one mole carries one equivalent and the two units are numerically identical. No conversion is needed.
Why can a low lithium level still mean serious toxicity?
Because chronic therapy loads the tissue compartment. A chronically treated patient at 2.0 mmol/L can be far sicker than someone at 3.0 mmol/L after an acute ingestion, in whom the drug is still largely intravascular.
What raises a lithium level in a patient on a stable dose?
Dehydration, vomiting or diarrhoea, NSAIDs, ACE inhibitors, angiotensin receptor blockers, thiazide diuretics, and any fall in glomerular filtration. Lithium is handled like sodium by the proximal tubule.
When is dialysis used in lithium toxicity?
The decision rests on the clinical picture and renal function rather than the level alone, with EXTRIP recommending it for impaired renal function with a high level, or for depressed consciousness, seizures or life-threatening arrhythmia. Poisoning management is time-critical and should be guided by a poisons centre or clinical toxicology service, which this tool supports rather than replaces.
Related calculators
References
- Decker BS, Goldfarb DS, Dargan PI, et al. Extracorporeal treatment for lithium poisoning: systematic review and recommendations from the EXTRIP workgroup. Clin J Am Soc Nephrol. 2015;10(5):875–887.
- Hedya SA, Avula A, Swoboda HD. Lithium toxicity. In: StatPearls. Treasure Island (FL): StatPearls Publishing.
- Baird-Gunning J, Lea-Henry T, Hoegberg LCG, et al. Lithium poisoning. J Intensive Care Med. 2017;32(4):249–263.