Lithium
| Indication | mood stabiliser |
|---|---|
| Mechanism of action | modulates intracellular signalling - numerous effects |
| Absorption | almost 100% oral bioavailability |
| Metabolism | Not metabolised |
| Distribution | Low volume of distribution + high water solubility (i.e. filtered by CRRT) |
| Elimination | Renal |
| Time course of action | |
| Adverse effects | See below Nephrogenic DI; tremor; |
| Contraindications | Brugada syndrome, heart failure, Arrhythmia Untreated hypothyroidism Low sodium diet Addison's disease |
Basically it pretends to be our friend magnesium :(
Lithium toxicity
pattern features which might point to the lithium toxidrome
- Acute: gastrointestinal symptoms
- Chronic: redistributes into intravascular space → CNS symptoms
| Acute | Chronic | |
|---|---|---|
| Clinical presentation | GI - N+V, diarrhoea, abdo pain | 1. Mild - tremor, hyperreflexia, ataxia 2. Moderate - stupor, rigidity, hypertonia, hypotension 3. Severe - coma, myoclonus, seizures |
| Bloods | Initially normal Low anion gap |
Renal impairment ?Low anion gap Check thyroid stimulating hormone, Ca (chronic lithium use is associated with hypothyroidism, hyperparathyroidism). |
| Levels | Lithium levels high - most useful as a one-off?? May not be proportionate to how sick the patient is | Lithium levels may be normal |
Danger is from lithium level in the brain, not the blood!
Looking for causes of the intoxication
- Trigger - infection
- Elimination altered e.g. renal impairment, NSAIDs, thiazides
Looking for sequelae
- Mortality is rare
- The terrifyingly named SILENT https://www.sciencedirect.com/science/article/abs/pii/S0303846720304005 - cerebellar signs, dyskinesia
Management
- ↑ elimination - fluid resuscitation