Take-home point on lithium toxicity: chronic lithium toxicity often presents with AMS and tremors! Urgent dialysis is indicated when lithium level is >4.
More PEARLS on lithium toxicity!
- Can be acute (eg intentional overdose), acute on chronic, or chronic (stable lithium regimen with reduction in renal function)
- Helpful to differentiate ACUTE vs CHRONIC lithium toxicity: neuro findings are LATE findings for acute toxicity, but are often the PRESENTING finding for chronic toxicity! Renal toxicity is seen in CHRONIC toxicity but not ACUTE toxicity.
Presentation: LITHIUM mnemonic:
- Insipidus (nephrogenic diabetes insipidus)
- Increased weight
- Misc – EKG changes (QT prolongation)
|· GI sxs (n/v/d) –> dehydration –> exacerbates lithium toxicity
· Cardiac (long QTc, bradycardia)
· Neuro findings develop LATE in acute Lithium toxicity (because it takes time to be absorbed into the CNS)
|· Neuro: sluggishness, ataxia, confusion or agitation, neuromuscular excitability (irregular coarse tremors, fasciculations, myoclonic jerks), seizures
· Cardiac: can also get long QT and bradycardia but more benign
· Renal: nephrogenic DI
- Diabetes Insipidus: Chronic lithium toxicity leads to renal resistance to ADH (inability of kidneys to concentrate urine) –> polyuria and polydipsia; hypernatremia is often not seen unless patient is altered and unable to take in po!
- SILENT SYNDROME: long-term neurologic sequelae of lithium toxicity despite removal by dialysis. Can persist for months to years!
- Cerebellar dysfunction, extrapyramidal symptoms, brainstem dysfunction, dementia
- Lithium levels often do not correlate with signs of toxicity!
- Hemodialysis is indicated if Li level is >4, regardless of clinical s/sx (this represents a large total body lithium burden), or >2.5 + sxs and/or renal insufficiency and/or IVF is contraindicated (eg decompensated CHF)
- Management of nephrogenic DI: often becomes irreversible or only partially reversible
- Discontinue lithium if possible
- Amiloride: blocks sodium channels in collecting tubules (only helpful if mild/moderate concentrating defect)
- Thiazide: paradoxically reduces UOP and increases urine osm and urine Na by increasing sodium excretion at distal convoluted tubule and reabsorption of water in proximal tubule, minimizing the effect of ADH at the collecting duct
- Desmopressin (to attain supraphysiologic level of ADH, as most patients only have partial resistance to ADH)
- Here is a reminder of the kidney and sites of action for various diuretics
More on dialysis for lithium toxicity: PMID 17288494 and 25583292
And a very recent (Oct 2015!) Nature Review article on management of nephrogenic DI, including potential future roles for molecular medicine! PMID 26077742
Evernote link: https://www.evernote.com/shard/s34/sh/1cfcde84-c4a5-4f39-a719-7d0a692b1afa/9e544457e5cea8d59e2ebbc492ad8e3b