| Lithium toxicity | |
|---|---|
| Other names | Lithium overdose, lithium poisoning |
 | |
| A bottle oflithium capsules | |
| Specialty | Toxicology |
| Symptoms | Tremor, increased reflexes, trouble walking, kidney problems,altered level of consciousness[1] |
| Complications | Serotonin syndrome, brain damage[1] |
| Types | Acute, chronic, acute on chronic[1] |
| Causes | Excessive intake, decreased excretion[1] |
| Risk factors | Dehydration, low sodium diet,kidney problems[1] |
| Diagnostic method | Based on symptoms and a lithium level[1][2] |
| Treatment | Gastric lavage,whole bowel irrigation,hemodialysis[1] |
| Prognosis | Low risk of death[3] |
Lithium toxicity, also known aslithium overdose, is the condition of having too muchlithium. Symptoms may include atremor,increased reflexes, trouble walking, kidney problems, and analtered level of consciousness. Some symptoms may last for a year after levels return to normal. Complications may includeserotonin syndrome.[1]
Lithium toxicity can occur due to excessive intake or decreased excretion.[1] Excessive intake may be either asuicide attempt or accidental.[1] Decreased excretion may occur as a result ofdehydration such as fromvomiting ordiarrhea, alow sodium diet, or fromkidney problems.[1] The diagnosis is generally based onsymptoms and supported by a lithium level in blood serum of greater than 1.2 mEq/L.[1][2]
Gastric lavage andwhole bowel irrigation may be useful if done early.[1]Activated charcoal is not effective.[1] For severe toxicityhemodialysis is recommended.[1] The risk of death is generally low.[3] Acute toxicity generally has better outcomes than chronic toxicity.[4] In the United States about 5,000 cases are reported topoison control centers a year.[2] Lithium toxicity was first described in 1898.[1]
Symptoms of lithium toxicity can be mild, moderate, or severe.[1]
Mild symptoms includenausea, feeling tired, and tremor occur at a level of 1.5 to 2.5 mEq/L in blood serum. Moderate symptoms includeconfusion, anincreased heart rate, andhypertonia occur at a level of 2.5 to 3.5 mEq/L.[1] Severe symptoms includecoma,seizures,low blood pressure andincreased body temperature which occur at a lithium concentration greater than 3.5 mEq/L.[1] When lithium overdoses produce neurological deficits or cardiac toxicity, the symptoms are considered serious and can be fatal.[5]
In acute toxicity, people have primarily gastrointestinal symptoms such asvomiting anddiarrhea, which may result involume depletion. During acute toxicity, lithium distributes later into thecentral nervous system causing dizziness and other mild neurological symptoms.[6]
In chronic toxicity, people have primarily neurological symptoms which includenystagmus,tremor,hyperreflexia,ataxia, andchange in mental status. During chronic toxicity, the gastrointestinal symptoms seen in acute toxicity are less prominent. The symptoms are often vague and nonspecific.[7]
In acute on chronic toxicity[clarification needed], people have symptoms of both acute and chronic toxicity.
People who survive an intoxication episode may develop persistent health problems.[8] This group of persistent health symptoms are called syndrome of irreversible lithium-effectuatedneurotoxicity (SILENT).[9] The syndrome presents with irreversible neurological and neuro-psychiatric effects.[10] The neurological signs arecerebellar dysfunction,extrapyramidal symptoms, andbrainstem dysfunction.[11] The neuro-psychiatric findings present with memory deficits, cognitive deficits, andsub-cortical dementia. For a diagnosis, the syndrome requires the absence of prior symptoms and persistence of symptoms for greater than 2 months after cessation of lithium.[12]
Lithium is readily absorbed from thegastrointestinal tract.[5] It is distributed to the body with higher levels in the kidney,thyroid, and bone as compared to other tissues. Since lithium is almost exclusively excreted by thekidneys, people with preexistingchronic kidney disease are at high risk of developing lithium intoxication.[13] The drug itself is also known to benephrotoxic, opening up the possibility of spontaneous emergence of toxicity at doses that were previously well-tolerated. Lithium toxicity can be mistaken for other syndromes associated with antipsychotic use, such asserotonin syndrome because lithium increasesserotonin metabolites in thecerebrospinal fluid.[14]
There are several drug interactions with lithium. Interactions can occur fromtypical antipsychotics oratypical antipsychotics. In particular, certain drugs enhance lithium levels by increasingrenal re-absorption at theproximal tubule. These drugs areangiotensin-converting enzyme inhibitors,non-steroidal anti-inflammatory drugs andthiazide diuretics.[13]
The diagnosis is generally based on symptoms and supported by a lithium level blood level.[1][2] Blood levels are most useful six to twelve hours after the last dose.[2] The normal blood serum lithium level in those on treatment is between 0.6 and 1.2 mEq/L.[1] Some blood tubes containlithium heparin which may result in falsely elevated results.[2]
When lithium toxicity is suspected tests may include:
Imaging tests are not helpful.
If the person's lithium toxicity is mild or moderate, lithium dosage is reduced or stopped entirely.[13] If the toxicity is severe, lithium may need to be removed from the body. The removal of lithium is done in ahospitalemergency department. It may involve:
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