Lithium-Induced Neurotoxic “Syndrome”
NOTE:
There is no established, specific, one neurologic syndrome caused by lithium, labeled as such. And yet, for the reason that the neurologic sequelae of lithium excess can be devastating for the patients, some of whom may require total care if they survive, that we choose to make the psychiatrist aware of this here.
Lithium poses a special danger because lithium has a very narrow therapeutic index, that is, its therapeutic dose closely correlates with the dose that may produce a toxic reaction. Neurotoxic effects may also occur with therapeutic lithium levels.
Do not start lithium on patients before doing the prelithium work-up (see Appendix A).
Use caution when using lithium in the following conditions:
Renal insufficiency—lithium is excreted through the kidneys, and it can accumulate rapidly in the presence of renal insufficiency.
Dehydration—patients who develop polyuria from lithium are at a risk of toxicity secondary to dehydration from the decreased ability of kidneys to concentrate urine.
Dehydration also causes fluid and electrolyte imbalance.
Infections, fever—fever (Adityanjee, 2005) may be a precipitant to the development of neurotoxicity, and is also a manifestation of neurotoxicity.
Gastroenteritis can cause dehydration as well.
Note: Leukocytosis without underlying infection can occur in the acute phase of lithium toxicity.
Hyponatremia—patients who have low serum sodium levels, or patients who are on sodium restricted diet, or patients who take medications that decrease sodium levels (thiazide diuretics, furosemide, ethacrynic acid, angiotensin-converting enzyme [ACE] inhibitors) are candidates for lithium toxicity because lithium excretion depends on normal sodium concentrations. Low serum sodium encourages the kidneys to reabsorb more lithium ions.
Neurologic conditions—patients prone to seizures or who have other neurologic illnesses are candidates for lithium toxicity.
Elderly patients—the elderly have a lower glomerular filtration rate and a lower creatinine clearance.
Their blood level of lithium may be high even if the given dose of lithium is small.
Drug interactions with lithium
ACE inhibitors decrease sodium levels.
Thiazides diuretics, furosemide, and ethacrynic acid decrease sodium levels.
Nonsteroidal anti-inflammatory drugs (NSAIDs) decrease lithium clearance, and thereby increase lithium levels.
Certain antibiotics
Macrolides
Antifungals (eg., metronidazole)
Trimethoprim (one case report noted)
Psychiatric medications
Selective serotonin reuptake inhibitors
Interaction can either increase or decrease lithium levels.
Lithium toxicity can be seen at normal lithium levels.
Tricyclic antidepressants (TCAs)
Because TCA and lithium can lower seizure threshold, there is the potential for an additive effect.
Specifically, there is an increased risk of neurotoxicity.
Antipsychotics
Concomitant use can increase risk of extrapyramidal side effects.Related posts:
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