Lithium toxicity

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Lithium toxicity
Other namesLithium overdose, lithium poisoning
Lithium300mg.jpg
A bottle of lithium capsules
Specialty Toxicology
Symptoms Tremor, increased reflexes, trouble walking, kidney problems, altered level of consciousness [1]
Complications Serotonin syndrome, brain damage [1]
TypesAcute, chronic, acute on chronic [1]
CausesExcessive 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 as lithium overdose, is the condition of having too much lithium. Symptoms may include a tremor, increased reflexes, trouble walking, kidney problems, and an altered level of consciousness. Some symptoms may last for a year after levels return to normal. Complications may include serotonin syndrome. [1]

Contents

Lithium toxicity can occur due to excessive intake or decreased excretion. [1] Excessive intake may be either a suicide attempt or accidental. [1] Decreased excretion may occur as a result of dehydration such as from vomiting or diarrhea, a low sodium diet, or from kidney problems. [1] The diagnosis is generally based on symptoms and supported by a lithium level in blood serum of greater than 1.2 mEq/L. [1] [2]

Gastric lavage and whole bowel irrigation may be useful if done early. [1] Activated charcoal is not effective. [1] For severe toxicity hemodialysis 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 to poison control centers a year. [2] Lithium toxicity was first described in 1898. [1]

Signs and symptoms

Symptoms of lithium toxicity can be mild, moderate, or severe. [1]

Mild symptoms include nausea, feeling tired, and tremor occur at a level of 1.5 to 2.5 mEq/L in blood serum. Moderate symptoms include confusion, an increased heart rate, and low muscle tone occur at a level of 2.5 to 3.5 mEq/L. [1] Severe symptoms include coma, seizures, low blood pressure and increased 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]

Acute toxicity

In acute toxicity, people have primarily gastrointestinal symptoms such as vomiting and diarrhea, which may result in volume depletion. During acute toxicity, lithium distributes later into the central nervous system causing dizziness and other mild neurological symptoms. [6]

Chronic toxicity

In chronic toxicity, people have primarily neurological symptoms which include nystagmus, tremor, hyperreflexia, ataxia, and change in mental status. During chronic toxicity, the gastrointestinal symptoms seen in acute toxicity are less prominent. The symptoms are often vague and nonspecific. [7]

Acute on chronic toxicity

In acute on chronic toxicity[ clarification needed ], people have symptoms of both acute and chronic toxicity.

Complications

People who survive an intoxication episode may develop persistent health problems. [8] This group of persistent health symptoms are called syndrome of irreversible lithium-effectuated neurotoxicity (SILENT). [9] The syndrome presents with irreversible neurological and neuro-psychiatric effects. [10] The neurological signs are cerebellar dysfunction, extrapyramidal symptoms, and brainstem dysfunction. [11] The neuro-psychiatric findings present with memory deficits, cognitive deficits, and sub-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]

Pathophysiology

Lithium is readily absorbed from the gastrointestinal 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 the kidneys, people with preexisting chronic kidney disease are at high risk of developing lithium intoxication. [13] The drug itself is also known to be nephrotoxic, 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 as serotonin syndrome because lithium increases serotonin metabolites in the cerebrospinal fluid. [14]

There are several drug interactions with lithium. Interactions can occur from typical antipsychotics or atypical antipsychotics. In particular, certain drugs enhance lithium levels by increasing renal re-absorption at the proximal tubule. These drugs are angiotensin-converting enzyme inhibitors, non-steroidal anti-inflammatory drugs and thiazide diuretics. [13]

Diagnosis

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 0.6-1.2 mEq/L. [1] Some blood tubes contain lithium heparin which may result in falsely positive results. [2]

When lithium toxicity is suspected tests may include:

Imaging tests are not helpful.

Treatment

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 a hospital emergency department. It may involve:

People may be sent home once their blood serum lithium level is less than 1.5 mEq/L and they have no symptoms. [1]

See also

Related Research Articles

<span class="mw-page-title-main">Serotonin syndrome</span> Symptoms caused by an excess of serotonin in the central nervous system

Serotonin syndrome (SS) is a group of symptoms that may occur with the use of certain serotonergic medications or drugs. The symptoms can range from mild to severe, and are potentially fatal. Symptoms in mild cases include high blood pressure and a fast heart rate; usually without a fever. Symptoms in moderate cases include high body temperature, agitation, increased reflexes, tremor, sweating, dilated pupils, and diarrhea. In severe cases, body temperature can increase to greater than 41.1 °C (106.0 °F). Complications may include seizures and extensive muscle breakdown.

<span class="mw-page-title-main">Neuroleptic malignant syndrome</span> Medical condition

Neuroleptic malignant syndrome (NMS) is a rare but life-threatening reaction that can occur in response to antipsychotic (neuroleptic) medications. Symptoms include high fever, confusion, rigid muscles, variable blood pressure, sweating, and fast heart rate. Complications may include rhabdomyolysis, high blood potassium, kidney failure, or seizures.

<span class="mw-page-title-main">Haloperidol</span> Typical antipsychotic medication

Haloperidol, sold under the brand name Haldol among others, is a typical antipsychotic medication. Haloperidol is used in the treatment of schizophrenia, tics in Tourette syndrome, mania in bipolar disorder, delirium, agitation, acute psychosis, and hallucinations from alcohol withdrawal. It may be used by mouth or injection into a muscle or a vein. Haloperidol typically works within 30 to 60 minutes. A long-acting formulation may be used as an injection every four weeks by people with schizophrenia or related illnesses, who either forget or refuse to take the medication by mouth.

Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. Symptoms can be absent, mild or severe. Mild symptoms include a decreased ability to think, headaches, nausea, and poor balance. Severe symptoms include confusion, seizures, and coma; death can ensue.

Iron poisoning typically occurs from ingestion of excess iron that results in acute toxicity. Mild symptoms which occur within hours include vomiting, diarrhea, abdominal pain, and drowsiness. In more severe cases, symptoms can include tachypnea, low blood pressure, seizures, or coma. If left untreated, iron poisoning can lead to multi-organ failure resulting in permanent organ damage or death.

<span class="mw-page-title-main">Kidney failure</span> Disease where the kidneys fail to adequately filter waste products from the blood

Kidney failure, also known as end-stage kidney disease, is a medical condition in which the kidneys can no longer adequately filter waste products from the blood, functioning at less than 15% of normal levels. Kidney failure is classified as either acute kidney failure, which develops rapidly and may resolve; and chronic kidney failure, which develops slowly and can often be irreversible. Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications of acute and chronic failure include uremia, hyperkalaemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.

<span class="mw-page-title-main">Kernicterus</span> Medical condition

Kernicterus is a bilirubin-induced brain dysfunction. The term was coined in 1904 by Christian Georg Schmorl. Bilirubin is a naturally occurring substance in the body of humans and many other animals, but it is neurotoxic when its concentration in the blood is too high, a condition known as hyperbilirubinemia. Hyperbilirubinemia may cause bilirubin to accumulate in the grey matter of the central nervous system, potentially causing irreversible neurological damage. Depending on the level of exposure, the effects range from clinically unnoticeable to severe brain damage and even death.

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<span class="mw-page-title-main">Uremia</span> Type of kidney disease, urea in the blood

Uremia is the term for high levels of urea in the blood. Urea is one of the primary components of urine. It can be defined as an excess in the blood of amino acid and protein metabolism end products, such as urea and creatinine, which would be normally excreted in the urine. Uremic syndrome can be defined as the terminal clinical manifestation of kidney failure. It is the signs, symptoms and results from laboratory tests which result from inadequate excretory, regulatory, and endocrine function of the kidneys. Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. The former denotation will be used for the rest of the article.

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Hypermagnesemia is an electrolyte disorder in which there is a high level of magnesium in the blood. Symptoms include weakness, confusion, decreased breathing rate, and decreased reflexes. Complications may include low blood pressure and cardiac arrest.

<span class="mw-page-title-main">Metabolic acidosis</span> Medical condition

Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low to high.

Nephrotoxicity is toxicity in the kidneys. It is a poisonous effect of some substances, both toxic chemicals and medications, on kidney function. There are various forms, and some drugs may affect kidney function in more than one way. Nephrotoxins are substances displaying nephrotoxicity.

Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater cyanobacteria crusts. Toxic encephalopathy can occur following acute or chronic exposure to neurotoxicants, which includes all natural toxins. Exposure to toxic substances can lead to a variety of symptoms, characterized by an altered mental status, memory loss, and visual problems. Toxic encephalopathy can be caused by various chemicals, some of which are commonly used in everyday life, or cyanotoxins which are bio-accumulated from harmful algal blooms (HABs) which have settled on the benthic layer of a waterbody. Toxic encephalopathy can permanently damage the brain and currently treatment is mainly just for the symptoms.

<span class="mw-page-title-main">Organophosphate poisoning</span> Medical condition

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<span class="mw-page-title-main">Salicylate poisoning</span> Medical condition

Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin. The classic symptoms are ringing in the ears, nausea, abdominal pain, and a fast breathing rate. Early on, these may be subtle, while larger doses may result in fever. Complications can include swelling of the brain or lungs, seizures, low blood sugar, or cardiac arrest.

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<span class="mw-page-title-main">Lithium (medication)</span> Mood-stabilizing psychiatric medication

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Antimanic drugs are psychotropic drugs that are used to treat symptoms of mania. Though there are different causes of mania, the majority is caused by bipolar disorder, therefore antimanic drugs are mostly similar to drugs treating bipolar disorder. Since 1970s, antimanic drugs have been used specifically to control the abnormal elevation of mood or mood swings during manic episodes. One purpose of antimanic drugs is to alleviate or shorten the duration of an acute mania. Another objective is to prevent further cycles of mania and maintain the improvement achieved during the acute episode. The mechanism of antimanic drugs has not yet been fully known, it is proposed that they mostly affect chemical neurotransmitters in the brain. However, the usage of antimanic drugs should be consulted with a doctor or pharmacist due to their side effects and interactions with other drugs and food.

References

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  2. 1 2 3 4 5 6 "Lithium Toxicity | California Poison Control System | UCSF". calpoison.org. Retrieved 22 December 2019.
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  4. 1 2 3 Waring, WS (2006). "Management of lithium toxicity". Toxicological Reviews. 25 (4): 221–30. doi:10.2165/00139709-200625040-00003. PMID   17288494. S2CID   22844004.
  5. 1 2 Watkins, J. B., Klaassen, C. D., & Casarett, L. J. (2010). Casarett & Doulls essentials of toxicology. Place of publication not identified: McGraw Hill Medical.
  6. ↑ Gitlin, Michael (2016-12-17). "Lithium side effects and toxicity: prevalence and management strategies". International Journal of Bipolar Disorders. 4 (1): 27. doi: 10.1186/s40345-016-0068-y . ISSN   2194-7511. PMC   5164879 . PMID   27900734.
  7. ↑ Netto, Ivan; Phutane, Vivek H. (2012). "Reversible Lithium Neurotoxicity: Review of the Literature". The Primary Care Companion for CNS Disorders. 14 (1). doi:10.4088/PCC.11r01197. ISSN   2155-7772. PMC   3357580 . PMID   22690368.
  8. ↑ Singh, Hemendra; Ganjekar, Sundernag; Kalegowda, Anand; Thyloth, Murali (2015-07-01). "Unusual manifestation of therapeutic dose of lithium as syndrome of irreversible lithium-effectuated neurotoxicity". Journal of Mental Health and Human Behaviour. 20 (2): 80. doi: 10.4103/0971-8990.174600 . S2CID   100832585.
  9. ↑ "Syndrome of Irreversible Lithium-Effectuated Neurotoxicity (Silent): Break the Silence". SHM Abstracts. Archived from the original on 2017-05-26. Retrieved 2018-10-30.
  10. ↑ Adityanjee, null; Munshi, Kaizad R.; Thampy, Anita (2005). "The syndrome of irreversible lithium-effectuated neurotoxicity". Clinical Neuropharmacology. 28 (1): 38–49. doi:10.1097/01.wnf.0000150871.52253.b7. ISSN   0362-5664. PMID   15714160. S2CID   2189764.
  11. ↑ Shah, Vivek C.; Kayathi, Pramod; Singh, Gurpreet; Lippmann, Steven (2015-06-04). "Enhance Your Understanding of Lithium Neurotoxicity". The Primary Care Companion for CNS Disorders. 17 (3). doi:10.4088/PCC.14l01767. ISSN   2155-7772. PMC   4578904 . PMID   26644952.
  12. ↑ Adityanjee; Munshi, Thampy (2005). "The syndrome of irreversible lithium-effectuated neurotoxicity". Clinical Neuropharmacology. 28 (1): 38–49. doi:10.1097/01.wnf.0000150871.52253.b7. PMID   15714160. S2CID   2189764.
  13. 1 2 3 Haussmann, R.; Bauer, M.; von Bonin, S.; Grof, P.; Lewitzka, U. (2015-10-22). "Treatment of lithium intoxication: facing the need for evidence". International Journal of Bipolar Disorders. 3 (1): 23. doi: 10.1186/s40345-015-0040-2 . ISSN   2194-7511. PMC   4615994 . PMID   26493348.
  14. ↑ Shahani, Lokesh (2012). "Venlafaxine Augmentation With Lithium Leading to Serotonin Syndrome". The Journal of Neuropsychiatry and Clinical Neurosciences. 24 (3): E47. doi:10.1176/appi.neuropsych.11080196. ISSN   0895-0172. PMID   23037683.
  15. 1 2 Lavonas, Eric J; Buchanan, Jennie (2015-09-16). Cochrane Injuries Group (ed.). "Hemodialysis for lithium poisoning". Cochrane Database of Systematic Reviews. 2015 (9): CD007951. doi:10.1002/14651858.CD007951.pub2. PMC   8436884 . PMID   26374731.
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