- 1978 Jul 19;58(3):317-22. Psychopharmacology (Berl) – PMID: 98804
- 1982 77(4):348-55. Psychopharmacology (Berl)
- 1976; 11(2):84-92. Int Pharmacopsychiatry
- 1987; Nov-Dec; 50(6): 85-7. Farmakol Toksikol
- Lithium – Toxicity – https://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+hsdb:@term+@rn+7439-93-2
[Rumack BH POISINDEX(R) Information System Micromedex, Inc., Englewood, CO, 2017; CCIS Volume 172, edition expires May, 2017. Hall AH & Rumack BH (Eds): TOMES(R) Information System Micromedex, Inc., Englewood, CO, 2017; CCIS Volume 172, edition expires May, 2017.] **PEER REVIEWED**
Lithium effects on rat brain glucose metabolism in long-term lithium-treated rats studied in vivo.
- The time course of lithium effects on several brain energy metabolites has been investigated in rats. The rats were injected once daily with lithium chloride and killed by freezing in liquid nitrogen 1–8 h after the last injection. The effect of lithium was most marked in the period in which the brain lithium concentration was increasing, whereas the effect was wearing off when the brain lithium concentration had stabilized, even though the lithium concentration was higher. These results led to the hypothesis that the effect of lithium on several parameters depends on the increase in lithium concentration following the administration of lithium, rather than on the absolute concentration of lithium.
2. The effects of lithium on several brain energy metabolites were investigated in rats. Lithium was administered by three alternative routes: 1) in food, 2) via IP injection, or 3) intracisternally via the suboccipital route. Lithium given in food induced permanent changes, mainly in glycolytic processes and in glycogen content. Lithium injected IP induced, in addition, several changes which depended on the increase in brain lithium concentration following injection of lithium. These changes in brain metabolites disappeared as brain lithium concentration stabilized. Intracisternal injection of lithium produced brain lithium concentrations between 1 and 2 mmoles/kg wet wt., with a mean of about 1.6 mmoles/kg wet wt. Lithium concentrations below about 1.6 mmoles/kg wet wt. induced changes in brain metabolites which were similar to the changes seen after IP injection of lithium. Lithium concentrations above about 1.6 mmoles/kg wet wt. induced changes in several brain metabolites which were at variance with the changes induced by lower lithium concentrations. These changes were in many respects similar to changes in brain metabolites seen in rats exposed to convulsive treatment. It is hypothesized that such metabolic changes during lithium treatment, in discrete areas of the brain with higher concentration of lithium, e.g., hypothalamus, might be related to the prophylactic effect of lithium treatment in man.
3. Administration of LiCl to rats was found to affect brain glucose metabolism in the following ways. The concentrations of brain glucose, brain lactate and brain glycogen were increased, and the concentration of brain glutamate was decreased. The incorporation of (14)C from U-(14)C D-glucose, administered intraperitoneally to the rats, was increased in brain glucose and brain lactate, and decreased in brain glutamate. The results were explained by a lithium-induced increase in brain glucose uptake and an increased rate of glycolysis, and a slight inhibition of the oxidative decarboxylation of the Krebs cycle.
4. Selective activation of phosphofructokinase (PFK) and lactate dehydrogenase (LDG) in the cerebral cortex and an increase of glucose and lactate contents in all other brain areas were noted in acute alcoholic intoxication of rats (2.5 g/kg). Lithium carbonate potentiated the inhibitory action of alcohol on glycolysis in the brain tissue. In combination with ethanol it decreased the activity of PFK and LDG in all studied brain areas and increased glucose and lactate levels.
5. Toxicity Summary:
IDENTIFICATION AND USE: Elemental lithium is a silver white metal; body centered cubic structure it becomes yellowish on exposure to moist air and it reacts with water. It is soluble in liquid ammonia forming a blue solution. It is used in the manufacture of catalysts for polyolefin plastics; in fuels for aircraft and missiles.It is used in metallurgy, as a degasifier, deoxidizer, desulfurizer; as a grain refiner in non-ferrous metals. Chemical intermediate for butyllithium polymerization catalyst; in alloys with aluminum or magnesium for aerospace uses. It is used in the production of tritium, reducing and hydrogenating agents, alloy hardeners, pharmaceuticals and Grignard reagents. Scavenger and degassifier for stainless and mild steels in molten state, modular iron, soaps and greases, deoxidizer in copper and copper alloys, heat-transfer liquid, storage batteries (with sulfur, selenium, tellurium, and chlorine). Rocket propellants, vitamin A synthesis, silver solders, underwater bouyancy devices, nuclear reactor coolent. HUMAN EXPOSURE AND TOXICITY: Elemental lithium causes severe eye and skin burns. Industrial exposures to lithium may occur during extraction of lithium from its ores, preparation of various lithium compounds, welding, brazing, enameling, and from the use of lithium hydrides.
Animal Toxicity Studies:
IDENTIFICATION AND USE: Elemental lithium is a silver white metal; body centered cubic structure it becomes yellowish on exposure to moist air and it reacts with water. It is soluble in liquid ammonia forming a blue solution. It is used in the manufacture of catalysts for polyolefin plastics; in fuels for aircraft and missiles.It is used in metallurgy, as a degasifier, deoxidizer, desulfurizer; as a grain refiner in non-ferrous metals. Chemical intermediate for butyllithium polymerization catalyst; in alloys with aluminum or magnesium for aerospace uses. It is used in the production of tritium, reducing and hydrogenating agents, alloy hardeners, pharmaceuticals and Grignard reagents. Scavenger and degassifier for stainless and mild steels in molten state, modular iron, soaps and greases, deoxidizer in copper and copper alloys, heat-transfer liquid, storage batteries (with sulfur, selenium, tellurium, and chlorine). Rocket propellants, vitamin A synthesis, silver solders, underwater bouyancy devices, nuclear reactor coolent. HUMAN EXPOSURE AND TOXICITY: Elemental lithium causes severe eye and skin burns. Industrial exposures to lithium may occur during extraction of lithium from its ores, preparation of various lithium compounds, welding, brazing, enameling, and from the use of lithium hydrides. ANIMAL STUDIES: No animal studies could be located.
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|The information contained in the Truven Health Analytics Inc. products is intended as an educational aid only. All treatments or procedures are intended to serve as an information resource for physicians or other competent healthcare professionals performing the consultation or evaluation of patients and must be interpreted in view of all attendant circumstances, indications and contraindications. The use of the Truven Health Analytics Inc. products is at your sole risk. These products are provided “as is” and “as available” for use, without warranties of any kind, either express or implied. Truven Health Analytics Inc. makes no representation or warranty as to the accuracy, reliability, timeliness, usefulness or completeness of any of the information contained in the products. Additionally, Truven Health ANALYTICS INC. makes no representation or warranties as to the opinions or other service or data you may access, download or use as a result of use of the Truven Health ANALYTICS INC. products. All implied warranties of merchantability and fitness for a particular purpose or use are hereby excluded. Truven Health Analytics Inc. does not assume any responsibility or risk for your use of the Truven Health Analytics Inc. products.The following Overview, *** CORROSIVES-ALKALINE ***, is relevant for this HSDB record chemical.|
o This overview assumes that basic life support measures have been instituted.
0.2.1 SUMMARY OF EXPOSURE 0.2.1.1 ACUTE EXPOSURE A) USES: Used as drain openers, household cleaners (oven, bathroom), hair relaxers, dishwasher soap, and in automobile air bags. In industry used as cleaners, in cement, and as chemical precursors. B) TOXICOLOGY: Alkaline corrosives cause liquefaction necrosis. They saponify the fats in the cell membrane, destroying the cell and allowing deep penetration into mucosal tissue. In gastrointestinal tissue an initial inflammatory phase may be followed by tissue necrosis (sometimes resulting in perforation), then granulation and finally stricture formation. C) EPIDEMIOLOGY: Exposure is common. Serious effects are rare in the developed world (generally only seen in adults with deliberate ingestion), largely because mostly low concentration corrosives are present in products available in the home. Serious effects are more common in developing countries. D) WITH POISONING/EXPOSURE 1) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop grade II burns (superficial blisters, erosions and ulcerations) are at risk for subsequent stricture formation, particularly esophageal. Some patients (particularly young children) may develop upper airway edema. a) Alkaline corrosive ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases. b) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. 2) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Upper airway edema is common and often life threatening. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products available in the home are generally of low concentration. 3) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury. 4) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation. 5) DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Metabolic acidosis may develop in patients with severe burns or shock. Prolonged exposure or high concentration products can cause full thickness burns. 0.2.3 VITAL SIGNS
0.4.2 ORAL EXPOSURE A) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY 1) Perform early (within 12 hours) endoscopy in patients with stridor, drooling, vomiting, significant oral burns, difficulty swallowing or abdominal pain, and in all patients with deliberate ingestion. If burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation. B) SEVERE ORAL TOXICITY 1) Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation. C) DILUTION 1) Dilute with 4 to 8 ounces of water may be useful if it can be performed shortly after ingestion in patients who are able to swallow, with no vomiting or respiratory distress; then the patient should be NPO until assessed for the need for endoscopy. Neutralization, activated charcoal, and gastric lavage are all contraindicated. D) AIRWAY MANAGEMENT 1) Aggressive airway management in patients with deliberate ingestions or any indication of upper airway injury. E) ENDOSCOPY 1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after inadvertent ingestion. Endoscopy should also be considered in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion. Children and adults who are asymptomatic after inadvertent ingestion do not require endoscopy. The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. F) CORTICOSTEROIDS 1) The use of corticosteroids to prevent stricture formation is controversial. Corticosteroids should not be used in patients with grade I or grade III injury, as there is no evidence that it is effective. Evidence for grade II burns is conflicting, and the risk of perforation and infection is increased with steroid use. G) STRICTURE 1) A barium swallow or repeat endoscopy should be performed several weeks after ingestion in any patient with grade II or III burns or with difficulty swallowing to evaluate for stricture formation. Recurrent dilation may be required. Some authors advocate early stent placement in these patients to prevent stricture formation. H) SURGICAL MANAGEMENT 1) Immediate surgical consultation should be obtained on any patient with grade III or severe grade II burns on endoscopy, significant abdominal pain, metabolic acidosis, hypotension, coagulopathy, or a history of large ingestion. Early laparotomy can identify tissue necrosis and impending or unrecognized perforation, early resection and repair in these patients is associated with improved outcome. I) PATIENT DISPOSITION 1) OBSERVATION CRITERIA: Patients with alkaline corrosive ingestion should be sent to a health care facility for evaluation. Patients who remain asymptomatic over 4 to 6 hours of observation, and those with endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged home. 2) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting. J) PITFALLS 1) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal burns. 2) Patients may have severe tissue necrosis and impending perforation requiring early surgical intervention without having severe hypotension, rigid abdomen, or radiographic evidence of intraperitoneal air. 3) Patients with any evidence of upper airway involvement require early airway management before airway edema progresses. 4) The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn. All patients with corrosive eye injury should be evaluated by an ophthalmologist. K) DIFFERENTIAL DIAGNOSIS 1) Acid ingestion, gastrointestinal hemorrhage, or perforated viscus. 0.4.3 INHALATION EXPOSURE A) DECONTAMINATION 1) Administer oxygen as necessary. Monitor for respiratory distress. B) AIRWAY MANAGEMENT 1) Manage airway aggressively in patients with significant respiratory distress, stridor or any evidence of upper airway edema. Monitor for hypoxia or respiratory distress. C) BRONCHOSPASM 1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids. 0.4.4 EYE EXPOSURE A) DECONTAMINATION 1) Exposed eyes should be irrigated with copious amounts of 0.9% saline for at least 30 minutes, until pH is neutral and the cul de sacs are free of particulate material. 2) An eye examination should always be performed, including slit lamp examination. Ophthalmologic consultation should be obtained. Antibiotics and mydriatics may be indicated. 0.4.5 DERMAL EXPOSURE A) OVERVIEW 1) DECONTAMINATION a) Remove contaminated clothes and any particulate matter adherent to skin. Irrigate exposed skin with copious amounts of water for at least 15 minutes or longer, depending on concentration, amount and duration of exposure to the chemical. A physician may need to examine the area if irritation or pain persist.
A) LIQUID CORROSIVES – With highly concentrated liquids (30% sodium hydroxide) esophageal burns may occur in up to 100% of patients, even after accidental ingestion. B) Serious burns are less likely if the pH is less than 11.5. Injury is greater with large exposures and high concentrations. C) More recent series of caustic ingestions (mixed liquid and solid) in children report incidences of significant esophageal burns from 5% to 35%. Adults with deliberate ingestions are more likely to develop significant esophageal burns (30% to 80%). D) LOW PHOSPHATE DETERGENTS and electric dishwasher soaps may result in oral and esophageal burns.
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|The information contained in the Truven Health Analytics Inc. products is intended as an educational aid only. All treatments or procedures are intended to serve as an information resource for physicians or other competent healthcare professionals performing the consultation or evaluation of patients and must be interpreted in view of all attendant circumstances, indications and contraindications. The use of the Truven Health Analytics Inc. products is at your sole risk. These products are provided “as is” and “as available” for use, without warranties of any kind, either express or implied. Truven Health Analytics Inc. makes no representation or warranty as to the accuracy, reliability, timeliness, usefulness or completeness of any of the information contained in the products. Additionally, Truven Health ANALYTICS INC. makes no representation or warranties as to the opinions or other service or data you may access, download or use as a result of use of the Truven Health ANALYTICS INC. products. All implied warranties of merchantability and fitness for a particular purpose or use are hereby excluded. Truven Health Analytics Inc. does not assume any responsibility or risk for your use of the Truven Health Analytics Inc. products.The following Overview, *** LITHIUM SALTS ***, is relevant for this HSDB record chemical.|
SUMMARY OF EXPOSURE 0.2.1.1 ACUTE EXPOSURE A) USES: Lithium carbonate is used therapeutically, primarily to treat bipolar disorder; it is less commonly used today due to the wide availability of other psychiatric medications with lesser side effects. It is available in oral formulations, both regular and extended release. Lithium orotate is a dietary supplement. Lithium is an important industrial material used to make batteries, alloys, and flux. B) PHARMACOLOGY: Lithium is a naturally occurring alkali metal and monovalent cation chemically similar to Na+ and K+. The exact mechanism by which it stabilizes mood is not known. It is thought to affect the CNS by altering nerve conduction, cortisol and monoamine metabolism, and increasing serotonin. C) TOXICOLOGY: In the kidney, lithium competes with Na+ and K+ in the renal tubules; conditions that increase renal sodium reabsorption (dehydration) decrease lithium elimination. Chronic toxicity is typically due to decreased clearance caused by dehydration, medication interactions, or renal impairment. D) EPIDEMIOLOGY: Acute poisoning is typically less severe than chronic toxicity. Chronic toxicity develops primarily in elderly patients, those with intercurrent illnesses, and those started on drugs that decrease lithium clearance. E) WITH THERAPEUTIC USE 1) At therapeutic doses, effects such as blurred vision, nystagmus, GI irritation, tremors, slowed mentation, cerebellar dysfunction may occur. Polyneuropathy and Parkinsonian syndrome have been described. ECG changes such as nonspecific ST/T changes, sinus node blocks may be present. Brugada Syndrome has been reported in several chronic lithium users. Nephrogenic Diabetes Insipidus, reduced glomerular filtration, and thyroid abnormalities, particularly hypothyroidism, may also occur. Lithium carbonate crosses the placenta and is also present in breast milk. Congenital malformations have been documented after exposure to lithium during pregnancy. 2) DRUG INTERACTIONS: Lithium clearance is decreased by concomitant use of ACE inhibitors, angiotensin II antagonists, thiazide and loop diuretics, and nonsteroidal anti-inflammatory drugs. F) WITH POISONING/EXPOSURE 1) MILD TO MODERATE POISONING: Toxicity is categorized as acute or chronic. Acute overdose is typically less severe than chronic toxicity and results in gastrointestinal upset, while CNS manifestations are less common due to slow absorption into the brain. Chronic effects are usually less gastrointestinal and more neurological due to prior CNS saturation. Mild to moderate poisoning can cause nausea, vomiting, diarrhea, dehydration, nystagmus, and tremors. Hyperreflexia, cogwheel rigidity, ataxia, agitation, confusion, and lethargy are common. Bradycardia, T-wave abnormalities, hypoventilation may also occur. 2) SEVERE POISONING: Severe effects in acute exposures are rare. Patients with chronic toxicity may manifest severe toxicity despite relatively modestly elevated serum lithium concentrations. Effects include photophobia, dehydration, electrolyte imbalances, thyroid dysfunction, hyperthermia, seizure, coma, rigidity, myoclonus, serotonin syndrome. ECG changes such as nonspecific T-wave abnormalities, QTc prolongation, bundle branch block, bradycardia, junctional rhythm, and hypotension may occur. Hypoventilation, respiratory failure, and ARDS may rarely develop. Bezoars may form in large ingestions. 0.2.3 VITAL SIGNS 0.2.20 REPRODUCTIVE HAZARDS A) Lithium is classified as FDA pregnancy category D. Congenital malformations have been reported. The use of lithium should be avoided during pregnancy, especially in the first trimester and one week prior to delivery. Cardiovascular and other teratogenic or toxic effects have been reported in infants born to lithium-treated mothers. In addition, a prospective, observational study showed that significantly more miscarriages and preterm deliveries occurred with lithium exposure during pregnancy (n=183) compared with a group of women who were not exposed to any teratogen during pregnancy (n=748). However, other studies have revealed that outcomes of most pregnancies with in utero exposure to lithium have resulted in normal infants, and that use of lithium during pregnancy may possess a lower fetal risk than previously believed. Lithium is present in breast milk at 33% to 50% of the plasma lithium concentration, and may cause hypertonia, hypothermia, cyanosis, and ECG changes in nursing infants and neonates. 0.2.21 CARCINOGENICITY 0.2.21.1 IARC CATEGORY A) IARC Carcinogenicity Ratings for CAS554-13-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 1) Not Listed 0.2.21.2 HUMAN OVERVIEW A) At the time of this review, the manufacturer does not report any carcinogenic potential for lithium in humans. 0.2.22 GENOTOXICITY A) Lithium-treated patients did not demonstrate increased numbers of chromosomal lesions in blood lymphocytes compared with controls (Turecki et al, 1994).
A) Monitor vital signs, mental status, and urine output. B) Serial lithium levels should be followed until concentration has clearly peaked and declined. The correlation between clinical toxicity and serum concentration is poor; an acute overdose is often asymptomatic despite high serum concentration; chronic exposure may have neurologic manifestations at therapeutic concentrations. C) Monitor electrolytes (particularly sodium), urinalysis, and serum creatinine. D) Obtain thyroid function tests and arterial blood gases; lithium intoxication may cause a low anion gap. E) CT scan of brain may be indicated if etiology of altered mentation is in question. Monitor EEG if there is a concern for subclinical seizures. Chest x-ray may be indicated to monitor pulmonary edema. In those with worsening symptoms or known large ingestions, closely monitor airway, breathing, circulation, cardiac ectopy via continuous cardiac monitoring (including pulse oximetry, capnography), and ECGs.
0.4.2 ORAL EXPOSURE A) MANAGEMENT OF MILD TO MODERATE TOXICITY 1) Most acute lithium overdoses may be safely managed with supportive care that includes: antiemetics for nausea and vomiting, intravenous normal saline hydration to enhance renal lithium elimination, and correction of any electrolyte abnormalities. For chronic toxicity, address underlying causes of decreased renal clearance, including intravenous fluids for dehydration or ceasing medications that impair renal function. B) MANAGEMENT OF SEVERE TOXICITY 1) Orotracheal intubation for airway protection should be performed if recurrent seizures, increasing somnolence or coma develop. Consider gastric lavage for recent, large ingestion if airway is protected. Whole bowel irrigation with polyethylene glycol may be considered in large ingestions, especially if a sustained-release formulation. Administer intravenous normal saline to enhance renal elimination of lithium (Goal: urine output of 2 to 3 mL/kg/hr). Intravenous fluids and vasopressors (dopamine, norepinephrine) may be needed to treat hypotension. Treat agitation, rigidity, seizures, hyperthermia, serotonin syndrome with sedation (benzodiazepines, propofol), and cooling measures; intubation and paralysis may be necessary with severe toxicity. Consider hemodialysis for patients with severe toxicity not responding to hydration, or congestive heart failure or renal insufficiency. Dysrhythmias are treated with standard ACLS protocols. C) DECONTAMINATION 1) PREHOSPITAL: Charcoal does not adsorb lithium well; it is not recommended. 2) HOSPITAL: Consider gastric lavage in a patient with recent life-threatening ingestion, if airway is protected or patient is alert. Whole bowel irrigation with polyethylene glycol should be considered with a large ingestion or ingestion of a sustained-release product. D) AIRWAY MANAGEMENT 1) Intubate if unable to protect airway due to worsening agitation, somnolence or coma, or if respiratory distress develops. E) ANTIDOTE 1) None. F) ENHANCED ELIMINATION 1) Hemodialysis increases lithium clearance and decreases half-life. The decision to perform hemodialysis is largely clinical. The international expert Extracorporeal Treatments in Poisoning (EXTRIP) workgroup reviewed the available literature and despite a low quality of evidence recommended the following guidelines for extracorporeal treatment (ECTR) in patients with severe lithium toxicity with any of the following clinical conditions: a) In the presence of a reduced level of consciousness, seizures, or life-threatening dysrhythmias irrespective of lithium concentration. b) If kidney function is impaired and lithium concentration is greater than 4 mEq/L. 2) ECTR was also suggested for patients with any of the following clinical conditions: a) If lithium concentration is greater than 5 mEq/L, if confusion is present, or if the expected time to obtain a lithium concentration less than 1 mEq/L with optimal management is greater than 36 hours. 3) DISCONTINUATION of ECTR is recommended: a) In patients with apparent clinical improvement or lithium concentration less than 1 mEq/L. b) After a minimum of 6 hours of ECTR if the lithium concentration is not readily available. 4) Serum lithium levels typically rebound 6 to 12 hours after dialysis in chronically intoxicated patients due to equilibration with intracellular and CNS lithium stores. In order to determine the use of subsequent ECTR sessions, serial lithium concentrations should be determined over 12 hours after the cessation of ECTR. The preferred ECTR is intermittent hemodialysis, with an acceptable alternative being continuous renal replacement therapy (RRT), if intermittent hemodialysis is not available. Both continuous RRT and intermittent hemodialysis are equally acceptable after the first treatment. G) PATIENT DISPOSITION 1) HOME CRITERIA: Accidental ingestions in asymptomatic lithium naive patients who ingest less than the maximum daily dose (Children less than 6 years old: 900 mg/square meter/day; Children 6 to 12 years old: 30 mg/kg/day; Adults: less than 2400 mg) who have no synergistic co-ingestions may be monitored at home. Those chronically taking lithium that are accidentally exposed to additional doses needed to be evaluated on a case by case basis, but typically tolerate a double dose without significant effects. 2) OBSERVATION CRITERIA: Patients with deliberate ingestions, symptomatic patients, children and adults with ingestions of greater than maximum daily dose, acute-on-chronic ingestions, unknown dosing errors in chronic patients, synergistic co-ingestions, or those with unclear history should be sent to a health care facility for evaluation and observation. Patients should be monitored until serum lithium concentration has peaked and is consistently declining and clinical condition is improved. 3) ADMISSION CRITERIA: Patients with persistent or worsening gastrointestinal irritation, renal impairment, altered mentation, respiratory depression, dysrhythmias, unstable vital signs, or persistently rising serum lithium concentrations should be admitted. Intensive care admission is indicated for aggressive airway, cardiac monitoring, and emergent hemodialysis. 4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (agitation, hyperthermia, need for hemodialysis, respiratory depression, coma), concerns about decontamination, or in whom the diagnosis is not clear. Consult a nephrologist for emergent hemodialysis in patients with severe poisoning. H) PITFALLS 1) Patients with chronic toxicity often exhibit neurologic toxicity at levels lower than those with acute exposures. Close monitoring of electrolytes, renal function, urine output, neurologic exam, mental status, and temperature should be correlated with serial levels to assess efficacy of treatment. Anticipate early the need to transfer the patient to a higher level of care if unable to check serial lithium concentration, or if hemodialysis is not available. Diuretics should be avoided as they increase lithium reabsorption in the renal tubules. I) PHARMACOKINETICS 1) Well absorbed; peak concentrations within 2 to 5 hours. Lithium is not bound to plasma proteins. The volume of distribution is 0.79 L/kg. Primarily renal (8% to 98%) elimination. Initial half-life is 6 to 12 hours, slowing to 24 hours or greater due to slow redistribution from intracellular compartment. Nearly 80% of filtered lithium is reabsorbed in proximal tubule; reabsorption increases with sodium depletion or dehydration. Half-life in therapeutic dose is approximately 19 hours (14 to 24 hours). J) TOXICOKINETICS 1) Peak lithium concentrations delayed 4 to 17 hours after overdose of sustained release formulations. Half-life is shorter in acute overdose (10 to 20 hours) and prolonged in patients with chronic intoxication (mean 32 hours). Hemodialysis reduces half-life to 2 to 5 hours. Serum concentrations rebound after hemodialysis due to redistribution from intracellular compartments. K) DIFFERENTIAL DIAGNOSIS 1) Extrapyramidal effects from other medications, neuroleptic malignant syndrome, serotonin syndrome from other agents, sepsis, CNS infections, or intracranial catastrophes (massive hemorrhage or stroke).
Range of Toxicity:
A) TOXICITY: Toxic dose is not well defined. In some patients on chronic lithium therapy, the serum concentrations associated with toxic effects are close to therapeutic levels. Therapeutic concentration is 0.6 to 1.2 mEq/L. CHRONIC VS ACUTE: Acute poisoning is typically less severe than chronic for a given serum concentration. Mild to moderate toxic reactions may occur at 1.2 to 2.5 mEq/L in chronic intoxications. Patients with chronic toxicity and serum concentrations above 2.5 mEq/L may have more severe effects, and serum concentrations above 4 mEq/L are generally associated with severe CNS effects in patients with chronic toxicity. Patients with an acute lithium toxicity can develop high serum concentrations with limited distribution to the brain (which can be delayed up to 24 hours), and limited neurologic toxicity. Conversely, in patients on chronic therapy the serum lithium concentration is closer to steady state and correlates better with brain lithium levels. B) ADULTS: A 45-year-old man died after an acute ingestion of 90 sustained-release lithium tablets (450 mg each) with a peak level of 6.9 mEq/L despite hemodialysis. A 28-year-old man survived an acute ingestion with a lithium level of 10 mEq/L. An adult recovered after an acute ingestion of 84 grams (210 tablets of 400 mg) of lithium. Levels up to 14 mmol/L have been recorded in survivors of acute ingestions. PEDIATRIC: Accidental ingestions of an average of 2 pills typically causes drowsiness, while neurotoxicity has resulted after chronic therapy of 40 mg/kg/day. Mortality due to lithium as a single exposure is rare if recognized quickly and treated aggressively. C) Full recovery was reported after a 39-year-old man ingested 210 lithium carbonate tablets (400 mg each) following a suicide attempt. D) THERAPEUTIC DOSE: ADULT: Daily dose ranges from 600 to 2400 mg. PEDIATRIC: EXTENDED-RELEASE TABLETS: 12 YEARS OF AGE AND OLDER: The recommended dose is 900 to 1800 mg/day orally in 2 to 4 divided doses. IMMEDIATE-RELEASE AND CAPSULES: 12 YEARS OF AGE AND OLDER: maintenance, 300 mg orally 3 to 4 times daily; desired serum lithium levels ranging between 0.6 to 1.2 mEq/L. YOUNGER THAN 12 YEARS OF AGE: Safety and effectiveness have not been established.
Antidote and Emergency Treatment:
Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary … . Monitor for shock and treat if necessary … . Anticipate seizures and treat if necessary … . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during treatment … . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool … . Cover skin burns with dry sterile dressings after decontamination … . /Lithium and related compounds/
No physiological function has been reported for Li.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Lithium is widely distributed in nature; trace amounts are found in many minerals, in most rocks and soils, and in many natural waters. Lithium is a member of the alkali metals and does not occur as the free metal in nature. Lithium concentrations in the earth’s crust are estimated to be 20 to 70 ppm by weight; it is the 27th most abundant element. Lithium is found in small amounts in nearly all igneous rocks and in the waters of many mineral springs. Lepidolite, spodumene, petalite, and amblygonite are the most important lithium containing minerals. The production and use of lithium compounds in ceramics, glass and primary aluminum production, the manufacture of lubricants and greases, primary and secondary (rechargeable) batteries, the production of synthetic rubber, the manufacture of polyester fiber, the production of antioxidants and antihistamines, as catalysts, and in the treatment of mood disorders may result in the release of lithium compounds to the environment through various waste streams. If release to air lithium compounds should exist in the particulate phase in the ambient atmosphere since the ionic nature of lithium compounds makes them essentially non-volatile. Particulate-phase lithium may be physically removed from the air by wet and dry deposition. The adsorption of lithium was measured on aquifer material; Freundlich coefficients ranged from 4.5 to 5.5. Lithium has been found to sorb slightly to humic soils with a Kp of 4.6 at pH 5. These data indicate that lithium compounds are not expected to adsorb strongly to soils and sediments. Lithium ion would not be expected to undergo oxidation-reduction reactions under environmental conditions, and would exist in its +1 oxidation state either in compounds or as dissolved ions. The ionic nature of lithium compounds makes them essentially non-volatile; lithium compounds would not volatilized from dry soil surfaces. Due to the ionic nature of lithium compounds, volatilization from moist surfaces will not occur. In water, adsorption to suspended solids and sediments is not expected to be important fate processes for lithium compounds. Lithium ions may undergo precipitation, sorption, or ligand exchange reactions in the environment. Due to the ionic nature of most lithium compounds, volatilization from water surfaces will not occur. Bioconcentration is not expected to be an important fate process due to the ionic nature of lithium compounds. Occupational exposure to lithium compounds may occur through inhalation and dermal contact at workplaces where lithium compounds are produced or used. Since lithium is found various environmental media, the general public would be exposed to small amounts of lithium via inhalation of ambient air, ingestion of food and drinking water. (SRC)
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has statistically estimated that 3,455 workers (1,084 of these are female) are potentially exposed to lithium in the US(1).
Natural Pollution Sources:
Lithium is widely distributed in nature; trace amounts are found in many minerals, in most rocks and soils, and in many natural waters(1). Lithium is a member of the alkali metals and does not occur as the free metal in nature(2). The typical oxidation state of the alkali metals is +1; no other cations are known or expected for the alkali metals(4). Lithium concentrations in the earth’s crust are estimated to be 20 to 70 ppm by weight(1); it is the 27th most abundant element(3). Lithium is found in small amounts in nearly all igneous rocks and in the waters of many mineral springs(2). Lepidolite, spodumene, petalite, and amblygonite are the most important lithium containing minerals(2).
Soft silvery-white metal
Silvery-white metal; body centered cubic structure; becomes yellowish on exposure to moist air
1342 deg C
180.54 deg C
LIQUID METAL IS CORROSIVE, ATTACKING GLASS OR PORCELAIN AT A TEMPERATURE OF ABOUT 200 DEG C
Critical Temperature & Pressure:
Critical temperature = 3223 deg C; critical pressure = 68.9 MPa
0.534 g/cu cm at 25 deg C
Heat of Combustion:
-18,470 BTU/LB= -10,260 CAL/G= -429.3X10+5 J/KG
Heat of Vaporization:
ca. 21.3 kJ/g
Reacts with water
Soluble in liquid ammonia forming a blue solution
Emits characteristic crimson color (670.8 nm) in flame
Characteristic spectrum lines: 670.8 nm (red); 610.4 (orange)
Surface tension at the melting point: 398 mN/m
7.90X10-11 Pa (5.92X10-13 mm Hg) at 400 K (127 deg C); 0.000489 Pa (3.67X10-6 mm Hg) at 600 K (327 deg C); 1.08 Pa (0.00810 mm Hg) at 800 K (524 deg C); 109 Pa (0.818 mm Hg) at 1000 K (727 deg C)
Other Chemical/Physical Properties:
Atomic number: 3; valance: 1; group IA(1); alkali metal; hardest of the alkali metals; Mohs’ hardness: 0.6; Oxidation potential: 3.045 V; reacts with water forming the hydroxide and hydrogen (H2); reacts violently with inorganic acids; reacts slowly with cold sulfuric acid; does not react with oxygen at room temperature; forms Li2O when heated to 100 deg C or higher; artificial radioactive isotopes: 5, 8-11 (all are unstable, half-lives < 1 sec)
Two stable isotopes are present in natural lithium: 7 (92.4%); 6 (7.6%); remains untarnished in dry air, but in moist air, its surface becomes coated with a mixture of LiOH, LiOH.H2O, Li2CO3, Li3N; thin films are opaque to visible light, but are transparent to UV radiation; electrical resistivity at 20 deg C: 9.446 microohm cm; first ionization potential: 519 kJ/mol; electron affinity: 52.3 kJ/mol
Enthalpy of fusion at the melting point: 432 J/g; specific heat capacity at constant pressure at 25 deg C: 3.57 24.8 J/mol K
When heated above melting point it burns with an intense white light; liquid metal dissolves metals such as copper, zinc, tin and their alloys.
Lightest and least reactive of the alkali metals; lightest solid element; reacts exothermically with nitrogen in moist air at high temperatures; high electrical conductivity
Heat of solution: -31,500 btu/lb= -17,500 cal/g= -733X10+5 J/kg
Critical volume: 66 mL/mol
Highly electropositive; high ionization potential; does not generally form coordinate covalent compounds.
Decomposes in alcohol
Burns with a luminous white flame, forming a dense white smoke consisting of mainly lithium oxide
Violently reactive with water or moisture, carbon dioxide, halogens, strong acids, and chlorinated hydrocarbons.
Viscosity of liquid lithium is less than water
Chemical Safety & Handling:
DOT Emergency Guidelines:
/GUIDE 138 SUBSTANCES – WATER-REACTIVE (Emitting Flammable Gases)/ Fire or Explosion: Produce flammable gases on contact with water. May ignite on contact with water or moist air. Some react vigorously or explosively on contact with water. May be ignited by heat, sparks or flames. May re-ignite after fire is extinguished. Some are transported in highly flammable liquids. Runoff may create fire or explosion hazard.
… Flammable solid.
Fire Fighting Procedures:
Extinguish lithium fires only with chemicals designed for this purpose.
Toxic Combustion Products:
Combustion may produce irritants and toxic gases.
Corrosive … Water reactive … Evolves hydrogen and ignites on contact with water.
Explosive Limits & Potential:
… Atmospheric oxidation of molten lithium led to an explosion. A high degree of correlation of incidence of explosions with high atmospheric humidity was demonstrated, with the intensity of explosion apparently directly related to the purity of the sample of metal.
Hazardous Reactivities & Incompatibilities:
Reacts with water forming lithium hydroxide and hydrogen. Keep under mineral oil or other liquid free from oxygen or water.
Other Hazardous Reaction:
A highly luminous reaction occurs at room temp, between iodine and lithium …
Protective Equipment & Clothing:
Rubber or plastic gloves; face shield; fire-retardant clothing
SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.
Decomposes in water
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance … and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by … /the hazardous materials regulations (49 CFR 171-177)./
Store in a cool, dry, well-ventilated location. Separate from water.
Eliminate all ignition sources. Keep water away from release. Shovel into suitable dry container.
Waste Disposal: Package Lots. Place in a separate labeled container for recycling or disposal by burning. Burn in an open furnace. Use caution and limit to 100 g packages. Small Quantities. Wear eye protection, laboratory coat and nitrile rubber gloves. Work in the fume hood. Equip a 3-necked round-bottom flask with a stirrer, dropping funnel, condenser and heating mantle. Flush the flask with nitrogen and place the lithium (cut in small pieces) in it. Add 30 mL of 95% ethanol per gram of lithium at a rate that causes rapid refluxing. Stirring is started as soon as enough ethanol has been added to make it feasible. The mixture is stirred and heated under reflux until the lithium is dissolved. The heat is turned off, and an equal volume of water is added at a rate that causes no more than mild refluxing. The solution is then cooled, neutralized with 6 M hydrochloric acid (cautiously add a volume of concentrated acid to an equal volume of cold water) and washed down the drain with at least 50 times its volume of water.
View products that contain this chemical: LITHIUM, ELEMENTAL
As “getter” in vacuum tubes; manufacture of catalysts for polyolefin plastics; in fuels for aircraft, missiles.
E.I. du Pont de Nemours and Co., 1007 Market St., Wilmington, DE 19898, (302) 774-1000; DuPont Coatings & Color Technologies, DuPont Performance Coatings; Production site: Niagara Falls, NY 14302
Methods of Manufacturing:
Recovery of the ore, spodumene, followed by concentration by froth flotation, conversion to lithium chloride, and electrolysis from an anhydrous lithium chloride-potassium chloride mixture.
General Manufacturing Information:
Available as ingots, rods, wire, ribbon, & pellets.
Grade: 99.86% to 99.9999%
The purity of the meatal is 99.8% or better with the metallic impurities less than 0.1%
U. S. Production:
(1972) LESS THAN 5.6X10+8 GRAMS (USE)
U. S. Imports:
770 metric tons /compounds, concentrate, ores, and metal/
U. S. Exports:
(1975) 2.72X10+7 GRAMS
Synonyms and Identifiers:
Related HSDB Records:
6900 [Lithium Compounds]
Grade: 99.86% to 99.9999%
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1415; LithiumIMO 4.3; Lithium
Hazardous Substances Databank Number:
Last Review Date:
Reviewed by SRP on 5/14/2007
Last Revision Date:
Field Update on 2015-12-21, 9 fields added/edited/deleted
Field Update on 2014-12-05, 2 fields added/edited/deleted
Field Update on 2013-09-20, 1 fields added/edited/deleted
Complete Update on 2007-10-11, 40 fields added/edited/deleted
Field Update on 2007-06-07, 1 fields added/edited/deleted
Field Update on 2006-04-18, 2 fields added/edited/deleted
Field Update on 2006-04-17, 2 fields added/edited/deleted
Complete Update on 02/14/2003, 1 field added/edited/deleted.
Complete Update on 01/24/2003, 1 field added/edited/deleted.
Complete Update on 05/13/2002, 1 field added/edited/deleted.
Complete Update on 02/13/2002, 1 field added/edited/deleted.
Complete Update on 01/18/2002, 9 fields added/edited/deleted.
Field Update on 01/14/2002, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 05/15/2001, 1 field added/edited/deleted.
Complete Update on 06/12/2000, 1 field added/edited/deleted.
Complete Update on 03/28/2000, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 11/18/1999, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 02/27/1998, 1 field added/edited/deleted.
Complete Update on 01/26/1998, 71 fields added/edited/deleted.
Field Update on 10/17/1997, 1 field added/edited/deleted.
Field Update on 01/24/1997, 1 field added/edited/deleted.
Field Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 05/10/1996, 1 field added/edited/deleted.
Complete Update on 03/21/1996, 1 field added/edited/deleted.
Complete Update on 01/19/1996, 1 field added/edited/deleted.
Complete Update on 11/10/1995, 1 field added/edited/deleted.
Complete Update on 12/21/1994, 1 field added/edited/deleted.
Complete Update on 08/18/1994, 1 field added/edited/deleted.
Complete Update on 06/16/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 09/14/1993, 1 field added/edited/deleted.
Field update on 12/14/1992, 1 field added/edited/deleted.
Field update on 03/06/1990, 1 field added/edited/deleted.
Complete Update on 09/14/1989, 2 fields added/edited/deleted.
Complete Update on 04/13/1989, 1 field added/edited/deleted.
Complete Update on 10/14/1986
Created 19830401 by GCF
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