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LITHIUM TOXICITY

PREPARED BY: Reejan Paudel (RN)


MN 1 st year
LITHIUM

 Lithium is an element with atomic number 3 and atomic weight 7, which is the
smallest alkaline ion.

 The element was discovered in 1817 by Arfuedson, since then, it has been
used for treatment of gout and for salt replacement in cardiac disease, but its
use was restricted due to fatal toxicity.

 It was rediscovered in 1949 by John Cade, for use in treatment of mania but its
potential went unrecognized as it was discovered in Australia.

 Mogen Schou in 1957, had to rediscover it yet again before it became popular
as a treatment of mania.
 Pharmacokinetics:

 Lithium is very rapidly absorbed from the gastrointestinal tract.

 The peak serum levels occur between 30 min to 3 hours.

 Lithium is distributed rapidly in liver and kidney and more slowly in muscle,
brain and bone. Steady state levels are achieved in about 7 days.

 There is no metabolism of lithium in body and it is excreted almost entirely by


the kidneys.

 Proximal reabsorption is influenced by the sodium balance, and depletion of


sodium results in retention, causing higher blood levels of lithium.
 Mechanism of action

 Lithium alters sodium metabolism within nerve and muscle cells and enhance
(There are five known biogenic amines: dopamine, epinephrine,
norepinephrine, histamine and serotonin) the reuptake of biogenic amines in
the brain, lowering levels in the body and resulting in decreased hyperactivity.

 It may block development of sensitive dopamine receptors in the CNS of


manic patient.

 Lithium has both anti-manic and antidepressant properties.


 Indications

 Treatment of acute mania

 prophylaxis for bipolar and unipolar mood disorder

 Treatment of schizoaffective disorder

 Treatment of cyclothymia (mild form of bipolar disorder)

 Treatment of chronic alcoholism (in presence of significant depressive


symptoms) and psychoactive use disorder (e.g. cocaine dependence)

 Impulsivity and aggression.


 Other disorder:

 Premenstrual dysphoric disorder (severe form of PMS)


 bulimia nervosa
 episodes of binge drinking

 Trichotillomania: Trichotillomania, also known as trich, is when someone


cannot resist the urge to pull out their hair.
 cluster headaches

 
 Dosage

Lithium is available in the market in the form of the following


preparations:
 lithium carbonate: 300 mg tablets (Licab); 400 mg sustained
release tablets (e.g. Lithosun-SR)

 lithium citrate: 300 mg/5ml liquid

 The usual range of dose per day in acute mania is 900-2100 mg


given in 2-3 divided doses.
 The treatment is started after serial lithium estimation is done
after a loading dose of 600mg or 900mg of lithium to determine
the pharmacokinetics.
 BLOOD LITHIUM LEVEL:

 Therapeutic levels = 0.8 – 1.2 mEq/L (for treatment of acute mania)

 Prophylactic levels = 0.6 – 1.2 mEq/L for prevention of relapse in bipolar


disorder.

 Toxic lithium levels > 2.0 mEq/L


 Side effects:

 Neurological : Tremors, motor hyperactivity, muscular weakness, cogwheel


rigidity, seizure, neurotoxicity (delirium, abnormal involuntary movements,
seizures, coma)

 Renal: Polydipsia (excessive thirst), polyuria, tubular enlargement, nephrotic


syndrome

 Cardiovascular: T-Wave depression

 Gastrointestinal : nausea, vomiting, diarrhea, abdominal pain and metallic


taste.
 Endocrine : abnormal thyroid dysfunction, goiter and weight gain.

 Dermatological: acne form eruptions, papular eruptions, and exacerbation of


psoriasis.

 Side effects during pregnancy and lactation: Teratogenic possibility,


increased incidence of Ebstein’s anomaly (distortion and downward
displacement of tricuspid valve in right ventricle) when taken in first trimester.

 Secreted in milk and can cause toxicity in infant.

 Lithium toxicity: toxicity occurs when serum lithium level >2.0 mEq/L
Pappular eruptions
 Contraindications of lithium use

 Cardiac, renal, thyroid or neurological dysfunctions.

 Presence of body dystonia. (excessive involuntary muscle contractions leading


to abnormal postures)

 During first trimester of pregnancy and lactation.

 Severe dehydration.

 Hypothyroidism.

 History of seizures.
LITHIUM TOXICITY

 Lithium toxicity is a potentially serious condition caused by having too much


lithium in blood. Since Lithium’s primary medical use is as a disorder.

 According to the US Food and Drug Administration (FDA), in general the


desirable level is 0.6 to 1.2 mEq/L.

 However, they point out, “Patients unusually sensitive to Lithium may exhibit
toxic signs at serum levels below 1 mEq/L”.

 The higher the serum level, the likelier there will be both side effects and the
appearance of toxic symptoms (also called lithium intoxication).
 
TYPES OF LITHIUM TOXICITY

 Acute lithium toxicity:

 This most commonly occurs when someone who it’s taking lithium at all
ingests it. This could occurs when a family member takes pills from the whole
bottle, when a child gets into a parent’s medications, or in a suicide attempt.

 According to the researchers, acute toxicity can carry somewhat less medical
risk and less severe symptoms that the other types, depending on amount
taken.
 Chronic Lithium Toxicity:

 The chronic form of lithium intoxication occurs in people who


take lithium daily but the serum blood level has crept up into the
toxic range.

 Possible causes are a dosage increase, dehydration, interactions


with other medications, and problems with kidney function.
Causes

 Drugs related condition.

 Poisoning for suicide.

 Lithium toxicity is usually precipitated by dehydration,


concurrent use of diuretics drugs such as HCT
(Hydrochlorothiazide), usage of over the counter pain killers such
as NSAIDS, rapid increase in the dose and renal impairment.
Sign and symptoms of lithium toxicity

 Ataxia : Ataxia means without coordination.

 Coarse tremor (hand)

 Nausea and vomiting

 Impaired concentration

 Nephrotoxicity : rapid deterioration in the kidney function due to toxic effect


of medications and chemicals.

 Muscle weakness

 Convulsions
 Muscle twitching

 Dysarthria

 Lethargy

 Confusion

 Coma

 Hyper-reflexia : Hyper-reflexia refers to hyperactive or repeating (clonic)


reflexes. 

 Nystagmus : a vision condition in which the eyes make repetitive,


uncontrolled movements. 
Management of lithium toxicity

 Pre-hospital care:

 Stabilize life – threatening condition and initiate supportive therapy.

 Obtain intravenous access with isotonic (sodium chloride) solution.

 Monitor cardiac function to assess rhythm disturbances.

 Obtain all pill bottles available to the patient.


 Emergency department care: Supportive therapy is the mainstay of
treatment of lithium toxicity.

 Airway protection is crucial due to emesis and risk of aspiration.

 Seizures can be controlled with benzodiazepines, or phenobarbital.


 
 GI decontamination:

 Gastric lavage may be attempted if the patient presents within one hour of
investigation.

 Lithium is a monovalent cat-ion that does not bind to charcoal; therefore,


activated charcoal has no role.

 Whole- bowel irrigation with polyethylene glycol lavage can be effective in


preventing absorption from extended-release lithium.

 Because of its similarities to potassium, the use of sodium polystyrene


sulfonate has been proposed as a method of eliminating lithium.
 Multiple-dose sodium polystyrene sulfonate may be useful in lowering the
serum lithium level of select patients with acute lithium overdoses but is not a
substitute for hemodialysis in severely ill patients.

 Enhanced elimination:

 The mainstay of treatment is fluid therapy. The goal of saline administration


is to restore glomerular filtration rate (GFR), normalize urine output, and
enhance lithium clearance.
 Lithium is readily dialyzed because of water solubility, low volume of
distribution, and lack of protein binding.
 Hemodialysis is indicated for patient who have renal failure and are unable to
eliminate lithium.

 It is also indicated in patient who cannot tolerate hydration such patients with
congestive heart failure (CHF) or liver disease.

 Hemodialysis should be considered in patients who develop severe signs of


neurotoxicity such as profound altered mental status and seizure.

 An absolute level of 4 mEq/L in acute toxicity and a level of 2.5 mEq/L in


chronic toxicity in patients with symptoms should also be considered for
hemodialysis.
 Consultations

 Consult renal service personnel for hemodialysis in severe intoxication.

 Consult psychiatric service personnel for patient with intentional overdose.

 Consult the poison control center and a medical toxicologist regarding appropriate
treatment.
 REFERENCES
 
 P.Subedi Durga, Mental health and psychiatric nursing, 4th edition, Makalu
publication 2018, page no. 370-375.
 
 R Shreevani, A Guide to Mental Health & Psychiatric Nursing, 4th edition, Jaypee
Brothers Medical Publishers pvt. Ltd 2016, page no. 130 – 133.
  
 
 Ahuja Neeraj, A Short textbook of Psychiatric, 7th edition, Jaypee Brothers Medical
Publishers pvt Ltd 2011, page no. 172-175

 RETRIVED FROM:
 https://www.webmd.com/bipolar-disorder/what-to-know-about-lithium-toxicity
 https://www.healthline.com/health/lithium-toxicity
 

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