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Lithium Toxicity
 

Lithium Toxicity

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Discussion about Lithium Toxicity

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    Lithium Toxicity Lithium Toxicity Presentation Transcript

    • MN Arham
    • The Patient Mr X 53 years old Presented to OPD with  Loose Stool from last 2 Days  Nausea  Loss of Energy  Fatigue Known patient of Bipolar Disorder and under treatment by Psychiatry. On Lithium carbonate
    •  Pulse 108 BP: 100/70 T: 36.6 R/R: 17/min  Dehydrted  CNS: Irritable, Confused, Mild tremor, Ataxia  CVS: Tachycardia Noramal heart sounds  Resp: Normal  GIT: Soft non tender B/S present no viceromegaly
    •  FBC normal  Cusp normal  LFT’s normal  CRP 60  Lithium level 3.17 mmol/L Ref: 0.50-1.20
    •  Lithium Toxicity
    •  Admit in ward  I/V Fluids  Stop the lithium  Supportive care  Lithium level repeated after 4 days is 0.68 mmol/L  Discharged via Psychiatry after one week.
    • • Lithium is used in the treatment of depressive and bipolar affective disorders. • The CNS is the major organ system affected, although the renal, GIT, endocrine, and CVS also may be involved. • Lithium is available only for oral administration. • Absorbed from the GI tract. • Peak levels occur 2-4 hours postingestion,
    • • The half-life of a single dose of lithium is from 12-27 hours • The half-life increases to approximately 36 hours in elderly • Additionally, half-life may be considerably longer with chronic lithium use. • An estimated 10,000 toxic exposures occur per year. These data indicate a gradual increase over the past 10 years*. * From USA
    • • Lithium is similar to sodium • In addition, lithium may inhibit the release of monoamines from nerve endings and increase their uptake. • The exact mode of action of lithium in affective disorders is unknown. • Lithium has a narrow therapeutic ratio. • Blood concentration must be carefully monitored to avoid toxicity. • Early signs of lithium toxicity are vomiting and severe diarrhoea followed by tremor, ataxia, renal impairment and convulsions
    • •Acute poisoning - Voluntary or accidental ingestion in a previously untreated patient •Acute-on-chronic - Voluntary or accidental ingestion in a patient currently using lithium •Chronic or therapeutic poisoning - Progressive lithium toxicity, generally in a patient on lithium therapy 11
    • Drugs increase the lithium toxicity • nonsteroidal anti-inflammatory drugs [NSAIDs], • diuretics, • tetracyclines, • phenytoin,and • cyclosporine Symptoms • Nausea and vomiting • Diarrhea • Weakness and fatigue • Lethargy and confusion • Tremor • Seizure
    • Mild-to-moderate toxicity • Generalized weakness • Fine resting tremor • Mild confusion Moderate-to-severe toxicity • Severe tremor • Muscle fasciculations • Choreoathetosis • Hyperreflexia • Clonus • Opisthotonos • Stupor • Seizures • Coma • Signs of cardiovascular collapse
    • ACUTE CHRONIC GI (nausea, vomiting 42% 20% & diarrhoea) CNS (seizures) delayed Common > 2.mmol/L Renal Usualy non Universal signifiant ECG normal QT prolongation usual Thyroid none Hypothyroidism 20% Recovery Usual, rapid Disability 10% delayed Level correlation poor Good Hypertox. 2007 14
    • Mmol/L effects 0.5 None 1.0 Mild tremor 1.5 Coarse tremor 2.0 Hyperreflexia, dysarthria 2.5 Myoclonia, ataxia,confusion > 3.0 Delirium, coma, seizures Hypertox 2007 15
    • • Lithium toxicity is dose related • Lithium is minimally protein bound The therapeutic dose is 300-2700 mg/d with desired serum levels of 0.7-1.2 mEq/L. • Lithium clear via kidneys. • Most filtered lithium is reabsorbed in the PCT • Diuretics acting distally to the proximal tubule, such as thiazides and spironolactone • Reabsorption of lithium is increased and toxicity is more likely in patients who are hyponatremic or volume depleted, both of which are possible consequences of diuretic therapy.
    • Tubular Lithium handling Li+ THIAZIDES Li+ LOOP AGENTS 17
    •  Loop diuretics may increase serum lithium levels and potentiate the risk of lithium toxicity.  The exact mechanism is unknown but may be related to the sodium loss induced by loop diuresis, which produces a compensatory increase in proximal tubular reabsorption of sodium along with lithium.
    • Tubular lithium handling: Effect of Furosemide Li+ X Li+ 19
    •  Measure serum lithium concentration  Consider toxicology  CUSP  Imaging Studies  Electrocardiogram
    • Prehospital Care • Stabilize life-threatening conditions and initiate supportive therapy. • Obtain IV access with isotonic sodium chloride solution. • Monitor cardiac function to assess rhythm disturbances. • Obtain all pill bottles available to the patient. • Supportive therapy should take precedence.
    •  Gastric decontamination  Gastric lavage  Activated charcoal  Consider whole bowel irrigation.  Role of sodium polystyrene sulfonate (Kayexalate)  Hypokalemia.
    • • Avoid onset of hypernatremia. • Hemodialysis  In general, consider dialysis in patients with chronic toxicity and serum lithium concentrations higher than 4mEq/L; also consider dialysis in unstable chronic patients with lithium levels higher than 2.5 mEq/L.  Guidelines for hemodialysis are more controversial in patients with acute lithium intoxication but generally refer to higher serum lithium levels despite relatively minor symptoms.  Change in mental status assists in determining need for dialysis
    • • Admit patients with significant signs or symptoms of toxicity. • Admit symptomatic patients, regardless of serum lithium levels; admit patients with serum lithium levels higher than 2 mEq/L. • Admit to an ICU patients with chronically elevated lithium levels higher than 4 mEq/L. • Perform serial serum lithium determinations approximately 4 hours apart to confirm a declining trend.
    •  Accidental overdose Asymptomatic patients and patients with serum lithium concentrations in the therapeutic range and minor toxicity may be discharged with scheduled follow-up in 1-2 days.  Intentional overdose Obtain psychiatric clearance before discharge from the hospital
    •  Truncal and gait ataxia  Nystagmus  Hypertonicity  Short-term memory deficits  Dementia (rare) Prognosis  Most cases of lithium toxicity result in a favourable outcome; however, up to 10% of individuals with severe toxicity
    •  Astruc B, Petit P, Abbar M. Overdose with sustained-release lithium preparations. Eur Psychiatry. Jun 1999;14(3):172-4.  Bailey B, McGuigan M. Comparison of patients hemodialyzed for lithium poisoning and those for whom dialysis was recommended by PCC but not done: what lesson can we learn?. Clin Nephrol. Nov 2000;54(5):388-92.  Chen KP, Shen WW, Lu ML. Implication of serum concentration monitoring in patients with lithium intoxication. Psychiatry Clin Neurosci. Feb 2004;58(1):25-29.  Eyer F, Pfab R, Felgenhauer N. Lithium poisoning: pharmacokinetics and clearance during different therapeutic measures. J Clin Psychopharmacol. Jun 2006;26(3):325-30.  Groleau G. Lithium toxicity. Emerg Med Clin North Am. May 1994;5. 12(2):511-31.  E-medicine  Hypertox 2007 Tables
    • Thanks