Lithium intoxication can cause mild symptoms like weakness and nausea or more severe symptoms like delirium, coma, and organ damage. Long term effects are also possible and include neurological issues like cerebellar dysfunction. Diagnosis involves checking the history, lithium serum level, ECG, and other tests. Treatment focuses on hydration, blocking lithium reabsorption, gastric lavage if recent ingestion, and hemodialysis for moderate to severe cases to reduce the lithium level quickly. Special care is needed to avoid hypernatremia in patients with kidney issues.

1. 1
Lithium intoxication – S/S
• Mild: Sleepy, Proximal muscle weakness, Impaired
memory, G-I: nausea, vomiting, diarrhea.
• Moderate: Neurotoxic: Delirium, Convulsion, Coma,
Incontinence, hyper- reflexia, Fasciculation,
Parkinson-like s/s : Ataxia. Un-coordination.
• Severe: Nephrotoxic: Nocturia, Distal tubular acidosis,
Impaired RFT. Cardiotoxic: ST-T
change, QT prolong, Flat T
Conduction delay, Hypotension.
• Acute intoxication– Less CNS depression.

2. 2
Long-term neurologic sequelae (1)
• In some cases, neurologic complications persist
despite lithium removal by hemodialysis.
• The syndrome of irreversible lithium effectuated
neurotoxicity (SILENT) consists of prolonged
neurologic and neuropsychiatric symptoms
following lithium toxicity . In typical cases of SILENT,
neurologic toxicity develops along with an elevated
lithium concentration, but symptoms persist
despite successful removal of the drug.

3. 3
Long-term neurologic sequelae (2)
• Cerebellar dysfunction, extrapyramidal symptoms, brainstem
dysfunction, and dementia can develop as part of SILENT
(syndrome of irreversible lithium effectuated neurotoxicity ) .
• Other neurologic sequelae may include nystagmus,
choreoathetoid movements, myopathy, and blindness.
• A review of 90 published cases identified cerebellar
dysfunction as the most common sequelae, and proposed
that demyelination at multiple sites in the CNS may be the
cause .
• SILENT can continue for months and in rare cases effects
persist for years.

4. 4
Lithium intoxication - Diagnosis
• History: Psychiatry ( Mania ) P’t with conscious
change + S/S of lithium intoxication.
• Serum level: Therapeutic: 0.6 – 1.2 mEq/L.
• Intoxication: Mild- Moderate: 1.5 – 2.5 mEq/L.
Severe: 2.5 – 3.0 mEq/L.
Lethal dose: 3.0 – 4.0 mEq/L.
• ECG, ABG, Biochemistry, BR.

5. 5
Lithium intoxication - Tx
• Hydration and electrolyte balance, beware of hypernatremia.
• Gastric lavage if ingested within 1 hour.
Charcot is useless ( poor absroption ).
• Block proximal tubule re-absorption: Sod. Bicarbonate,
Diuretics, Amino-phylline.
• Moderate to severe intoxication with conscious change –
Hemo-dialysis: 11 hrs ( indication: Li level >4mEq/L )
Goal: Li level < 1 mEq/L 8 hrs later.

6. 6
Nephrogenic diabetes insipidus
• NDI is a known complication of chronic lithium poisoning. In
patients on chronic lithium therapy who are suspected of
concomitant NDI, the serum sodium concentration should be
followed closely, particularly in patients receiving IV
hydration and those with altered mentation who may not
drink in response to thirst.
• In patients admitted with chronic lithium toxicity, measure
the serum sodium concentration every 6 to 11 hours for the
first 24 to 48 hours. Care must be taken to avoid
hypernatremia from IV hydration in patients with
inadequate free water intake.

7. 7
H.D for lithium intoxication (1)
• Lithium is readily dialyzable due to its low molecular weight,
negligible protein binding, and small volume of distribution.
Therefore, hemodialysis is the treatment of choice for severe
lithium toxicity.
• The appropriate indications for the treatment of lithium
poisoning with hemodialysis remain controversial.
• We recommend treatment with hemodialysis for lithium
poisoning in the following settings regardless of the nature of
the ingestion (ie, acute, acute-on-chronic, or chronic) :