lithium carbonate / lithium citrate

Brand: Lithobid, Eskalith

⚠ BBW Beers Criteria TDM Required Prototype Drug
Drug Class: mood stabilizer
Drug Family: mood stabilizer
Subclass: alkali metal ion
Organ Systems: cns

Mechanism of Action

Inhibits inositol monophosphatase (depleting inositol and reducing phosphoinositide signaling) and GSK-3 (affecting neuronal plasticity); also modulates neurotransmitter release and receptor sensitivity; mechanism of mood stabilization not fully established.

inositol monophosphataseglycogen synthase kinase-3 (GSK-3)

Indications

  • bipolar disorder (acute mania — first-line)
  • bipolar maintenance prophylaxis
  • augmentation of antidepressants in treatment-resistant depression
  • cluster headache prophylaxis

Contraindications

  • severe renal impairment
  • dehydration or sodium depletion
  • concurrent diuretics and NSAIDs (relative)
  • pregnancy (first trimester — Ebstein's anomaly risk)

Adverse Effects

Common

  • fine tremor
  • polyuria
  • polydipsia
  • weight gain
  • cognitive dulling
  • nausea
  • diarrhea
  • acne

Serious

  • lithium toxicity (coarse tremor, confusion, ataxia, seizures, coma)
  • nephrogenic diabetes insipidus
  • hypothyroidism
  • cardiac conduction abnormalities
  • Ebstein's anomaly (first-trimester exposure)

Pharmacokinetics (ADME)

Absorption Complete oral absorption; distributed throughout total body water
Distribution Not protein-bound; Vd ~0.7–1.0 L/kg; distributes like sodium; crosses BBB and placenta
Metabolism Not metabolized; excreted unchanged
Excretion Entirely renal; proximal tubule reabsorption competes with sodium — sodium depletion increases lithium reabsorption and toxicity risk
Half-life 18–36 hours
Onset 5–7 days for antimanic effect
Peak 0.5–3 hours (immediate release); 4–12 hours (extended release)
Duration 12–24 hours
Protein Binding 0%
Vd 0.7–1.0 L/kg

Drug Interactions

Drug / Agent Mechanism Severity
NSAIDs and COX-2 inhibitors reduce renal prostaglandin synthesis, decreasing lithium clearance by up to 20–25% major
thiazide diuretics sodium depletion increases proximal tubular lithium reabsorption; levels may increase 25–40% major
ACE inhibitors / ARBs reduce aldosterone, impairing lithium excretion; levels can double major

Nursing Considerations

  1. Therapeutic drug monitoring is mandatory: target serum trough level 0.8–1.2 mEq/L (acute mania) or 0.6–0.8 mEq/L (maintenance); toxic above 1.5 mEq/L — draw 12 hours after last dose
  2. Maintain consistent sodium intake and hydration; instruct patient to avoid dehydration, low-salt diets, excessive sweating, and OTC NSAIDs
  3. Lithium toxicity signs: coarse tremor, confusion, ataxia, nausea, vomiting (early); seizures, coma, cardiac arrhythmias (severe) — hold and notify provider immediately
  4. Monitor thyroid function (TSH) every 6–12 months; hypothyroidism occurs in ~30% of long-term users; monitor renal function annually (polyuria and nephrogenic DI are common)

Clinical Pearls

  • Lithium is the only medication with level-1 evidence for antisuicidal effect in bipolar disorder — this unique benefit makes it irreplaceable despite its narrow therapeutic index
  • The sodium-lithium competition in the proximal tubule explains the many drug interactions: anything that depletes sodium (diuretics, low-sodium diet, vomiting, diarrhea) will cause lithium retention and toxicity

Safety Profile

Pregnancy use-with-caution
Lactation avoid
Renal Adjustment Required
Hepatic Adjustment Not required
TDM Required