A 52-year-old woman with bipolar disorder type I has been on lithium carbonate 900 mg daily for 3 years with good mood stabilization. She presents to the emergency department with a 2-day history of coarse tremor, confusion, ataxia, and slurred speech. Her husband reports she had acute gastroenteritis with vomiting and diarrhea for 48 hours, after which she did not reduce her lithium dose. On examination: BP 128/82 mmHg, HR 96/min, temperature 37.2°C, coarse tremor of hands, hyperreflexia, and nystagmus. Serum lithium level is 2.8 mEq/L (normal therapeutic range 0.6–1.2 mEq/L). Serum creatinine 1.4 mg/dL (baseline 0.9 mg/dL), serum sodium 132 mEq/L. What is the most appropriate immediate management?

Explanation

## Acute Lithium Toxicity: Recognition and Management ### Clinical Presentation This patient exhibits classic signs of **moderate-to-severe lithium toxicity**: - **Neurological:** coarse tremor, confusion, ataxia, slurred speech, nystagmus, hyperreflexia - **Precipitant:** acute gastroenteritis with volume depletion → reduced renal clearance of lithium - **Serum level:** 2.8 mEq/L is in the toxic range (>2.0 indicates toxicity; >3.5 is life-threatening) - **Renal dysfunction:** creatinine elevated from 0.9 to 1.4 mg/dL (acute kidney injury from dehydration) - **Hyponatremia:** 132 mEq/L (lithium impairs nephrogenic ADH response) ### Management Algorithm for Acute Lithium Toxicity ```mermaid flowchart TD A[Acute Lithium Toxicity]:::outcome --> B{Serum Li+ level & symptoms?}:::decision B -->|Mild: Li+ 1.5-2.0, GI/tremor only| C[Supportive care, IV fluids, monitor]:::action B -->|Moderate: Li+ 2.0-3.5, neuro signs| D[IV normal saline + hemodialysis]:::action B -->|Severe: Li+ >3.5, seizures/coma| E[Urgent hemodialysis + ICU]:::urgent C --> F[Repeat Li+ level 4-6 hrs]:::action D --> G[Lithium clearance & symptom resolution]:::outcome E --> H[Continuous monitoring, supportive care]:::action ``` ### Why Hemodialysis Is Indicated | Feature | Rationale | |---------|----------| | **Serum level 2.8 mEq/L** | Clearly toxic; symptomatic with CNS involvement | | **Moderate-to-severe symptoms** | Coarse tremor, ataxia, confusion = CNS penetration | | **Acute kidney injury** | Reduced renal clearance; dialysis removes lithium directly | | **Hyponatremia** | Worsens neurological toxicity; IV normal saline helps | | **Volume depletion** | Precipitated by gastroenteritis; IV fluids essential | **Key Point:** Hemodialysis is the definitive treatment for moderate-to-severe lithium toxicity (Li+ >2.0 with symptoms, or >3.5 regardless of symptoms). Lithium is water-soluble, has a small volume of distribution, and is NOT protein-bound—it is readily removed by dialysis. **High-Yield:** Lithium has a **narrow therapeutic window** (0.6–1.2 mEq/L). Toxicity occurs when: - Volume depletion (vomiting, diarrhea, diuretics, NSAIDs) → reduced renal clearance - Renal impairment (acute or chronic) - Drug interactions (ACE inhibitors, thiazide diuretics increase renal reabsorption) - Intentional or accidental overdose **Clinical Pearl:** In acute gastroenteritis, patients on lithium should **stop the drug immediately** and rehydrate aggressively. Resumption should occur only after serum levels normalize and renal function recovers. ### Why IV Normal Saline? - Restores intravascular volume → increases glomerular filtration rate (GFR) - Increases urinary lithium excretion (lithium is reabsorbed in proximal tubule like sodium; high Na+ load promotes lithium wasting) - Corrects hyponatremia cautiously (avoid overcorrection; risk of osmotic demyelination) ### Monitoring Post-Dialysis - Serum lithium level 4–6 hours after dialysis (may rebound as intracellular lithium redistributes) - Repeat dialysis if level remains >2.0 or symptoms persist - Monitor serum creatinine, electrolytes, and neurological status - Resume lithium only after level <0.8 mEq/L and renal function normalized [cite:Kaplan & Sadock's Synopsis of Psychiatry 12e, Ch. 31]