A 28-year-old man with bipolar disorder on lithium carbonate 1200 mg daily presents to the emergency department with tremor, confusion, ataxia, and diarrhea. His serum lithium level is 2.8 mEq/L (normal: 0.6–1.2 mEq/L). Which investigation should be performed immediately to assess the severity of lithium toxicity and guide management?

Explanation

## Acute Lithium Toxicity: Investigations ### Clinical Presentation of Lithium Toxicity The patient presents with classic signs of **acute lithium toxicity**: - **Mild toxicity (1.5–2.0 mEq/L):** Tremor, nausea, diarrhea - **Moderate toxicity (2.0–3.0 mEq/L):** Confusion, ataxia, coarse tremor, polyuria - **Severe toxicity (>3.0 mEq/L):** Seizures, arrhythmias, coma, renal failure This patient's level of **2.8 mEq/L** indicates **moderate-to-severe acute toxicity** requiring urgent investigation. ### Why ECG and Serum Electrolytes? (Option D — Correct) **Key Point:** ECG and serum electrolytes (Na⁺, K⁺, Ca²⁺) are the most critical *immediate* investigations in acute lithium toxicity because lithium causes: 1. **Cardiac arrhythmias** (ECG findings): - Flattened or inverted T waves - Prolonged QT interval - Bradycardia and sinus node dysfunction - Atrioventricular (AV) block in severe cases - Risk of sudden cardiac death 2. **Electrolyte disturbances**: - **Hyponatremia** — lithium competes with Na⁺ in renal tubular reabsorption; sodium depletion also increases lithium reabsorption, worsening toxicity - **Hyperkalemia** — from renal dysfunction and cellular shifts - **Hypocalcemia** — rare but can potentiate QT prolongation - These disturbances worsen both cardiac arrhythmias and neurological symptoms **High-Yield:** Hyponatremia in lithium toxicity is particularly dangerous because it worsens cerebral edema and seizure risk. Correction must be gradual to avoid osmotic demyelination syndrome. ### Why Not the Other Options? - **Option A — TSH and free T4:** Lithium causes hypothyroidism with *chronic* use (inhibits thyroid hormone synthesis and release). In *acute* toxicity, thyroid function is not the immediate threat and does not guide emergency management. - **Option B — ABG and serum glucose:** While ABG may be useful if respiratory compromise or metabolic acidosis is suspected, it is not the *first-line* investigation in acute lithium toxicity. Glucose disturbance is not a primary feature of lithium toxicity. ABG does not directly guide the most critical management decisions (cardiac monitoring, dialysis). - **Option C — Serum creatinine and BUN:** Renal function is *important* in lithium toxicity because lithium is exclusively renally excreted, and impaired renal clearance can worsen toxicity and influence the decision for hemodialysis. However, renal function tests are *secondary* to the immediate cardiac and electrolyte assessment. ECG and electrolytes identify life-threatening arrhythmias and electrolyte crises that require intervention within minutes, whereas creatinine/BUN results guide longer-term management decisions. In clinical practice, both are ordered, but ECG + electrolytes take priority. ### Management Implications - **ECG abnormalities** → determine need for cardiac monitoring and antiarrhythmic therapy - **Electrolyte imbalances** → guide IV fluid and electrolyte replacement - **Hyponatremia + seizures** → hypertonic saline (3%) may be needed - **Severe toxicity (>3.0 mEq/L) or renal failure** → hemodialysis (guided by creatinine/BUN as a secondary step) **Clinical Pearl:** In moderate-to-severe acute lithium toxicity, the combination of ECG changes and hyponatremia is the strongest predictor of poor outcome. These investigations directly guide ICU admission, dialysis decisions, and pharmacological interventions. ### Mnemonic: LITE Toxicity **L** — Lithium level (>1.5 mEq/L = toxicity) **I** — Investigate **ECG** (arrhythmias) and **Ions** (Na⁺, K⁺) **T** — Tremor, confusion, ataxia (neurological signs) **E** — Emergency management (dialysis if severe) [cite: KD Tripathi 8e Ch 12; Harrison 21e Ch 383]