A 32-year-old patient on long-term lithium 900 mg daily for bipolar I disorder presents with a 2-day history of vomiting, coarse hand tremor, ataxia, slurred speech, and confusion. The patient began ibuprofen 400 mg three times daily four days ago for ankle pain. Vital signs: T 37.2 °C, HR 108, BP 102/64. Serum lithium drawn on arrival: 1.8 mEq/L (therapeutic 0.6–1.2). Which is the nurse's priority action?

A lithium level of 1.8 mEq/L with vomiting, coarse tremor, ataxia, slurred speech, and confusion represents at least moderate lithium toxicity in a patient who has compounded the risk by adding an NSAID (which reduces renal lithium clearance) and now has volume depletion from vomiting (which further reduces clearance). The priority action bundle is to (1) hold lithium and the offending NSAID, (2) establish IV access with isotonic saline to restore volume and renal clearance, (3) place the patient on continuous cardiac monitoring (lithium causes QT prolongation and dysrhythmias at toxic levels), and (4) prepare for possible hemodialysis if level rises, neurologic findings worsen, or renal function declines. Choice 1 continues a toxic drug. Choice 3 underestimates the severity and the role of NSAID and dehydration. Choice 4 is wrong: activated charcoal does not bind lithium because lithium is a small ion.

In-depth explanation

This patient illustrates the classic triad of lithium toxicity precipitants: chronic lithium therapy plus a new NSAID plus volume depletion from GI losses. The NSAID inhibits afferent arteriolar prostaglandins, drops glomerular filtration, and reduces renal lithium clearance because sodium and lithium share tubular handling — when sodium is retained, so is lithium. The clinical picture is not from a single overdose but from a steadily climbing level over four days. Priority is concurrent action in four domains: (1) stop the offending drugs, (2) restore intravascular volume with isotonic saline to support renal clearance, (3) monitor cardiac rhythm continuously because lithium prolongs QT and can precipitate dysrhythmias as the level rises, and (4) apply hemodialysis criteria — level >4.0, or level >2.5 with severe symptoms, neurologic compromise, or renal failure. Sustained-release formulations may continue to absorb after admission, so monitoring for a rising level after holding the dose is essential.

Clinical scenario

<p>A <strong>32-year-old patient</strong> on long-term <strong>lithium 900 mg/day</strong> for bipolar I disorder presents with <strong>2 days of vomiting, coarse hand tremor, ataxia, slurred speech, and confusion</strong>. The patient began <strong>ibuprofen 400 mg three times daily</strong> four days ago for ankle pain. <strong>HR 108, BP 102/64</strong>. <strong>Serum lithium 1.8 mEq/L</strong> (therapeutic 0.6–1.2).</p>

Key concepts

• Lithium Toxicity — Mild: 1.5–2.0 mEq/L (coarse tremor, GI upset, lethargy). Moderate: 2.0–2.5 (ataxia, dysarthria, blurred vision). Severe: >2.5 (seizures, coma, dysrhythmias, AKI). Hemodialysis is indicated for level >4.0, level >2.5 with severe symptoms, neurologic compromise, or renal failure.
• NSAID-Lithium Interaction — NSAIDs (ibuprofen, naproxen, indomethacin) reduce renal lithium clearance by inhibiting prostaglandin-mediated afferent arteriolar dilation, raising serum lithium 25–60% within days. Aspirin and sulindac have less interaction. Acetaminophen is preferred for occasional pain in lithium-treated patients.
• Activated Charcoal Limitation — Effective for many drug overdoses but not for ions like lithium, iron, or lead, or for alcohols. For sustained-release lithium overdose, whole-bowel irrigation with polyethylene glycol may be considered within 1 hour of ingestion. The mainstay of acute lithium toxicity management is volume restoration and dialysis.