IHD vs. CRRT in Acute Lithium Toxicity

[tab_nav type=”two-up”][tab_nav_item title=”Clinical Case” active=”true”][tab_nav_item title=”Answer” active=””][/tab_nav][tabs][tab active=”true”] A 24 y/o male with a history of bipolar disorder and depression is admitted to your ICU from the Emergency Department after taking approximately 60 – 450mg ER lithium pills an hour prior to presentation in suicide attempt.  He is currently vomiting with VS as follows: 37.5 C    HR 115   BP: 120’s/70’s    RR: 22      SpO2: 99% on RA.  His exam is unremarkable and his EKG shows only sinus tachycardia.  His initial lithium level in the ED is 3.0 mmol/L.

You quickly place an NG tube, start whole bowel irrigation, and put in an right IJ dialysis catheter to prepare the patient for emergent HD.  His 2 hour repeat lithium level is 6.6 mmol/L so you decide to start HD. The patient’s 2 & 4 hour levels are down to  <1 mmol/L, but the next morning you find his level just jumped back up to 4.0 mmol/L after his HD stopped.

Your friendly nephrologist comes to see the patient and recommends another course of standard hemodialysis followed by 18 hours of CVVHD.  What’s the deal?
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Lithium Toxicity

• Small molecule (7 Da), low protein binding, water soluble drugs
• One of the dialyzable drugs (“I STUMBLE”)
  • Isopropyl Alcohol
  • Salycylates
  • Theophylline
  • Uremia
  • Methanol
  • Barbiturates, beta-blockers (water soluble, such as atenolol)
  • Lithium
  • Ethylene glycol
• Lithium pharmacokinetics follow a two compartment model [active drug found in both intra- & extracellular compartment]
  • Central compartment: Highly perfused tissues (e.g. blood, extracellular fluid, liver, kidneys, etc.)
  • Peripheral compartment: Poorly perfused tissues (e.g. muscle, fat, etc.)
• Causes a reduced GFR and urinary concentrating ability by 15% of normal maximum (Nephrogenic DI)
• Many preparations of lithium are sustained release forms (longer absorption times)

Treatment of Acute Toxicity

• Goal:  Prevent and lower intracellular lithium levels
• Consider whole bowel irrigation if the patient who ingested extended release lithium tabs
• Forget activated charcoal – lithium is not absorbed by AC
• Hydrate the patient aggressively to improve renal clearance of lithium (it doesn’t get metabolized)
• Extracorporeal elimination
  • Indications
    • Renal failure
    • Severe neurologic dysfunction
    • Inability to tolerate fluid replacement
    • Lithium concentration > 4 mmol/L (acute ingestion), >=2.5 mmol/L (chronic ingestion)
    • Improvement of clinical symptoms will occur after hemodialysis, however
    • After HD, a rebound in serum lithium levels may occur because of the slow diffusion of lithium from the peripheral compartment.

• Hemodialysis: The most effective method for clearing lithium in the extracellular compartment.
  • Mode of choice if hemodynamically stable
  • Can clear 70-160 mL/min (Normal renal clearance 15-30 mL/min)
  • As extracellular clearance occurs, intracellular lithium diffuses along gradient back into extracellular compartment for HD to clear.
  • After IHD stops, diffusion of lithium from the gut and from the peripheral compartment will commonly cause a rebound lithium levels 6-10 hours after cessation of IHD – just enough time to think you are in the clear.
    
• Sustained low-efficiency dialysis (SLED):  A longer, slower session of dialysis (6-8 hrs) shown to provide adequate clearance of lithium level – disadvantage is it is still intermittent.
• Continuous veno-venous hemodialysis (CVVHD/CVVHDF): Continuous solute clearance that may be better tolerated by those with hemodynamic collapse (lower Qb’s)
• If CRRT unavailable, strongly consider arranging for a repeat IHD session as you trend serial (q2h) lithium levels should rebound toxicity occur.

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