0071643192.pdf

TOXICOLOGY

DIAGNOSIS

■ Clinical diagnosis based on history and examination

■ Lithium levels:

■ Measure 4–6 hours postingestion, follow until clear peak and decline.

■ Peak serum level with large ingestion, especially sustained-release

preparations, may occur >12 hours postingestion.

■ Falsely elevated if placed in a green-top tube (lithium heparin)

TREATMENT

■ Supportive therapy

■ GI decontamination for acute ingestions (ineffective for chronic

ingestions)

■ Lithium does notbind to charcoal.

■ Gastric lavage—if <1 hour and large ingestion.

■ Whole-bowel irrigation

■ Kayexelateadministration has been shown to decrease serum lithium levels

due to lithium’s similarity to K+, but its effect on outcome is uncertain.

■ Hydrationis essential to correct dehydration and increase GFR.

■ Hemodialysis

■ Lithium is effectively removed by hemodialysis (see Table 6.21).

■ Because HD removes lithium only from the plasma, a “rebound

lithium level” may occur. Levels should be checked after HD and

6 hours later.

■ Benzodiazepines for seizures and agitation

■ Avoid

■ Phenytoin:Decreases renal excretion of lithium

■ Forced diuresis or diuretics (not effective)

COMPLICATIONS

■ Hypothyroidism (concentrates in the thyroid)

■ Nephrogenic diabetes insipidus (via blockage of antidiuretic hormone)

■ Increased risk of serotonin syndrome when taken with serotonergic agents

LOCAL ANESTHESTICS

Local anesthetics are typically divided into two classes:

■ Esters: Procaine, tetracaine, benzocaine

■ Amides: Lidocaine, bupivacaine, mepivacaine

TABLE 6.21. Indications for Hemodialysis in Lithium Toxicity

Renal failure

Inability to handle aggressive hydration

Severe CNS toxicity

Level >4.0 mEq/L in acute ingestion

Level >2.5 mEq/L with moderate CNS symptoms in chronic ingestion