Lithium
Lithium excreted renally on sodium transporter, so if serum sodium is decreased, more lithium and sodium will be reabsorbed at proximal tubule, like in states pf dehydration
Blocks actions of ADH so leads to DI
Hypothyroidism
CNS is the major site of toxicity
EKG-t wave flattening, ST changes, prolonged QRS and rarely QT
If on lithium and c/o GI stuff, it is lithium toxicity until proven otherwise
Ther. Levels usually .6-1.2
AC does not bind
Dialyse if >4.0 serum. Renal failure, CHF, comatose
Fine tremor=side effect, coarse tremor=toxicity
Severe toxicity=seizures and coma
Whole Bowel Irrigation with PEG if sustained release tabs
Hydration
Lithium level, repeat in 2 hours for acute, 6 hours for chronic. Best course is to get levels Q 1-2 hrs regardless if first is back yet, if truly suspect.
Kayexalate for overdose. The usual dose is 30 grams of SPS in sorbitol orally every four hours. Binds lithium in gut, gut dialysis, and sodium load.
Chronic lithium toxicity can occur with even mild renal fx and they can be toxic at near normal levels
acute often has GI side effects, chronic not as much
Back to topAntiseizure Medications
Present c CNS effects, sedation, confusion, dizziness,
Phenytoin (Dilantin)
Therapeutic Levels 10-20
Class 1B antidysrhythmic.
do not give in patients with bradycardia or heart block
Most dysrhythmias are probably from diluent (propylene glycol)
Carbamazepine (Tegratol)
Therapeutic Levels 4-12
Levels above 40 mg/L assoc c adverse effects
Nystagmus, ataxia, dysarthria, stupor, encephalopathy, myoclonus, dystonia
Seizures and tachycardia
Valproic Acid (Depakote)
Therapeutic Levels 50-120
Has toxic metabolite, so sx of overdose can be present c normal serum levels at presentation.
Releases GABA
Sedation, ataxia, dizziness, myoclonus, GI sx,
Can cause hepatic failure
Causes carnitine deficiency and blocks fatty acid metabolism, eventually leading to hyperammonemia
VPE (a metabolite of valproate) combines with carnitine and is excreted in the urine. Lacking carnitine, fats must undergo alpha oxidation instead of beta oxidation. This produces ammonia. Ammonia normally metabolized through the urea cycle, but VPE also binds the first enzyme there. Fatty acyl groups also inhibit the urea cycle. All increase ammonia levels.
Send ammonia levels, possibly administer carnitine (15-50 mg/kg IV or PO to take VPE out of urea cycle)
GABAergic action on CNS also increases endogenous opioids (enkephalen)
AC
Nalaxalone may reverse CNS depressant effects (JEM 22:1, pp.67-70)
In order to clear, need two consecutive valproate levels that are clearing by at least 20% and are three hours apart
Onset is 3 hours after ingestion, so first level should be after 3 hours
Elimination half life is 6-17 hours
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