At higher concentrations, phenytoin delays activation of outward potassium currents in nerves and prolongs the neuronal refractory period. Those who have decreased protein binding, such as neonates and elderly patients, have a higher risk than the general population. metabolism and elimination of phenytoin.2,4,7 Signs of phenytoin toxicity usually manifest at phenytoin levels above 15 mcg/mL. At higher levels in the therapeutic range, any increase in the daily dose will result in a disproportionate increase in the plasma level.
Individuals who are be suffering from uncontrollable The medication phenytoin is classified as an anticonvulsant and acts primarily on the motor cortex of the brain.
Deaths from oral ingestion of phenytoin are extremely rare.The chronic administration of phenytoin is associated with numerous side effects that involve a variety of organ systems. If the patient receives phenytoin intravenously, they may experience The neurologic toxicity symptoms may include abnormal gait, confusion, irritability, agitation, respiratory distress, tremors, hallucinations, mental status alterations, peripheral neuropathy, dysphagia or difficulty in swallowing and the presence of more seizures. Given the long and erratic absorption phase of phenytoin after oral overdose, the decision to discharge or medically clear a patient for psychiatric evaluation cannot be based on a single serum level. This is further evidence for its etiologic role in intravenous phenytoin toxicity, a phenomenon which is almost always related to infusion rate. Marked phenytoin toxicity can occur in critically ill patients with hypoalbuminemia and can often be detected only by direct measurement of free phenytoin levels. Thus, at phenytoin doses above 300 mg (~5 mg/kg) per day, incremental doses should be limited to 30 mg. After each increase in dose, the patient should be maintained on the new dose for at least 2 weeks and the plasma level should be reassessed before any further increase.Because phenytoin's half-life is 24 h or less, once-a-day regimens may result in erratic levels and become problematic for patients requiring tight control. Background: Phenytoin is a commonly used sedative antiepileptic medication in many countries. Phenytoin intoxication can occur either with repeated supra therapeutic dosing or an acute overdose. However, some patients have a greater propensity to side effects than others. The use of activated charcoal is effective especially if it is given within an hour after the ingestion has taken place. Recently, prodrugs of phenytoin have been synthesized that are more soluble and less irritating to the tissues. All patients had documented serum phenytoin levels of more than 20 g/mL, clinical evidence of toxicity at pre- sentation, and improvement of clinical symptoms and signs after the serum phenytoin level declined to around the therapeutic level. Phenytoin also affects the metabolism of various other agents (Table 1).The acute cardiovascular toxicity seen with intravenous phenytoin infusion has frequently been ascribed to its diluent.
Epub 2014 Sep 2.
It is useful in the treatment of status epilepticus in conjunction with other more rapidly acting anticonvulsants. Disease states resembling phenytoin toxicity include hypoglycemia, Wernicke encephalopathy, and posterior fossa hemorrhage or tumor. Nystagmus usually appears first at phenytoin levels of 20 mg/mL but may occur at lower levels or not appear until much higher levels are attained.
The signs and symptoms associated with The degree of protein binding in the body plays a major role in the metabolism of this medication. Due to its saturation (zero-order) pharmacokinetics, phenytoin carries a special risk of dose-related toxicity that is an important issue in emergency medicine.
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