{"id":414,"date":"2019-11-19T16:58:43","date_gmt":"2019-11-19T21:58:43","guid":{"rendered":"https:\/\/opentextbc.ca\/nursingpharmacology\/chapter\/8-10-anticonvulsants\/"},"modified":"2022-12-15T12:32:05","modified_gmt":"2022-12-15T17:32:05","slug":"8-10-anticonvulsants","status":"publish","type":"chapter","link":"https:\/\/opentextbc.ca\/nursingpharmacology\/chapter\/8-10-anticonvulsants\/","title":{"raw":"8.10 Anticonvulsants","rendered":"8.10 Anticonvulsants"},"content":{"raw":"
\r\n\r\nMedications used for seizures are called anticonvulsants or antiseizure drugs. Antiseizure drugs stabilize cell membranes and suppress the abnormal electric impulses in the cerebral cortex. These drugs prevent seizures but do not provide a cure. Antiseizure drugs are classified as CNS depressants. There are many types of medications used to treat seizures such as phenytoin, phenobarbital, benzodiazepines, carbamazepine, valproate, and levetiracetam.[footnote]McCuistion, L., Vuljoin-DiMaggio, K., Winton, M, & Yeager, J. (2018). Pharmacology: A patient-centered nursing process approach.<\/em> pp. 227-305. Elsevier.[\/footnote]\r\n\r\nThere are three main pharmacological effects of antiseizure medications. First, they increase the threshold of activity in the motor cortex, thus making it more difficult for a nerve to become excited. Second, they limit the spread of a seizure discharge from its origin by suppressing the transmission of impulses from one nerve to the next. Third, they decrease the speed of the nerve impulse conduction within a given neuron.\r\n\r\nSome drugs work by enhancing the effects of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), which plays a role in regulating neuron excitability in the brain.[footnote]Lilley, L., Collins, S., & Snyder, J. (2020). Pharmacology and the Nursing Process.<\/em> pp. 246-272. Elsevier.[\/footnote] Gabapentin, although structurally similar to GABA and classified as an anticonvulsant, is commonly used to control chronic neuropathic pain. Neuropathic pain is defined by the International Association for the Study of Pain as \u201cpain caused by a lesion or disease of the somatosensory nervous system.\u201d[footnote]Murnion B. P. (2018, June 1). Neuropathic pain: current definition and review of drug treatment. Australian prescriber, 41<\/em>(3), 60\u201363. https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6003018\/<\/a>[\/footnote] An example of neuropathic pain is tingling or burning in the lower extremities that often occurs in clients with diabetes.\r\n

Phenytoin<\/h1>\r\nPhenytoin, which was discovered in 1938, was the first anti-seizure medication and is still being used to control seizures.[footnote]McCuistion, L., Vuljoin-DiMaggio, K., Winton, M, & Yeager, J. (2018). Pharmacology: A patient-centered nursing process approach.<\/em> pp. 227-305. Elsevier.[\/footnote]\r\n

Mechanism of Action<\/h2>\r\nPhenytoin improves evidence of seizures by interfering with sodium channels in the brain, resulting in a reduction of sustained high-frequency neuronal discharges.\r\n

Indications for Use<\/h2>\r\nPhenytoin is indicated for the treatment of tonic-clonic (grand mal) and psychomotor (temporal lobe) seizures and for the prevention and treatment of seizures occurring during or following neurosurgery.\r\n

Nursing Considerations Across the Lifespan<\/h2>\r\nPhenytoin should not be administered to pregnant women because it will cause harm to the fetus. When given intravenously, there is a Black Box Warning that the rate of administration should not exceed 50 mg per minute in adults and 1 to 3 mg\/kg\/min (or 50 mg per minute, whichever is slower) in pediatric clients because of the risk of severe hypotension and cardiac arrhythmias. Careful cardiac monitoring is needed during and after administering intravenous phenytoin.\r\n\r\nPhenytoin has a narrow therapeutic drug level, usually between 40 - 80 uM\/L, so serum drug monitoring is required.[footnote]London Health Science Center. (2021). Phenytoin.\u00a0https:\/\/www.lhsc.on.ca\/critical-care-trauma-centre\/phenytoin-dilantin<\/a>[\/footnote]Serum levels of phenytoin sustained above the therapeutic range may produce confusional states referred to as delirium, psychosis, or encephalopathy. Accordingly, at the first sign of acute toxicity, serum levels should be immediately checked.\r\n\r\nAbrupt discontinuation can cause status epilepticus, so in the event of an allergic or hypersensitivity reaction, rapid substitution of alternative therapy may be necessary.\r\n\r\nUse with caution in clients with renal or hepatic impairment. Elderly clients may require dosage adjustment.\r\n\r\nThere are many potential drug interactions with phenytoin. Read drug label information before administering. Phenytoin is extensively bound to plasma proteins and is prone to competitive displacement. Phenytoin is metabolized by hepatic cytochrome P450 enzymes, so it is susceptible to inhibitory drug interactions, which may produce significant increases in circulating phenytoin concentrations and enhance the risk of drug toxicity.\r\n

Adverse\/Side Effects<\/h2>\r\nSerious and sometimes fatal dermatologic reactions, including toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS), have been reported with phenytoin treatment. The onset of symptoms is usually within 28 days but can occur later. Phenytoin should be discontinued at the first sign of a rash.\r\n\r\n[pb_glossary id=\"741\"]Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)[\/pb_glossary]<\/strong> has been reported in clients taking antiepileptic drugs, including phenytoin. Some of these events have been fatal or life-threatening. DRESS typically presents with fever, rash, lymphadenopathy, and\/or facial swelling, in association with other organ system involvement. These findings should be immediately reported to the provider. Acute hepatotoxicity has been reported with phenytoin. These events may be part of the spectrum of DRESS or may occur in isolation.\r\n\r\nHematopoietic complications, some fatal, have occasionally been reported in association with the administration of phenytoin. These have included thrombocytopenia, leukopenia, granulocytopenia, agranulocytosis, and pancytopenia with or without bone marrow suppression.\r\n\r\nThe most common adverse reactions encountered with phenytoin therapy are nervous system reactions and are usually dose-related. Reactions include nystagmus, ataxia, slurred speech, decreased coordination, somnolence, and mental confusion.[footnote]This work is a derivative of Daily Med<\/a> by U.S. National Library of Medicine<\/a> in the public domain<\/a>. \u00a0[\/footnote]\r\n

Client Teaching & Education<\/h2>\r\nClients should be advised to take medications as directed and that doses should be evenly spaced throughout the day.\u00a0 It may take several weeks to obtain the desired medication effect.\u00a0 Abrupt withdrawal of medication may cause status epilepticus. Clients should avoid alcohol and other CNS depressants while taking anticonvulsant drug therapy.\u00a0 Additionally, diabetic clients should monitor their blood glucose levels carefully.\r\n

Phenytoin Medication Card<\/h1>\r\nNow let's take a closer look at the medication card for phenytoin.[footnote]This work is a derivative of Daily Med<\/a> by U.S. National Library of Medicine<\/a> in the public domain<\/a>. <\/span>[\/footnote] <\/span>Medication cards like this are intended to assist students to learn key points about each medication. Because information about medication is constantly changing, nurses should always consult evidence-based resources to review current recommendations before administering specific medication. Basic information related to each class of medication is outlined below.\u00a0 Prototype or generic medication examples are also hyperlinked to a free resource at Daily Med<\/a>. On the home page, enter the drug name in the search bar to read more about the medication.\r\n
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Medication Card 8.10.1: Phenytoin<\/h2>\r\n<\/header>\r\n
\r\n\r\nGeneric Name: <\/strong>phenytoin<\/a>\r\n\r\nPrototype\/Brand Name: <\/strong>Dilantin\r\n\r\nMechanism: <\/strong>interfering with sodium channels in the brain, resulting in a reduction of sustained high-frequency neuronal discharges.\r\n

Therapeutic Effects<\/h3>\r\n