PHENYTOIN SODIUM
PHENYTOIN SODIUM
What it does
Phenytoin is a medication used to prevent and control seizures.
Commonly used for: seizures (epilepsy), status epilepticus
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Sourcing - Kenya onlyRegistration & product details
Source: Medicines Control Authority of Zimbabwe · fetched 2026-04-18 08:22:09 · updated 2026-09-16 04:30:09
Drug Interactions
109Pharmacodynamic Warnings
Phenytoin appears in TABLE 12: Drugs that cause peripheral neuropathy
Severe (13)
Antiepileptics - decreases absorption
Iron chelators (dexrazoxane) might decrease the absorption of antiepileptics (fosphenytoin, phenytoin). Avoid.
Antiepileptics - decreases exposure
Lumacaftor is predicted to decrease the exposure to antiepileptics (carbamazepine, fosphenytoin, phenobarbital, phenytoin, primidone). Avoid.
Antiepileptics - decreases concentration
St John’s wort is predicted to decrease the concentration of antiepileptics (fosphenytoin, phenobarbital, phenytoin, primidone). Avoid.
Antiepileptics - increases risk of overheating and dehydration
Hydroxyzine potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.
Antiepileptics - increases risk of overheating and dehydration
Haloperidol potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.
Moderate (43)
Antiepileptics - increases concentration
Intravenous chloramphenicol increases the concentration of antiepileptics (fosphenytoin, phenytoin) and antiepileptics (fosphenytoin, phenytoin) affect the concentration of intravenous chloramphenicol
Antiepileptics - decreases concentration
Diazoxide decreases the concentration of antiepileptics (fosphenytoin, phenytoin) and antiepileptics (fosphenytoin, phenytoin) are predicted to decrease the effects of diazoxide. Monitor concentration
Antiepileptics - increases concentration
Disulfiramincreasestheconcentrationofantiepileptics (fosphenytoin,phenytoin).Monitorconcentrationandadjust dose.rStudy →AlsoseeTABLE12p.1520
Antiepileptics - increases concentration
Fluorouracilincreasestheconcentrationofantiepileptics (fosphenytoin,phenytoin).Monitorconcentrationandadjust dose.rAnecdotal 1xidneppA|snoitcaretnI A1 https://www.facebook.c (Books-Courses-Medic
Antiepileptics - decreases concentration
Folates are predicted to decrease the concentration of antiepileptics (fosphenytoin, phenobarbital, phenytoin, primidone). Monitor concentration and adjust dose.
Unknown (53)
Aminophylline - decreases exposure
Phenytoin decreases the exposure to aminophylline. Adjust dose.
Anaesthetics,local - decreases exposure
Phenytoin is predicted to decrease the exposure to anaesthetics, local (ropivacaine).
Antiepileptics - increases risk of overheating and dehydration
Acetazolamide potentially increases the risk of overheating and dehydration when given with antiepileptics (zonisamide). Avoid in children.
Antiepileptics - increases risk of visual disturbances
Alcohol potentially increases the risk of visual disturbances when given with antiepileptics (retigabine).
Antiepileptics - decreases exposure
Enzalutamide is predicted to slightly decrease the exposure to antiepileptics (brivaracetam).
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: class
About this medicine
Phenytoin is a medication used to prevent and control seizures.
What it treats
- seizures (epilepsy)
- status epilepticus
How it works
Phenytoin works by stabilizing electrical activity in the brain, which helps to prevent seizures.
Who it's for
This medication is for people who have epilepsy or other conditions that cause seizures.
Drug class
Antiepileptics
Cautions
- • Be cautious if you are taking other medications that can cause nerve damage.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Phenytoin
BNF-referencedPhenytoin is an antiepileptic drug primarily used in the management of epilepsy and other seizure disorders. It is particularly effective against tonic-clonic seizures and focal seizures. Phenytoin works by stabilizing neuronal membranes and inhibiting the spread of seizure activity in the brain. It has a narrow therapeutic index, making careful monitoring of serum levels essential to avoid toxicity.
Indications
- Tonic-clonic seizures
- Focal seizures
- Prevention and treatment of seizures during or following neurosurgery or severe head injury
Dosage
Children: For children aged 1 month to 11 years, the initial dose is 1.5-2.5 mg/kg twice daily, adjusted according to response, with maintenance doses of 2.5-5 mg/kg twice daily (maximum per dose is 7.5 mg/kg twice daily).
Adults: Initial dose of 30 mg daily, with maintenance doses usually between 200-500 mg per day, taken in divided doses preferably with or after food. Doses should be titrated based on clinical response and plasma-phenytoin levels.
Mechanism of action
Phenytoin acts primarily by blocking voltage-gated sodium channels, thereby inhibiting the influx of sodium ions into neurons. This action stabilizes neuronal membranes and prevents excessive neuronal firing, which is crucial in controlling seizures. It also decreases calcium influx and synaptic transmission, which further helps in reducing neuronal excitability.
Pharmacodynamics
Phenytoin exhibits a narrow therapeutic index, with effective serum concentrations typically between 10-20 mg/L. The pharmacological effect is influenced by factors such as protein binding, genetics, and concurrent medications. Variations in albumin levels and genetic polymorphisms in metabolizing enzymes like CYP2C9 can significantly affect phenytoin metabolism and overall therapeutic outcomes.
Pharmacokinetics
Phenytoin is primarily absorbed in the gastrointestinal tract and is highly protein-bound, which may impact its free concentration. The drug undergoes hepatic metabolism through the cytochrome P450 system, particularly CYP2C9, and has a nonlinear pharmacokinetic profile at higher doses. The elimination half-life varies widely among individuals, typically ranging from 7 to 42 hours. Due to this variability, therapeutic drug monitoring is recommended.
Contra-indications
- Hypersensitivity to phenytoin or any of its excipients
- History of previous severe cutaneous adverse reactions to phenytoin
- Severe hepatic impairment
- Pregnancy (due to embryotoxic effects in animal studies)
Adverse effects
- Dizziness
- Nausea
- Vomiting
- Gingival hyperplasia
- Ataxia
- Rash
- Hirsutism
- Nystagmus
- Skin reactions (e.g., Stevens-Johnson syndrome)
- Suicidal thoughts and behaviors
Interactions
- Iron chelators may decrease absorption of phenytoin
- St John's Wort may decrease phenytoin concentration
- Thrombin inhibitors may decrease exposure to phenytoin
- Antipsychotics (second generation) may decrease exposure to phenytoin
- Cenobamate may increase exposure to phenytoin
- Intravenous chloramphenicol may increase concentration of phenytoin
Precautions
- Monitor plasma-phenytoin concentrations regularly
- Caution in patients with hepatic impairment
- Caution in patients with renal impairment
- Dose adjustment may be necessary when switching between different formulations
- Avoid abrupt discontinuation to prevent seizure exacerbation
Pregnancy
Avoid-embryotoxic in animal studies.
Breast-feeding
Avoid-present in milk in animal studies.
Storage
Store in a cool, dry place away from direct sunlight. Keep out of reach of children.
Formulations
- Oral suspension (e.g., 125 mg/5 mL)
- Tablets (various strengths including 100 mg and 300 mg)
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Phenytoin
PubChem CID 1775Molecular formula: C15H12N2O2
Mechanism of action
Although phenytoin first appeared in the literature in 1946, it has taken decades for the mechanism of action to be more specifically elucidated. Although several scientists were convinced that phenytoin altered sodium permeability, it wasn’t until the 1980’s that this phenomenon was linked to voltage-gated sodium channels. Phenytoin is often described as a non-specific sodium channel blocker and targets almost all voltage-gated sodium channel subtypes. More specifically, phenytoin prevents seizures by inhibiting the positive feedback loop that results in neuronal propagation of high frequency action potentials. The mechanism of action is not completely known, but it is thought to involve stabilization of neuronal membranes at the cell body, axon, and synapse and limitation of the spread of neuronal or seizure activity. In neurons, phenytoin decreases sodium and calcium ion influx by prolonging channel inactivation time during generation of nerve impulses. Phenytoin blocks the voltage-dependant sodium channels of neurons and inhibits the calcium flux across neuronal membranes, thus helping to stabilize neurons. It also decreases synaptic transmission, and decreases post-tetanic potentiation at the synapse. Phenytoin enhances the sodium ATPase activity of neurons and/or glial cells. It also influences second messenger systems by inhibiting calcium-calmodulin protein phosphorylation and possibly altering cyclic nucleotide production or metabolism. Phenytoin may act to normalize influx of sodium and calcium to cardiac Purkinje fibers. Abnormal ventricular automaticity and membrane responsiveness are decreased. Also, phenytoin shortens the refractory period, and therefore shortens the QT interval and the duration of the action potential. Exact mechanism is unknown. Phenytoin may act in the CNS to decrease synaptic transmission or to decrease summation of temporal stimulation leading to neuronal discharge (antikindling). Phenytoin raises the threshold of facial pain and shortens the duration of attacks by diminishing self-maintenance of excitation and repetitive firing. Phenytoin's mechanisms of action as a muscle relaxant is thought to be similar to its anticonvulsant action. In movement disorders, the membrane stabilizing effect reduces abnormal sustained repetitive firing and potentiation of nerve and muscle cells. A number of studies suggest that keratinocyte growth factor (KGF) plays a major part in reepithelialization after injury, via binding to the specific KGF receptor (KGFR). Several pharmacological agents, including the anti-epileptic drug phenytoin (PHT), have been widely used clinically to promote wound healing. Although the mechanism of action of PHT in this process is still not well understood, it is possible that the activity of PHT in wound healing is mediated via KGF and the KGFR. In the present study, using the enzyme-linked immunosorbant assay and flow cytometry we have shown that PHT increases KGF secretion and KGFR expression by more than 150% in gingival fibroblasts and epithelial cells, respectively. Moreover, semi-quantitative reverse transcriptase-polymerase chain reaction analysis showed that PHT also markedly increased both KGF and KGFR gene transcription by these cells.
Pharmacodynamics
Phenytoin is an anticonvulsant with a narrow therapeutic index. Although the recommended therapeutic range is cited to be between 10-20 mg/L, differences in albumin levels, genetics, comorbidities, and body composition can make achieving an ideal phenytoin dose challenging. For example, studies have confirmed that phenytoin metabolism is impacted by CYP2C9 genotype polymorphisms and possibly by CYP2C19 genotype polymorphisms (the latter has not been as extensively studied). It is worth nothing that although phenytoin is highly protein bound, only the fraction unbound is able to exert a pharmacological effect. Therefore, factors that reduce or increase the percentage of protein bound phenytoin (for example: concomitant administration of drugs that can cause displacement from protein binding sites) can have a marked impact on phenytoin therapy.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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