Phenytoin is an anticonvulsant drug which can be useful in the treatment of epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Phenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures.
The plasma half-life in man after oral administration of phenytoin averages 22 hours, with a range of 7 to 42 hours. Steady state therapeutic levels are achieved at least 7 to 10 days (5 to 7 half-lives) after initiation of therapy with recommended doses of 300 mg/day.
When serum level determinations are necessary, they should be obtained at least 5 to 7 half-lives after treatment initiation, dosage change, or addition or subtraction of another drug to the regimen so that equilibrium or steady state will have been achieved. Trough levels provide information about clinically effective serum level range and confirm patient compliance and are obtained just prior to the patient's next scheduled dose. Peak levels indicate an individual's threshold for emergence of dose-related side effects and are obtained at the time of expected peak concentration. For Dilantin capsules, peak serum levels occur 4 to 12 hours after administration. For Dilantin Infatabs, Dilantin suspensions and Dilantin with Phenobarbital capsules, peak serum levels occur 1 1/2 to 3 hours after administration.
Optimum control without clinical signs of toxicity occurs more often with serum levels between 10 and 20 mcg/mL, although some mild cases of tonic-clonic (grand mal) epilepsy may be controlled with lower serum levels of phenytoin.
In most patients maintained at a steady dosage, stable phenytoin serum levels are achieved. There may be wide interpatient variability in phenytoin serum levels with equivalent dosages. Patients with unusually low levels may be noncompliant or hypermetabolizers of phenytoin.
Unusually high levels result from liver disease, congenital enzyme deficiency or drug interactions which result in metabolic interference. The patient with large variations in phenytoin plasma levels, despite standard doses, presents a difficult clinical problem. Serum level determinations in such patients may be particularly helpful.
Most of the drug is excreted in the bile as inactive metabolites which are then reabsorbed from the intestinal tract and excreted in the urine. Urinary excretion of phenytoin and its metabolites occurs partly with glomerular filtration but more importantly by tubular secretion. Because phenytoin is hydroxylated in the liver by an enzyme system which is saturable at high plasma levels small incremental doses may increase the half-life and produce very substantial increases in serum levels, when these are in the upper range. The steady state level may be disproportionately increased, with resultant intoxication, from an increase in dosage of 10% or more.
Clinical studies show that chewed and unchewed Infatabs are bioequivalent and yield approximately equivalent plasma levels.
Phenobarbital produces its anticonvulsant effect by depressing the motor cortex and raising the seizure threshold.
Phenobarbital is absorbed completely, although slowly, following oral administration and undergoes partial biotransformation in the liver by hydroxylation. Phenobarbital is excreted via the kidneys, 10% to 25% as free drug and the remainder primarily as the inactive para-hydroxyphenyl metabolite. The plasma half-life is long, approximately 2 to 6 days in adults, and shorter and more variable in children.
In adults, the oral anticonvulsant dose of 1 to 3 mg/kg will produce therapeutic concentrations of 10 to 30 mcg/mL in the serum, the levels usually necessary for seizure control. At this dose, approximately 3 weeks may be required for the serum levels to achieve steady state.
High serum levels occur when liver disease, diminished urinary flow, acidosis, or obesity is present. Low serum levels in adults may be due to poor patient compliance.
When used as an anticonvulsant, the clinical phenomenon of breakthrough seizures has been seen. Whether this is a case of true pharmacologic tolerance or some form of spontaneous variation is not known. Physical dependence does develop and may produce accentuation of seizures in epileptics when the drug is abruptly withdrawn.
For the control of generalized tonic-clonic and psychomotor (grand mal and temporal lobe) seizures and prevention and treatment of seizures occurring during or following neurosurgery.
Dilantin Infatabs and Suspensions:
For the control of generalized tonic-clonic (grand mal) and complex partial (psychomotor, temporal lobe) seizures.
Phenytoin serum level determinations may be necessary for optimal dosage adjustments (see Dosage).
Dilantin with Phenobarbital:
For the control of generalized tonic-clonic (grand mal) and complex partial (psychomotor, temporal lobe) seizures, only in those patients who require both drugs for seizure control and who previously have had their daily anticonvulsant requirements determined by the administration of the two drugs separately. Combinations should not be used to initiate anticonvulsant therapy and are provided as a convenience for epileptic patients.
In those patients who are hypersensitive to phenytoin or other hydantoins.
Phenobarbital is contraindicated in the following conditions: Latent or manifest porphyria or familial history of intermittent porphyria, history of confusion or restlessness from hypnotics, history of abnormal reaction or known hypersensitivity to barbital and its derivatives, including phenobarbital, or a known previous addiction to sedative-hypnotics. Other contraindications include renal and hepatic impairment and severe pulmonary insufficiency.
Phenobarbital may be habit forming.
Abrupt withdrawal of phenytoin in epileptic patients may precipitate status epilepticus. When, in the judgment of the clinician, the need for dosage reduction, discontinuation, or substitution of alternative antiepileptic medication arises, this should be done gradually. However, in the event of an allergic or hypersensitivity reaction, rapid substitution of alternative therapy may be necessary. In this case, alternative therapy should be an antiepileptic drug not belonging to the hydantoin chemical class.
There have been a number of reports suggesting a relationship between phenytoin and the development of lymphadenopathy (local or generalized) including benign lymph node hyperplasia, pseudolymphoma, lymphoma, and Hodgkin's Disease. Although a cause and effect relationship has not been established, the occurrence of lymphadenopathy indicates the need to differentiate such a condition from other types of lymph node pathology. Lymph node involvement may occur with or without symptoms and signs resembling serum sickness, e.g. fever, rash and liver involvement.
In all cases of lymphadenopathy, follow-up observation for an extended period is indicated and every effort should be made to achieve seizure control using alternative antiepileptic drugs.
Acute alcoholic intake may increase phenytoin serum levels while chronic alcoholic use may decrease serum levels.
A number of reports suggests an association between the use of antiepileptic drugs by women with epilepsy and a higher incidence of birth defects in children born to these women. Data are more extensive with respect to phenytoin and phenobarbital, but these are also the most commonly prescribed antiepileptic drugs; less systematic or anecdotal reports suggest a possible similar association with the use of all known antiepileptic drugs.
The reports suggesting a higher incidence of birth defects in children of drug-treated epileptic women cannot be regarded as adequate to prove a definite cause and effect relationship. There are intrinsic methodologic problems in obtaining adequate data on drug teratogenicity in humans; genetic factors or the epileptic condition itself may be more important than drug therapy in leading to birth defects. The great majority of mothers on antiepileptic medication deliver normal infants. It is important to note that antiepileptic drugs should not be discontinued in patients in whom the drug is administered to prevent major seizures, because of the strong possibility of precipitating status epilepticus with attendant hypoxia and threat to life. In individual cases where the severity and frequency of the seizure disorder are such that the removal of medication does not pose a serious threat to the patient, discontinuation of the drug may be considered prior to and during pregnancy, although it cannot be said with any confidence that even minor seizures do not pose some hazard to the developing embryo or fetus. The prescribing physician will wish to weigh these considerations in treating or counseling epileptic women of childbearing potential.
In addition to the reports of the increased incidence of congenital malformations, such as cleft lip/palate and heart malformations in children of women receiving phenytoin and other antiepileptic drugs, there have more recently been reports of a fetal hydantoin syndrome. This consists of prenatal growth deficiency, microcephaly and mental deficiency in children born to mothers who have received phenytoin, barbiturates, alcohol, or trimethadione. However, these features are all interrelated and are frequently associated with intrauterine growth retardation from other causes.
There have been isolated reports of malignancies, including neuroblastoma, in children whose mothers received phenytoin during pregnancy.
An increase in seizure frequency during pregnancy occurs in a high proportion of patients, because of altered phenytoin absorption or metabolism. Periodic measurement of serum phenytoin levels is particularly valuable in the management of a pregnant epileptic patient as a guide to an appropriate adjustment of dosage. However, postpartum restoration of the original dosage will probably be indicated.
Neonatal coagulation defects have been reported within the first 24 hours in babies born to epileptic mothers receiving phenobarbital and/or phenytoin. Vitamin K has been shown to prevent or correct this defect and has been recommended to be given to the mother before delivery and to the neonate after birth.
The liver is the chief site of biotransformation of phenytoin; patients with impaired liver function, elderly patients, or those who are gravely ill may show early signs of toxicity.
A small percentage of individuals who have been treated with phenytoin have been shown to metabolize the drug slowly. Slow metabolism may be due to limited enzyme availability and lack of induction; it appears to be genetically determined.
Phenytoin should be discontinued if a skin rash appears (see Warnings regarding drug discontinuation). If the rash is exfoliative, purpuric, or bullous or if lupus erythematosus, Stevens-Johnson syndrome or toxic epidermal necrolysis is suspected, use of this drug should not be resumed and alternative therapy should be considered (see Adverse Effects). If the rash is of a milder type (measles-like or scarlatiniform), therapy may be resumed after the rash has completely disappeared. If the rash recurs upon reinstitution of therapy, further phenytoin medication is contraindicated.
Hyperglycemia, resulting from the drug's inhibitory effects on insulin release, has been reported. Phenytoin may also raise the serum glucose level in diabetic patients.
Osteomalacia has been associated with phenytoin therapy and is considered to be due to phenytoin's interference with vitamin D metabolism.
Phenytoin is not indicated for seizures due to hypoglycemic or other metabolic causes. Appropriate diagnostic procedures should be performed as indicated.
Phenytoin is not effective for absence (petit mal) seizures. If tonic-clonic (grand mal) and absence (petit mal) seizures are present, combined drug therapy is needed.
Serum levels of phenytoin sustained above the optimal range may produce confusional states referred to as delirium, psychosis, or encephalopathy, or rarely, irreversible cerebellar dysfunction. Accordingly, at the first sign of acute toxicity, plasma level determinations are recommended. Dose reduction of phenytoin therapy is indicated if plasma levels are excessive; if symptoms persist, termination is recommended (see Warnings).
Information for the Patient:
Patients taking phenytoin should be advised of the importance of adhering strictly to the prescribed dosage regimen, and of informing the physician of any clinical condition in which it is not possible to take the drug orally as prescribed, e.g. surgery, etc.
Patients should also be cautioned on the use of other drugs or alcoholic beverages without first seeking the physician's advice.
Patients should be instructed to call their physician if skin rash develops.
The importance of good dental hygiene should be stressed in order to minimize the development of gingival hyperplasia and its complications.
Do not use capsules which are discolored.
Phenytoin serum level determinations may be necessary to achieve optimal dosage adjustments.
There are many drugs which may increase or decrease phenytoin levels or which phenytoin may affect. The most commonly occurring drug interactions are listed below.
Drugs which may increase phenytoin serum levels include: chloramphenicol, dicumarol, disulfiram, tolbutamide, isoniazid, phenylbutazone, acute alcohol intake, salicylates, chlordiazepoxide, phenothiazines, diazepam, estrogens, ethosuximide, halothane, methylphenidate, sulfonamides, cimetidine, trazodone.
Drugs which may decrease phenytoin levels include: carbamazepine, chronic alcohol abuse, reserpine. Moban brand of molindone HCl contains calcium ions which interfere with the absorption of phenytoin. Ingestion times of phenytoin and antacid preparations containing calcium should be staggered in patients with low serum phenytoin levels to prevent absorption problems.
Drugs which may either increase or decrease phenytoin serum levels include: phenobarbital, valproic acid, and sodium valproate. Similarly, the effect of phenytoin on phenobarbital, valproic acid and sodium valproate serum levels is unpredictable.
Although not a true drug interaction, tricyclic antidepressants may precipitate seizures in susceptible patients and phenytoin dosage may need to be adjusted.
Drugs whose efficacy is impaired by phenytoin include: corticosteroids, coumarin anticoagulants, oral contraceptives, quinidine, vitamin D, digitoxin, rifampin, doxycycline, estrogens, furosemide.
Serum level determinations are especially helpful when possible drug interactions are suspected.
Drug/Laboratory Test Interactions:
Phenytoin may cause decreased serum levels of protein-bound iodine (PBI). It may also produce lower than normal values for dexamethasone or metyrapone tests. Phenytoin may cause increased serum levels of glucose, alkaline phosphatase, and gamma glutamyl transpeptidase (GGT).
Infant breast-feeding is not recommended for women taking this drug because phenytoin appears to be secreted in low concentrations in human milk.
Withdrawal symptoms, including convulsions and delirium, may occur upon discontinuance of phenobarbital in patients with chronic intoxication. Analgesics, if used with phenobarbital, should be prescribed with caution because of possible additive effects. Caution should be exercised in prescribing this drug to patients with suicidal tendencies or with a predilection to abusive use of barbiturates.
Phenobarbital should be used with caution in debilitating and pulmonary diseases.
Phenobarbital should be used with caution in patients with severely impaired liver function, severe anemia, congestive heart failure, fever, neuroses, hyperthyroidism, diabetes mellitus, and any conditions in which respiratory depression may be characteristic. Marked excitement rather than depression may occur in aged or debilitated patients, particularly those with cerebral arteriosclerosis.
Confusion or euphoria may result from use of this drug. Symptoms in mentally ill, phobic, and emotionally disturbed patients may be accentuated. Prolonged usage may produce psychological habituation. Sudden discontinuation or radical reduction of dosage may precipitate withdrawal symptoms in patients who have taken the drug for prolonged period; dosage should be gradually reduced to the point of complete discontinuation.
Barbiturates should be prescribed with extreme caution for persons known or suspected of routinely or periodically consuming large quantities of alcoholic beverages. Potentiation of effect, even to the extent of causing death, may result from consumption of barbiturates by patients with a high serum alcohol level.
Phenobarbital may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks, such as driving a motor vehicle or other such activity requiring alertness; therefore, the patient should be cautioned accordingly.
The effects of phenobarbital may be increased by many drugs including antihistamines, tranquilizers, corticosteroids, MAO inhibitors, narcotic analgesics, amitriptyline, imipramine, and rauwolfia alkaloids.
Evidence that phenobarbital is secreted in human milk is inadequate. The drug appears to be secreted in low concentrations which are unlikely to affect the infant. If the mother is receiving large doses of phenobarbital, however, the drug concentration in milk might increase. For this reason, artificial feeding of the infant is recommended for women taking this drug.
Labor and Delivery:
Barbiturates readily cross the placental barrier and, if administered during labor, may have a depressant effect on the fetus; infants born of mothers receiving barbiturates may have difficulty breathing spontaneously.
The most common manifestations encountered with phenytoin therapy are referable to this system and are usually dose-related. These include nystagmus, ataxia, slurred speech, decreased coordination and mental confusion. Dizziness, insomnia, transient nervousness, motor twitchings, and headaches have also been observed. There have also been rare reports of phenytoin induced dyskinesias, including chorea, dystonia, tremor and asterixis, similar to those induced by phenothiazine and other neuroleptic drugs.
A predominantly sensory peripheral polyneuropathy has been observed in patients receiving long-term phenytoin therapy.
Nausea, vomiting, and constipation.
Dermatological manifestations sometimes accompanied by fever have included scarlatiniform or morbilliform rashes. A morbilliform rash (measles-like) is the most common; other types of dermatitis are seen more rarely. Other more serious forms which may be fatal have included bullous, exfoliative or purpuric dermatitis, lupus erythematosus, Stevens-Johnson syndrome and toxic epidermal necrolysis (see Precautions).
Hemopoietic complications, some fatal, have occasionally been reported in association with administration of phenytoin. These have included thrombocytopenia, leukopenia, granulocytopenia, agranulocytosis, and pancytopenia with or without bone marrow suppression. While macrocytosis and megaloblastic anemia have occurred, these conditions usually respond to folic acid therapy. Lymphadenopathy including benign lymph node hyperplasia, pseudolymphoma, lymphoma, and Hodgkins's Disease have been reported (see Warnings).
Coarsening of the facial features, enlargement of the lips, gingival hyperplasia, hypertrichosis and Peyronie's Disease.
Systemic lupus erythematosus, periarteritis nodosa, toxic hepatitis, liver damage, and immunoglobulin abnormalities may occur.
With larger doses, the most common manifestations relate to this system. These include drowsiness, vertigo, ataxia, hebetude, headache, delirium, and stupor.
Phenobarbital may cause gastrointestinal discomfort and nausea.
Hypersensitivity reactions are rare. Cutaneous eruptions are principally due to idiosyncrasy. Fatalities from exfoliative dermatitis and cutaneous eruptions have been reported. There are two syndromes associated with phenobarbital administration: Stevens-Johnson and a phenobarbital sensitivity syndrome. The phenobarbital sensitivity syndrome, which has resulted in fatalities, is characterized by an erythematous rash, high fever, jaundice, mental confusion, and toxic damage of parenchymatous organs.
Megaloblastic anemia has been reported. This condition usually responds to folic acid therapy.
The therapeutic ranges for phenytoin and phenobarbital in adults are 10 to 20 mcg/mL and 10 to 30 mcg/mL, respectively. Following acute overdosage of this combination, the patient at steady state may experience evidence of phenytoin toxicity ahead of phenobarbital toxicity because phenytoin plasma levels rise more rapidly than phenobarbital levels. Phenytoin also has a narrower margin between therapeutic and toxic levels than does phenobarbital.
The lethal dose in children is not known. The lethal dose in adults is estimated to be 2 to 5 g. The initial symptoms are nystagmus, ataxia, and dysarthria. Other signs are tremor, hyperflexia, lethargy, slurred speech, nausea, vomiting. The patient may become comatose and hypotensive. Death is due to respiratory and circulatory depression.
There are marked variations among individuals with respect to phenytoin plasma levels where toxicity may occur. Nystagmus, on lateral gaze, usually appears at 20 mcg/mL, ataxia at 30 mcg/mL, dysarthria and lethargy appear when the plasma concentration is over 40 mcg/mL, but as high a concentration as 50 mcg/mL has been reported without evidence of toxicity. As much as 25 times the therapeutic dose has been taken to result in a serum concentration over 100 mcg/mL with complete recovery.
The lethal dose of phenobarbital is believed to be 5 g. The highest known blood level from which a patient recovered was 580 mcg/mL. An overdose of phenobarbital will induce the classical picture of progressive CNS depression. In its severest form, this syndrome leads to respiratory arrest as a result of general reflex paralysis. The milder forms of this syndrome may mimic any stage of clinical anesthesia. Except for a rapid (and weak) pulse, vital signs are characteristically reduced. In addition to direct inhibition of the cardiac contractile mechanism with consequent hypotension, circulatory insufficiency may be aggravated by hypoxia from inadequate pulmonary ventilation. Early deaths are usually due to respiratory arrest, but delayed fatalities may arise from one or any combination of the following complications: hypostatic pneumonia, bronchopneumonia, lung abscess, pulmonary edema, cerebral edema, circulatory collapse, and irreversible renal shutdown.
Treatment is nonspecific since there is no known antidote.
The adequacy of the respiratory and circulatory systems should be carefully observed and appropriate supportive measures employed. Hemodialysis can be considered since phenytoin is not completely bound to plasma proteins. Total exchange transfusion has been used in the treatment of severe intoxication in children.
In acute overdosage the possibility of other CNS depressants, including alcohol, should be borne in mind.
The treatment of barbiturate poisoning consists of removing any unabsorbed drug from the stomach, supporting the respiration and circulation, and expediting elimination of the drug which has been absorbed.
Serum concentrations should be monitored when switching a patient from the sodium salt to the free acid form.
Dilantin capsules, Dilantin parenteral and Dilantin with Phenobarbital are formulated with the sodium salt of phenytoin. The free acid form of phenytoin is used in Dilantin-30 Pediatric and Dilantin-125 suspensions and Dilantin Infatabs. Because there is approximately an 8% increase in drug content with the free acid form than the sodium salt, dosage adjustments and serum level monitoring may be necessary when switching from a product formulated with the free acid to a product formulated with the sodium salt and vice versa.
The combination of Dilantin with Phenobarbital capsules is provided as a convenience for epileptic patients who require both drugs for seizure control. Anticonvulsant therapy should be initiated with either phenytoin or phenobarbital and, if indicated, the other drug can be added. If the total daily doses of the 2 drugs used separately are within those given below, the combination of Dilantin with Phenobarbital capsules can then be substituted in equivalent amounts. When plasma level determinations are necessary for optimal dosage adjustments, the clinically effective level of Dilantin is usually 10 to 20 mcg/mL and for phenobarbital 10 to 30 mcg/mL in adults. Serum blood level determinations are especially helpful when possible drug interactions are suspected.
If either the phenytoin or phenobarbital dosage requires adjustment, this should be done by switching the patient to separate phenytoin and phenobarbital dosage forms in order to enable subsequent dosage adjustments of either or both drugs.
Dilantin Infatabs and suspensions are not for once-a-day dosing.
Dosage should be individualized to provide maximum benefit. In some cases, serum blood level determinations may be necessary for optimal dosage adjustments. The clinically effective serum level is usually 10 to 20 mcg/mL. Serum blood level determinations are especially helpful when possible drug interactions are suspected. With recommended dosage, a period of 7 to 10 days may be required to achieve therapeutic blood levels with Dilantin and changes in dosage (increase or decrease) should not be carried out at intervals shorter than 7 to 10 days. Dilantin Infatabs can be either chewed thoroughly before being swallowed or swallowed whole.
Patients who have received no previous treatment may be started on 100 mg 3 times daily, and the dose then adjusted to suit individual requirements. For most adults, the satisfactory maintenance dosage will be 3 to 4 capsules (300 to 400 mg) daily. An increase to 6 capsules daily may be made, if necessary.
Infatabs and Suspensions:
Patients who have received no previous treatment may be started on 2 Infatabs 3 times daily or on 5 mL of Dilantin-125 suspension 3 times daily, and the dose then adjusted to suit individual requirements. For some adults, the satisfactory maintenance dosage will be 8 Infatabs daily; an increase to 12 may be made, if necessary. With Dilantin-125, an increase to 25 mL daily may be made if necessary.
Dilantin with Phenobarbital:
For maintenance, usually 3 to 4 capsules daily. An increase to 6 capsules daily may be made, if necessary.
Capsules, Infatabs and Suspensions:
Initially, 5 mg/kg/day in 2 or 3 equally divided doses, with subsequent dosage individualized to a maximum of 300 mg daily. A recommended daily maintenance dosage is usually 4 to 8 mg/kg. Children over 6 years old may require the minimum adult dose (300 mg/day). If the daily dosage cannot be divided equally, the larger dose should be given before retiring. Pediatric dosage forms available include a 30 mg capsule, a 50 mg palatably flavored Infatab, or an oral suspension form containing 30 mg of phenytoin in each 5 mL.
Dilantin with Phenobarbital:
The recommended starting phenobarbital dose for children is 2 to 3 mg/kg/day in 2 or 3 equally divided doses. The recommended starting Dilantin dose for children is 5 mg/kg/day in 2 to 3 equally divided doses.
For maintenance individualized to a maximum of 300 mg of Dilantin daily.
Alternative Dose (Capsules only):
Once-a-day dosage for adults with 300 mg may be considered if seizure control is established with divided doses of three 100 mg capsules daily. Studies comparing divided doses of 300 mg with a single daily dose of this quantity indicated that absorption, peak plasma levels, biologic half-life, difference between peak and minimum values, and urinary recovery were equivalent. Once-a-day dosage offers a convenience to the individual patient or to nursing personnel for institutionalized patients, and is intended only to be used for patients requiring this amount of drug daily. A major problem in motivating noncompliant patients may also be lessened when the patient can take all of his medication once a day. However, patients should be cautioned not to inadvertently miss a dose.
Extended Phenytoin Sodium Capsules USP:
Each white capsule with pale pink cap contains: Phenytoin sodium 30 mg. Energy: 3.0 kJ (0.7 kcal). Sodium: <1 mmol (2.52 mg). Also contains lactose 74 mg and sucrose. Bottles of 100.
Each white capsule with orange cap contains: Phenytoin sodium 100 mg. Also contains lactose 57 mg and sucrose. Energy: 2.6 kJ (0.6 kcal). Sodium: <1 mmol (8.39 mg). Unit packages of 100. Bottles of 100 and 1000.
Dilantin with Phenobarbital Capsules:
Each white capsule with garnet cap contains: Phenytoin sodium 100 mg and phenobarbital 15 mg. Also contains lactose 99 mg. Energy: 2.1 kJ (0.5 kcal). Sodium: <1 mmol (8.79 mg). Bottles of 100.
Each white capsule with black cap contains: Phenytoin sodium 100 mg and phenobarbital 30 mg. Also contains lactose 84 mg. Energy: 2.1 kJ (0.5 kcal). Sodium: <1 mmol (8.39 mg). Bottles of 100.
All capsules are gluten-free, paraben-free, sulfite-free and tartrazine-free.
Each flavored, triangular shaped, grooved tablet contains: Phenytoin 50 mg. Also contains sucrose. Energy: 8.0 kJ (1.88 kcal). Gluten-free, lactose-free, paraben-free, sodium-free, sulfite-free and tartrazine-free. Unit packages of 100. Bottles of 100.
Each 5 mL of flavored, colored suspension contains: Phenytoin 30 mg (red, Dilantin-30) or 125 mg (orange, Dilantin-125). Also contains alcohol 0.4 to 0.5% and sucrose. Energy: 23.9 kJ (5.7 kcal/5 mL). Sodium: <1 mmol (9.5 to 9.7 mg/5 mL). Gluten-free, lactose-free, paraben-free, sulfite-free and tartrazine-free. Bottles of 250 mL.
Store at room temperature below 30°C. Protect from light and moisture.