Prophylactic administration of various fast-acting agents, given during fever
episodes, has been studied as an alternative to continuous treatment for the
prevention of febrile seizures. Agents in both the AED and antipyretic drug classes
have been studied in this regard, but no clinically important benefits have been
155–159 Thus, AED prophylaxis for febrile seizures is probably not warranted for
J.J., even though she is at risk for both development of epilepsy and recurrence of
febrile seizures. No evidence supports that medication will significantly affect her
later development of epilepsy. Close medical follow-up of J.J. is warranted. Her
parents should be counseled to contact a physician if J.J.’s febrile seizure is
accompanied by focal features or last longer than 15 minutes; or, if J.J. experiences
afebrile seizures. Although antipyretic measures (tepid sponge baths, acetaminophen
or ibuprofen) are of questionable benefit, they can be considered at the onset of fever
because these interventions are usually safe and well tolerated. Many febrile seizures
occur early in the course of an illness before fever is detected
vigilance by her parents and early antipyretic therapy may help prevent further febrile
Skin Rash: Hypersensitivity Reactions to Antiepileptic
QUESTION 1: R.S., a 34-year-old man, has been taking phenytoin 200 mg BID for the past 7 weeks to
extremities and torso, and the mucous membranes of his mouth appear to be mildly inflamed. Cervical
rash and other signs and symptoms? Are these likely to be related to his phenytoin therapy?
Skin-related adverse reactions (e.g., rash, urticarial) are relatively common (2%–
3% of patients) side effects related to AED therapy. Skin rash is most commonly
associated with phenytoin, lamotrigine, carbamazepine, and phenobarbital. Most
cases are relatively mild, but severely affected patients may exhibit Stevens–Johnson
syndrome or a systemic hypersensitivity syndrome accompanied by severe hepatic
damage. In R.S.’s case, signs and symptoms suggesting hepatic involvement
accompany the skin rash. Fever, lymphadenopathy, and apparent inflammation of
mucous membranes also suggest a hypersensitivity reaction to phenytoin with
multisystem involvement and the potential for progression to Stevens–Johnson
syndrome. Viral infection (e.g., hepatitis, influenza, infectious mononucleosis) should
be considered and ruled out as a possible cause of R.S.’s symptoms before they are
attributed to phenytoin therapy.
DRESS syndrome (which stands for Drug Reaction with Eosinophilia and
Systemic Symptoms) is a type of hypersensitivity syndrome that can occur with some
drugs, including phenytoin and other AEDs, that is most commonly seen in adults.
Typically, patients with this syndrome present with complaints of fever, skin rash,
and lymphadenopathy during the first 2 months of AED therapy. Hepatomegaly,
splenomegaly, jaundice, or bleeding manifestations may occur. Laboratory
manifestations often include leukocytosis with eosinophilia, elevated serum bilirubin,
and elevated AST and ALT. When a phenytoin hypersensitivity reaction includes
significant hepatotoxicity, fatality may occur in as many as 38% of affected
A high likelihood exists that R.S. has developed a severe reaction to phenytoin; the
clinical manifestations and the timing of their appearance are typical of this reaction.
Phenytoin should be discontinued immediately pending diagnostic clarification. R.S.
should be hospitalized for evaluation of other possible causes of his symptoms such
as viral illness and treatment. Treatment of phenytoin-related hypersensitivity and
hepatotoxicity is symptomatic and supportive. Intensive therapy with corticosteroids
has commonly been used, although little objective evidence exists for beneficial
effects of this treatment. Potential complications of this reaction include sepsis and
hepatic failure; these conditions should be treated specifically.
CASE 60-10, QUESTION 2: R.S. was hospitalized and treated with oral prednisone and topical
guide selection of an alternative AED for R.S.?
Further administration of phenytoin to R.S. is contraindicated on the basis of his
history of a severe hypersensitivity reaction to this drug. Although the mechanism of
this reaction is not fully understood, research implicates reactive arene oxide
of phenytoin (and other chemically similar AEDs) as possible causative agents for
hypersensitivity reactions. Affected patients purportedly are predisposed genetically
to the development of hypersensitivity, possibly because a relative deficiency of
epoxide hydrolase enzymes allows the accumulation of toxic concentrations of
reactive epoxide metabolites. These metabolites are believed to exert a direct
cytotoxic effect and to interact with cellular macromolecules, thereby functioning as
haptens that stimulate an immunologic reaction.
166 Carbamazepine, phenytoin, and
phenobarbital all are metabolized by similar pathways and converted to reactive
arene oxides. It is hypothesized that carbamazepine-induced liver damage also may
result from the effects of accumulation of reactive epoxide metabolites; these reactive
metabolites differ from the 10,11-epoxide metabolite that accumulates during
carbamazepine therapy. For this reason, these drugs potentially cross-react in
susceptible patients. Cases of apparent cross-reactivity between phenytoin and
phenobarbital or carbamazepine have been documented.
carbamazepine and phenobarbital can produce hypersensitivity reactions similar to
those seen with phenytoin. This potential for cross-reactivity should be considered
when an alternative AED is selected for R.S. An analysis of cases of AED-related
skin rashes found that the most significant nondrug predictor of skin rash was the
occurrence of a rash with another AED.
Valproate has been suggested as the preferred alternative AED for patients who
have exhibited hypersensitivity reactions to phenytoin.
metabolized to arene oxides and also is chemically dissimilar to all other AEDs.
Because valproate often shows good efficacy for complex partial seizures with
secondary generalization, it would seem to be a safe and potentially effective
alternative AED for R.S. Of the newer AEDs, lamotrigine should probably be
avoided in R.S. because of its likelihood of causing skin rash and apparent
hypersensitivity reactions. Oxcarbazepine is potentially an alternative AED for R.S.
because it is not metabolized through the arene oxide pathway. Nevertheless, 25% to
30% of patients who experience a rash in response to carbamazepine will also
experience a rash with oxcarbazepine.
171 Therefore, many clinicians would avoid
oxcarbazepine. Gabapentin, lacosamide, levetiracetam, pregabalin, tiagabine,
topiramate, or zonisamide could be considered as alternative medications for R.S.
These medications appear less likely to cause skin rash or hypersensitivity
It is suggested that R.S. be advised to add phenytoin to his list of medication
Additional recognized genetic risk factors for AED-related hypersensitivity
reactions in specific populations are presented in Table 60-6.
Although epilepsy affects men and women equally, many health issues are of specific
importance to women, such as contraceptive interactions with AEDs, teratogenicity,
pharmacokinetic changes during pregnancy, breast-feeding, menstrual cycle
influences on seizure activity (catamenial epilepsy), AED impact on bone, and sexual
It is noteworthy that the latter two issues can also occur in men. A
great need exists to educate both health care professionals and patients about the
many complex issues facing women with epilepsy.
For women of childbearing potential, prepregnancy planning and counseling are
important, because significant AED exposure of the fetus often occurs by the time
pregnancy is confirmed. This is especially important because of the potential for
unplanned pregnancies from the AED–contraceptive drug interactions. Prepregnancy
counseling also should include the importance of at least 0.4 mg/day of folic acid
supplementation and medication adherence. Patients should be informed about the
risk of teratogenicity and the importance of prenatal care.
Although complete seizure control is desirable for all patients with epilepsy, it is
especially favorable for a woman’s seizures to be well controlled before conception.
Monotherapy is preferred whenever possible, because the relative risk of birth
defects dramatically increases with AED polytherapy.
improves patient adherence. The AED should be given at the lowest effective dose to
reduce the possibility of birth defects.
154 Gradual discontinuation of AED before
pregnancy may be considered if a woman has been seizure-free for 2 years or longer.
Antiepileptic Drug–Oral Contraceptive Interaction
ago. What is the relationship between P.Z.’s apparent contraceptive failure and her AED therapy?
There have been several reports of reduced efficacy of oral contraceptives in
patients receiving various AEDs.
178 These reports describe both breakthrough
bleeding and pregnancy. Phenobarbital, phenytoin, carbamazepine, oxcarbazepine,
eslicarbazepine, perampanel, and felbamate have been shown to increase the
metabolism of ethinylestradiol and progestogens.
179 This effect is not associated with
valproate, lamotrigine, gabapentin, tiagabine, zonisamide, levetiracetam, lacosamide,
179 Topiramate in polytherapy and at high dosages (200–800 mg/day)
appears to have a mild, though measurable, effect on oral contraceptive
pharmacokinetics; apparent clearance of the estrogen component of combined oral
contraceptives is increased in patients taking topiramate.
monotherapy in lower dosages (50–200 mg/day) has a lesser impact on the
pharmacokinetics of the oral contraceptive.
A lack of contraceptive efficacy may present as irregular or breakthrough
menstrual bleeding. Decreased efficacy is not always associated with breakthrough
bleeding, however. Oral contraceptive doses can be increased to compensate for the
182 However, estrogens also may exacerbate seizures in some
183 Women older than 35 years of age and those who smoke must consider the
risk of thromboembolic complications associated with higher doses of
contraceptives. A second contraceptive method (e.g., condoms, intrauterine devices,
or spermicide) is recommended to avoid contraceptive failure.
also an alternative. An additional alternative that could be considered is injectable
depot medroxyprogesterone acetate. Although there is a lack of clinical studies
substantiating its effectiveness in patients on enzyme-inducing AED, the
pharmacokinetic characteristics of this agent suggest that its effect is not reduced by
enzyme induction. Medroxyprogesterone is a high-clearance drug; its clearance is
directly dependent on hepatic blood flow. Thus, enzyme induction would have little
effect on the metabolism of this drug when it is administered by injection. Depot
medroxyprogesterone acetate may, however, have other negative effects that would
limit its choice as an alternative contraceptive in this situation.
Assuming P.Z. was taking her contraceptive pills on a regular basis, it is possible
that her enzyme-inducing AED (phenytoin) is responsible for their failure. Patients
receiving enzyme-inducing AED should be prospectively informed that this
interaction can occur and advised concerning the use of alternative contraceptives
(see Chapter 47, Contraception).
Interestingly, a different drug interaction exists between oral contraceptives and
lamotrigine. The estrogen component in oral contraceptives increases the clearance
of lamotrigine. Lamotrigine clearance may increase twofold when contraceptive
steroids are begun and fall by 50% when contraceptive steroids are discontinued.
Changes in lamotrigine levels associated with initiation and discontinuation of
contraceptive steroids can result in increased seizure activity in some patients and
might be taken to minimize these risks?
P.Z.’s child is at risk of congenital malformations because of exposure to several
potentially teratogenic drugs: estrogen–progestin combination oral contraceptives,
valproate, and phenytoin (also see Chapter 49, Obstetric Drug Therapy).
Many AEDs have teratogenic effects.
186 Animal data regarding the teratogenic
potential of the new AEDs are encouraging, but conclusions regarding the teratogenic
potential of these AEDs cannot be made because of limited experience in pregnant
women. A good resource for clinicians to educate women is the American Epilepsy
Society and the American Academy of Neurology series of three Practice Parameter
updates on management issues for women with epilepsy focused on pregnancy. They
deal with obstetric complications and change in seizure frequency; teratogenesis and
perinatal outcomes; and vitamin K, folic acid, blood levels, and breast-feeding.
The authors evaluated the available evidence based on a structured literature review
Most AEDs are believed to exert their teratogenic effects (and possibly other
adverse effects such as hepatotoxicity) partly via reactive epoxide metabolites.
Enhancement of the formation of these metabolites via hepatic enzyme induction (e.g.,
by carbamazepine or phenobarbital) or inhibition of their breakdown (e.g., through
inhibition of epoxide hydrolase by valproate) would increase the risk of
teratogenicity. Combined administration of enzyme inducers and valproate
(specifically the combination of carbamazepine, phenobarbital, and valproate with or
without phenytoin) is associated with an especially high risk of teratogenicity.
addition, each of the present major AEDs has been associated with congenital
malformations when administered alone. Meador et al.
pregnancies in women with epilepsy taking an AED in monotherapy and enrolled in
the Neurodevelopmental Effects of Antiepileptic Drugs (NEAD) study. Serious
adverse outcomes (major malformations and fetal death) were significantly more
likely to occur with exposure to valproate (20.3%) than with carbamazepine (8.2%),
phenytoin (10.7%), or lamotrigine (1%). In addition to physical malformations, AED
exposure in utero has an adverse effect on neurodevelopment.
evaluated age-6 IQ and found that valproate-exposed children had significantly lower
scores (mean 97), even after controlling for the mother’s IQ and seizure type.
age-6 IQ scores were significantly lower for children exposed in utero to valproate
compared with scores of children exposed to carbamazepine (mean 105), phenytoin
(mean 108), and lamotrigine (mean 108) monotherapy. A European task force of
epilepsy experts recommends that, where possible, valproate should be avoided in
women of childbearing potential.
Several strategies can be used to reduce the potential adverse effects of AEDs on
pregnancy outcomes. If feasible, before conception, seizure control should be
optimized using the AED of first choice for the prospective mother’s seizure type or
epilepsy syndrome. Monotherapy at the lowest effective dose is the goal.
Maintenance of adequate folic acid stores before conception and during fetal
organogenesis is also important. Folic acid supplementation can reduce the risk of
congenital neural tube malformations in infants at risk who are born to women
without epilepsy, but folate supplementation does not reliably reduce the teratogenic
effects of AED. Nevertheless, supplementation of folic acid (and ensuring adequate
folate levels) is recommended. Because about half of pregnancies are unplanned and
not evident until weeks after conception, folate supplementation should be given
routinely to women of childbearing age with epilepsy. No study has been conducted
to determine the optimal dose of folic acid supplementation in patients taking AEDs.
Clinicians engage in much discussion of this topic, but the current practices are not
evidence-based. Even though this is the case, P.Z. should start taking 4 mg of folic
acid supplementation each day.
Physiologic changes in pregnant women may affect the pharmacokinetics of
171 Absorption can be influenced by nausea and vomiting. Hepatic metabolism
and renal function both increase during pregnancy. The binding capacity of albumin is
decreased during pregnancy, resulting in decreased protein binding for highly bound
drugs. Unbound fractions of phenobarbital, phenytoin, and valproate increase with
decreased concentrations of albumin.
195–197 For drugs predominately metabolized by
the liver with a restrictive clearance (e.g., carbamazepine and valproate), decreased
protein binding without changes in intrinsic clearance should result in a decrease in
total drug concentrations; unbound drug concentrations usually remain unchanged. For
drugs with both increased hepatic metabolism and decreased protein binding (e.g.,
phenytoin and phenobarbital), both total and unbound plasma concentrations
decrease, but not necessarily proportionately.
The clearance of lamotrigine increases as pregnancy progresses, presumably
related to the impact of estrogen on lamotrigine metabolism.
clearance changes immediately postpartum. Preliminary data suggest that
oxcarbazepine concentrations may also decrease as pregnancy progresses.
The effects of changes in renal function during pregnancy on AED concentrations
199 Renal blood flow and glomerular filtration rate increase
during pregnancy. Thus, the renal clearance of drugs that are predominately excreted
through the kidneys, such as gabapentin, levetiracetam, and pregabalin, may increase
During pregnancy, serum levels of AEDs (including free serum levels for highly
protein-bound drugs) can be monitored. In this case, a prepregnancy level would be
optimal for comparison. Dosage adjustments may help to prevent the increase in
seizure frequency that is seen in approximately 25% of pregnant women with
epilepsy. Because falls and anoxia associated with uncontrolled generalized tonic–
clonic seizures may increase the risk to the unborn baby, P.Z. should be educated on
the value of adherence to her AED regimen.
For P.Z., it can be presumed that significant exposure of the fetus to any teratogenic
influence of AED has already occurred. Optimization of seizure control is now the
primary concern for her. Any major alterations in P.Z.’s AED regimen should be
made cautiously to avoid precipitating seizures. In addition, she should be instructed
to contact the AED pregnancy registry at Massachusetts General Hospital (1-888-
233-2334 or www.aedpregnancyregistry.org). Information provided to the registry
will aid in the ongoing monitoring of outcomes of babies born to mothers taking
AEDs. Reports from this registry have provided
risk information on many AEDs and regular visits to their website is helpful to
Babies born to women with epilepsy who are taking enzyme-inducing AED are at
risk of hemorrhage owing to decreased vitamin-K-dependent clotting factors.
Although some question the evidence, women taking carbamazepine, phenobarbital,
primidone, or phenytoin should receive vitamin K 10 mg orally every day from 36
weeks of gestation until delivery, and babies should also receive vitamin K 1 mg IM
In a lactating woman who is taking medications, the risk of drug exposure to the
infant needs to be weighed against the benefits of breast-feeding.
into milk to some extent. The extent of protein binding of the drug is the most
important predictor of drug passage into milk.
intersubject variability in the milk/plasma (M/P) ratio exists, presumably owing to a
difference in volume and composition of the milk. Thus, the M/P ratio is not useful
for predicting infant AED exposure. Reviews on AED and breast-feeding are
204 For most first-generation AEDs (carbamazepine, phenytoin, valproic
acid), breast-feeding results in negligible AED plasma concentrations in the infants.
For the newer AEDs, breast-feeding should be done cautiously and the infant should
be monitored for excess AED plasma concentrations and toxicity, if possible. This
information should be presented to P.Z. in an appropriate manner. Once she delivers
her baby, re-evaluation and optimization of P.Z.’s AED therapy should occur.
Characteristics and Pathophysiology
generalized tonic–clonic seizures. For the past 3 months, he has been treated with 600 mg/day of
are associated with status epilepticus?
Status epilepticus (SE) is operationally defined as “either continuous seizures
lasting at least 5 minutes or 2 or more discrete seizures between which there is
incomplete recovery of consciousness.”
205 Because V.S. has had three seizures within
slightly more than 30 minutes and did not return to his baseline level of
consciousness between seizures, his present condition meets this definition. V.S. is
experiencing generalized convulsive SE; this is the most common type and it is
associated with the greatest risk of systemic and neurologic damage. SE also may be
characterized by nonconvulsive seizures that produce a persistent state of impaired
consciousness, or by partial seizures (with or without impaired consciousness).
These forms of SE are associated with much lower morbidity and mortality than
Uncontrolled, convulsive SE can cause severe metabolic and hemodynamic
alterations. V.S.’s vital signs (tachycardia, elevated blood pressure, increased
respiratory rate, and elevated body temperature) are typical for a patient in SE.
Prolonged, severe muscle contractions and CNS dysfunction from uncontrolled
seizure discharges result in hyperthermia, cardiorespiratory collapse, myoglobinuria,
renal failure, and neurologic damage. Even in the absence of convulsive muscle
movements, neurologic damage can occur from excessive electrical activity and the
resultant alterations in brain metabolism. When seizure activity persists longer than
approximately 30 minutes, failure of mechanisms that regulate cerebral blood flow is
more likely; this failure accompanies dramatic increases in brain metabolism and
demand for glucose and oxygen. Failure to meet the metabolic demands of brain
tissue results in accumulation of lactate and cell death. Peripherally, lactate
accumulates and serum glucose and electrolytes are altered. After 30 minutes of
seizure activity, the body often fails to compensate for increased metabolic demands,
and cardiovascular collapse can occur.
207 For these reasons, SE is considered a
medical emergency that requires immediate treatment to prevent or lessen both
systemic and neurologic damage. Mortality in adults with SE is approximately
; fatal outcome is often the result of the condition that precipitated SE (e.g.,
acute symptomatic causes, such as cardiopulmonary arrest, stroke). Long-term
neurologic consequences of severe SE may include cognitive impairment, memory
loss, and worsening of seizure disorders.
General Treatment Measures and Antiepileptic Drug
CASE 60-12, QUESTION 2: Describe a general treatment plan for V.S.’s episode of status epilepticus.
The immediate therapeutic concern in V.S. is to ensure ventilation, stabilize vital
signs, and terminate current seizure activity. If possible, an airway should be placed
for airway protection and if ventilatory support is needed; however, this may not be
possible while he is convulsing. Objects (e.g., spoons, tongue blades) should never
be placed into the mouth of a patient during a seizure. If airway placement is
impossible, V.S. should be positioned on his side to allow drainage of saliva and
mucus from the mouth and prevent aspiration. An IV line should be established using
normal saline, and blood should be obtained for serum chemistries (especially
glucose and electrolytes), AED serum concentrations, and toxicology screens.
Glucose, 25 g (50 mL of 50% dextrose solution) by IV push should be administered
to correct any hypoglycemia, which may be responsible for SE. Glucose
administration should be preceded by IV thiamine 100 mg or vitamin B complex to
prevent Wernicke encephalopathy.
IV administration of rapid-acting anticonvulsant medication should begin as soon
as possible to terminate V.S.’s seizure activity. Status epilepticus becomes more
resistant to treatment the longer the seizure continues; thus, treatment is more likely to
stop seizures the sooner it is administered.
205 For in-hospital treatment of SE, IV
medication administration is usually preferred.
CASE 60-12, QUESTION 3: Which anticonvulsants are available for IV administration? Evaluate the
available drugs and recommend a drug, dosage, and regimen for initial treatment of SE in V.S.
Lorazepam, phenytoin, and fosphenytoin are the agents most commonly used as IV
therapy in the initial treatment of SE.
209 Phenytoin and fosphenytoin are indicated
for treatment of SE, but owing to limitations on their rates of infusion, the onset of
peak effect may be delayed. Therefore, phenytoin or fosphenytoin is usually used
after initial treatment with lorazepam.
IV sodium valproate (Depacon) is available, but it is not FDA-approved for the
treatment of SE. Although the manufacturer recommends that Depacon be
administered slowly (<20 mg/minute), it has been administered safely at high doses
208 There is growing experience with the use of IV valproate
for SE that fails to respond to lorazepam and phenytoin, and for patients in whom
phenytoin is contraindicated (e.g., phenytoin allergy).
209 An IV form of levetiracetam
is available. This drug also is FDA-approved only for patients who cannot receive
oral dosage forms of levetiracetam. Rapid IV administration of levetiracetam has
been used; however, experience with this agent is limited.
available in an IV formulation and there are several case reports of its successful use
for refractory nonconvulsive SE.
IV phenobarbital is usually reserved for SE
that does not respond to benzodiazepines and phenytoin.
Four IV regimens for generalized convulsive SE were directly compared in one
213 The study evaluated diazepam followed by phenytoin,
lorazepam alone, phenobarbital alone, and phenytoin alone. For initial IV treatment
of overt generalized SE, lorazepam was more effective than phenytoin alone.
Lorazepam was as effective as the other two regimens, and it was easier to use.
IV administration of either diazepam or lorazepam is usually effective for rapid
termination of seizure activity in SE.
214 Owing to diazepam’s higher lipid solubility,
it redistributes from the CNS to peripheral tissues rapidly after administration; this
results in a short duration of action (<60 minutes).
solubility prevents rapid redistribution and accounts for its longer duration of
215 Lorazepam may be effective for up to 72 hours.
duration, lorazepam is the preferred benzodiazepine for immediate treatment of
Lorazepam 0.1 mg/kg given intravenously at 2 mg/minute would be appropriate
208 Lorazepam may cause significant venous irritation, and the
manufacturer recommends dilution with an equal volume of normal saline solution or
water for injection before IV administration. Lorazepam may be repeated after 5
minutes if seizures continue. The efficacy of lorazepam depends on rapid
achievement of high serum and CNS concentrations. Although lorazepam can be
administered IM, this route should not be used for treatment of SE because it is
unlikely that it would achieve serum concentrations necessary for termination of
seizure activity and there is little experience with its use for terminating SE.
Midazolam given IM has been shown to quickly and effectively terminate SE when
219 The most common adverse effects
after IV administration of benzodiazepines are sedation, hypotension, and respiratory
215 These side effects are usually short-lived and, when adequate facilities are
available for assisted ventilation and administration of fluids, they usually can be
managed without major risk to the patient. Respiratory depression occurs most
commonly in patients who receive multiple IV medications for control of SE.
INTRAVENOUS PHENYTOIN AND FOSPHENYTOIN
injection was completed. What drug should be administered to V.S. for prolonged control of seizures?
Recommend a dose, route, and method of administration.
Continued effective seizure control is important for patients who experience SE.
Previously, when diazepam was the benzodiazepine predominantly used for
immediate control of SE, a long-acting AED such as phenytoin was routinely
administered at the same time to ensure continued suppression of seizure activity.
Routine use of phenytoin has been somewhat de-emphasized with increased use of
; lorazepam’s apparent longer duration of effect may make routine use of
IV phenytoin less necessary. Nevertheless, many centers still use phenytoin in
The availability of fosphenytoin for IV administration has provided an additional
option for administration of phenytoin in the treatment of SE, and in most centers,
fosphenytoin is preferred over phenytoin. Use of this phenytoin prodrug allows more
rapid administration of large IV loading doses of phenytoin with less risk of injection
site complications. Fosphenytoin is also better tolerated than phenytoin.
Fosphenytoin itself is inactive; the therapeutic effect results from its conversion to
In the U.S., phenytoin (administered as either sodium phenytoin injection or as
sodium fosphenytoin injection) is considered the long-acting anticonvulsant of choice
for most patients with generalized convulsive SE.
209 Phenytoin causes much less
sedation and respiratory depression than drugs such as phenobarbital when it is used
in conjunction with IV benzodiazepines.
208 V.S.’s maintenance carbamazepine
therapy was previously effective. Without obvious precipitating factors such as head
trauma, CNS infection, and drug or alcohol abuse, SE, in a patient with a history of
epilepsy, most commonly results from poor adherence with maintenance AED
medication. Therefore, IV fosphenytoin is a good choice for re-establishing effective
AED therapy for V.S. Phenytoin is an acceptable alternative if fosphenytoin is
No comments:
Post a Comment
اكتب تعليق حول الموضوع