You are in: eMedicine Specialties > Neurology > Seizures and Epilepsy Seizures in the Emergency DepartmentArticle Last Updated: Nov 14, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Jeffrey S Nicholl, MD, Director of Clinical Neurophysiology Training, Associate Professor of Clinical Neurology, Department of Psychiatry and Neurology, Section of Neurology, Tulane University School of Medicine Jeffrey S Nicholl is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Editors: Edward B Bromfield, MD, Associate Professor of Neurology, Faculty Member, Division of Sleep Medicine, Harvard Medical School; Chief, Division of EEG, Epilepsy and Sleep Neurology, Consulting Neurologist, Brigham and Women's Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Jose E Cavazos, MD, PhD, Assistant Professor, Departments of Medicine (Neurology), Pharmacology, and Physiology, University of Texas Health Science Center at San Antonio; Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital; Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants Author and Editor Disclosure Synonyms and related keywords: anticonvulsant medications, antiepilepsy drugs, antiepilepsy medications, antiseizure medications, epilepsy, pseudoseizures, psychogenic seizures, status epilepticus INTRODUCTIONSection 2 of 10
  Seizures are a common cause of visits to the emergency department (ED). One estimate states that approximately 1% of patients coming to the ED do so because of seizures (Krumholz et al, 1989). At any given time, approximately 1% of the general population has epilepsy (ie, recurrent unprovoked seizures), although as many as 10% of individuals have at least one seizure during their lifetime. The role of the neurologist in the ED evaluation and treatment of patients presenting with seizures varies with the specifics of the individual case and also among institutions. Most often the neurologist is called as a consultant. In institutions with neurologic house staff, patients with seizures almost always are seen by a neurology resident. In other hospitals, the neurologist often is called by the emergency physician to consult by telephone and arrange follow-up care, but rarely is asked to observe the patient in the ED. The exception to this is status epilepticus, in which the neurologist may be called in to review the EEG, if obtained, and take over care of the patient. Usually, ED physicians have already examined these patients and stabilized their condition and often have treated them prior to contacting a neurologist. Frequently, routine labs, including CBC, chemistries, and toxicology, as well as CT scanning have been performed. The neurologist's role is to direct the further treatment and evaluation of each patient. The neurologist also should play a key role in educating ED physicians in evaluation and treatment of patients with seizures. Do all patients who have had a seizure need to be seen in the ED? Do all patients need lab work, CT scans, and treatment? What is the best treatment in the ED for patients with seizures? TYPES OF SEIZURESSection 3 of 10
Seizures may be divided into two main categories, partial and generalized, and partial seizures in turn are classified simple, complex, and partial with secondary generalization (International League Against Epilepsy [ILAE], 1981). Seizures involving no impairment of consciousness are simple partial seizures. These may be characterized by behavioral and/or motor, sensory, or experiential phenomena. Clonic jerking of a part of the body, olfactory hallucinations, and déją vu are examples of simple partial seizures. Preservation of consciousness implies that simple partial seizures have not spread beyond a very limited region of the cortex. Because of the small area of cortex involved, the EEG, even during simple partial status epilepticus, may show no ictal activity (Kaplan and Lesser, 1997). Auras are simple partial seizures that sometimes progress to complex partial or secondarily generalized seizures. Complex partial seizures involve impairment but not necessarily complete loss of consciousness. These patients demonstrate incomplete awareness of and ability to respond to their environment, and amnesia for the event. Complex partial seizures commonly consist of staring with oroalimentary and/or extremity automatisms. Patients are usually unable to converse, answer questions, or follow commands during complex partial seizures, but in some cases can perform these tasks slowly and inaccurately. Complex partial seizures are the manifestation of ictal activity involving limited areas of both hemispheres and usually have an EEG correlate. Partial seizures with secondarily generalization involve the entire cerebrum, and typically progress from a simple or complex partial seizure typical for the patient to a generalized convulsion involving bilateral, though sometimes asymmetric, tonic posturing followed by clonic jerking. Generalized seizures involve the whole cortex, as well as variable subcortical structures, and always should be visible on EEG, although the activity may be obscured by muscle and movement artifact. Several types of generalized seizures occur: tonic-clonic, tonic, clonic, clonic-tonic-clonic, typical absence, atypical absence, atonic, and myoclonic. Generalized tonic-clonic seizures always cause complete unconsciousness, and the other generalized seizures usually involve at least brief loss of consciousness, unless the duration is too short for this to be noticeable, as in myoclonic seizures. Also see Seizures and Epilepsy: Overview and Classification. TYPES OF EPILEPSYSection 4 of 10
Epilepsy may be idiopathic (which usually means genetic) or symptomatic, indicating a focal or diffuse structural abnormality as the cause of the seizures, even if this abnormality cannot be seen on neuroimaging. The term "cryptogenic" is sometimes used if a brain insult is known to cause the epilepsy but cannot be identified precisely. Epilepsy also may be characterized as localization-related or generalized (ILAE, 1989). These two dimensions yield 4 categories of epilepsy syndromes: (1) idiopathic generalized (eg, childhood absence or juvenile myoclonic epilepsy), (2) idiopathic localization-related (eg, benign epilepsy of childhood with centrotemporal spikes [rolandic epilepsy]), (3) symptomatic generalized (eg, West syndrome, Lennox-Gastaut syndrome), and (4) symptomatic localization-related (eg, temporal or frontal lobe epilepsy). The type of epilepsy is important to determine, since this guides treatment and assists in determining the prognosis of the patient. EVALUATION AND TREATMENTSection 5 of 10
Patient known to be epileptic with a single seizure Sometimes the ED physician may be able to ascertain that a patient who has had a seizure has a history of epilepsy. A Medic Alert bracelet or necklace may be visible, or the patient or someone who knows the patient may be able to supply this important information. A patient with known epilepsy who has had a single, typical seizure and whose mental status has returned to baseline need not be transported to the ED unless other injuries require treatment (Engel and Starkman, 1994). Transportation to and evaluation and treatment in the ED are extremely expensive. The cost of recurrent trips to the ED may be devastating financially to the patient and the family. Since noncompliance is the most frequent cause of breakthrough seizures, patients must be encouraged to take medications as prescribed and to arrange follow-up care with their own physician as soon as possible. If the patient has run out of medication and has no refills on his prescription, he or she should be told to go to the ED or an urgent care clinic if someone can provide transportation. If not, the patient should be transported to the ED by ambulance. If the patient arrives at the ED, only testing of the anticonvulsant level is necessary. "Routine" lab work and neuroimaging are not necessary if the patient has returned completely to baseline and has no significant head injury caused by the seizure. If anticonvulsant levels are low, particularly if below the patient's usual levels, he or she will need a partial or full loading dose of the anticonvulsant. The following is a convenient formula for determining how much of the drug to give the patient: Dose (mg) = weight (kg) X volume of distribution for the drug (L/kg) X [the desired level – the current level (mcg/mL)] (Treiman, 1997). The volume of distribution for phenytoin and carbamazepine is approximately 0.8; for phenobarbital, 0.6; and for valproate, 0.2 (Bourgeois, 1996). If the specific patient's optimal levels are unknown, reasonable target levels are at the upper end of the usual therapeutic ranges, approximately 20 mcg/mL for phenytoin, 40 mcg/mL for phenobarbital, and 100 mcg/mL for valproate. Intravenous loading can be performed with phenobarbital, phenytoin/fosphenytoin, valproate, or levetiracetam. Oral loading often is limited by the neurotoxic adverse effects of most antiepileptic drugs, including nausea and vomiting, but the required calculated dose can be spread out over a day or more if necessary. For example, phenytoin can be administered 400 mg orally every 4 hours as needed to reach the final dosage. Advise the patient of the importance of complying with the medication regimen. If the patient stopped taking medication because he or she was drinking alcohol, advise the patient to continue taking antiseizure medication even if drinking, while warning against respiratory depressive effects of sedating drugs when combined with alcohol. Detoxification or alcohol abstinence programs should also be encouraged, even if the perceived chance of compliance is low. Patient with no history of epilepsy who has returned to baseline following a seizure This patient should be taken to the ED and evaluated. The evaluation should include vital signs, general and neurologic examinations, basic chemistry studies, and a toxicology screen. Investigate circumstances that may have precipitated a seizure, such as alcohol withdrawal, stimulant use, or head injury. If the patient has no history of head trauma and is being seen in a setting where MRI, EEG, and rapid follow-up care with a neurologist can be obtained as an outpatient (and the patient is deemed reliable regarding follow-up care), CT scan of the head is not necessary (Roth and Drislane, 1998). With no recent head injury and completely normal findings on neurologic examination, CT scanning is extremely unlikely to show an abnormality requiring emergent intervention, such as a space-occupying lesion. Regardless of whether a CT scan is done, the patient needs an MRI, as the latter is much more sensitive in detecting structural lesions likely to cause epilepsy (Pellegrino, 1994). The patient also requires an EEG. An EEG performed soon after the event is more likely to show an abnormality than one performed later (Gotman and Marciani, 1985). EEG after sleep deprivation increases the yield in detecting epileptiform abnormalities (Mattson et al, 1965), although background abnormalities may be obscured by excessive drowsiness. If the patient has a history of recent head trauma, abnormal neurologic examination findings, or inability to ensure close follow-up care, perform a CT scan of the head while the patient is in the ED. If the patient has a fever or history of subacute behavioral change or new headaches, perform a lumbar puncture to look for evidence of herpes encephalitis or other CNS infection. After a single unprovoked seizure, the chance of a second seizure (ie, likelihood of going on to develop epilepsy) is approximately 30-60%. The patient with a single seizure who has returned to baseline does not need to be started on an antiepileptic drug in the ED. Treatment does lower the rate of recurrence, but patients who would not have had a recurrent seizure are subjected needlessly to the potential toxicity of these medications. Recurrence is more likely in those with a history of significant head injury or other CNS insult. If the patient has a normal MRI and EEG, the likelihood of a second seizure is approximately 1 in 3; if either test result is abnormal, the chances are approximately 1 in 2; if both are abnormal, the probability rises to 2 in 3 (Berg and Shinnar, 1991). The other argument against starting antiseizure medications in this situation involves eventual medication withdrawal. If the patient remains seizure free for 2 years, the minimum recommended in patients with established epilepsy, and the decision is made to withdraw medication, the patient needs to stop driving during the taper and for some months thereafter. Since a patient who has had one seizure typically should not drive for 6-12 months (depending on state regulations), monitoring this individual to see whether he or she is going to develop epilepsy during this period makes more sense than requiring the individual to stop driving again later, or needlessly leaving him or her on medication indefinitely. Instruct the patient regarding seizure precautions. Advise the patient not to operate a motor vehicle for the length of time required by state law. In a few states, notifying the state that the patient has had a seizure is mandatory. In addition to not driving, warn patients to avoid any activities or situations during which sudden loss of consciousness would be dangerous, such as climbing ladders, operating heavy equipment, swimming alone, taking baths (as opposed to showers), and cooking (other than with a microwave). Instructions to the patient should be documented very well in the chart. If possible, make appointments for an MRI, EEG, and follow-up care with a neurologist while the patient is still in the ED. Patients are more likely to comply with follow-up care if they have premade appointments. Stress the importance of follow-up care to exclude serious intracranial pathology requiring intervention (eg, tumor), establishing the cause of the seizure, and estimating prognosis. MRI is the most sensitive test for a structural abnormality causing seizures. EEG helps establish the type of seizure and epilepsy syndrome, which are important for prognosis and treatment. Patient with no history of epilepsy who does not return to baseline following seizure During the postictal period, patients often are confused or lethargic. This usually lasts 20-30 minutes. If the postictal state is longer than this or a new focal neurological abnormality is detected (eg, Todd paralysis), perform a CT scan of the head as soon as possible. Unless contraindicated because of findings on the CT scan suggestive of increased intracranial pressure, a lumbar puncture also should be performed to look for evidence of bleeding or infection. Prolonged postictal confusion suggests either ongoing seizure activity or that the seizure and altered mental status are symptomatic of another condition, which can be toxic, metabolic, infectious, or structural. If available, an urgent EEG can discriminate between ongoing seizure activity (ie, status epilepticus) and an encephalopathic state, whether due to a prolonged postictal state or some other underlying abnormality. Patient in status epilepticus Most seizures do not last beyond 2-3 minutes and already have ended by the time the patient reaches the ED. Status epilepticus traditionally has been defined as a continuous seizure lasting longer than 30 minutes or recurrent seizures over this period without a return to baseline between ictal events. We now know that a seizure lasting longer than 5 minutes has a much higher chance of progressing to status epilepticus (Lowenstein et al, 1999). Therefore, these patients should be treated early and aggressively. As always, attend to the ABCs first. Some have taught that patients should be rolled onto their side during a seizure. Recent indications demonstrate that this may cause more harm than good. Patients who have been rolled onto their side during a major motor seizure are at greater risk for self-injury, such as a dislocated shoulder (DeToledo and Lowe, 2001). As patients are not breathing during a generalized tonic-clinic seizure, they are not at high risk for aspiration until the event ends. Immediately following the seizure, patients usually take a deep breath. Therefore, roll the patient onto his or her side immediately after the motor activity ceases. Likewise, to prevent injury to the patient, wait to suction the oropharynx until the end of the seizure. If the seizure lasts longer than 2 minutes, place an intravenous (IV) line and simultaneously draw blood for a bedside blood glucose check and further tests later as indicated. If the patient is hypoglycemic, immediately administer 100 mg of thiamine followed by 50 mL of dextrose 50% in water solution (D50W) as an IV push. If the seizure continues beyond 5 minutes, then begin treatment with a benzodiazepine. The drug of choice is lorazepam. Diazepam, which is very lipid soluble, has rapid onset of action, but it has a short effective half-life in the brain because of rapid redistribution to adipose tissue (Schmidt, 1995). Even though lorazepam has a much shorter elimination half-life than diazepam, the effective half-life in the brain in the brain is longer (Bleck, 1999). Reports also exist of using midazolam as the initial treatment of status epilepticus, but this has a very short half-life and must be given as a continuous infusion or multiple boluses. Benzodiazepines may on occasion cause respiratory depression; therefore, means to ventilate the patient must be immediately at hand. At this point, the patient should be loaded with IV fosphenytoin. Although IV phenytoin is much less expensive, the risk of the "purple glove syndrome" argues for use of the newer prodrug. The purple glove syndrome is the progressive development of edema, discoloration, and pain in the limb after extravasation of IV phenytoin. This syndrome rarely has necessitated amputation of the limb (O'Brien et al, 1998). Hypotension and arrhythmia are risks of both phenytoin and fosphenytoin, requiring frequent or continuous monitoring of vital signs. The usual dose is 20 mg of phenytoin, or of phenytoin equivalents (PEs) of fosphenytoin, per kilogram. If this fails, another 5-10 mg of phenytoin or PE/kg of fosphenytoin may be administered. Maximum rate of administration is 50 mg/min of phenytoin or 150 PE/min of fosphenytoin; therefore, the fosphenytoin load can be completed more quickly than the phenytoin load. An alternative to fosphenytoin/phenytoin is IV valproic acid. Though not yet approved by the US Food and Drug Administration (FDA) for treatment of status epilepticus, this has been found to be safe and effective. A dose of 25 mg/kg of valproate can be administered at a rate of 3-6 mg/kg/min to yield a blood level of approximately 130 mcg/mL (Sinha and Naritoku, 2000; Venkataraman and Wheless, 1999; Limdi and Faught, 2000; Wheless, 2004). It is particularly useful in patients with documented hypersensitivity to phenytoin or in patients who already are taking phenytoin but in whom the blood level of phenytoin is not yet known. In patients with epilepsy, noncompliance with the medication regimen is the most common cause of status epilepticus. Some concern exists that administering fosphenytoin to a patient who is taking phenytoin may raise the level to a point at which the drug actually becomes proconvulsant (Bruni, 1995). This is extremely unlikely to occur when the phenytoin level is less than 40 mcg/mL. Intravenous levetiracetam has recently (2006) become available. At this time, levetiracetam is indicated only for the treatment of partial-onset epilepsies and not generalized epilepsies or status epilepticus. Eventually, it may be useful in the treatment of status epilepticus, as a full loading dose can be given safely in 5 minutes (Ramael, 2006). If the patient continues to be in status epilepticus after receiving 30 mg PE/kg of fosphenytoin, several options are available. One is to load the patient with 25 mg/kg of IV valproic acid. If this too fails, all the remaining options carry a high risk of respiratory depression. Therefore, the patient should be intubated at this point, if he or she has not been intubated already. Traditionally, the next step was to load the patient with IV phenobarbital, 20 mg/kg (at 60 mg/min) (Willmore, 1998). An additional dose of 10 mg/kg, or more, then could be given if the first dose was not successful. Phenobarbital given IV may cause profound hypotension. If phenobarbital was unsuccessful in terminating the seizures, pentobarbital was administered as a 10-15 mg/kg loading dose (at 50 mg/min) and then as an infusion of 0.5-1 mg/kg/h. As with phenobarbital, IV pentobarbital has been associated with severe hypotension, which has led to the recommendation to use midazolam or propofol first (Lowenstein and Alldredge, 1998). Begin these medications with a bolus of 0.2 mg/kg for midazolam or 1 mg/kg for propofol, followed by a continuous infusion (0.045 mg/kg/h for midazolam, 2 mg/kg/h for propofol, titrated to effect). Although these drugs are less likely than phenobarbital or pentobarbital to cause severe hypotension, patients who have received them may require rapid administration of fluid or pressors. At this time, transfer the patient to an intensive care unit. Once the decision has been made to put the patient into drug-induced coma, continuous EEG monitoring is important to judge the effect of the medication. Although the patient may cease to convulse clinically, he or she may be in nonconvulsive status epilepticus, which can be evaluated only by EEG. EEG also helps to judge the depth of the coma. The aim is to eliminate all epileptiform activity. Reaching a burst-suppression pattern or electrocerebral silence on the EEG may be necessary to achieve this. If the seizures still cannot be controlled, the patient is beyond the purview of the ED; then general anesthesia using an inhaled anesthetic may work (Ramsay, 1993). After the patient has been free of seizures for 12-24 hours, and levels of a long-acting antiepileptic drug such as phenytoin, phenobarbital, or valproate are stable and high, an attempt may be made to wean the patient off the medication administered by continuous infusion. If seizure activity returns, the level of the coma must be deepened again. An argument has been made that 2 types of nonconvulsive status epilepticus exist, a "twilight" confusional state and that in which the patient is comatose. The latter occurs following some CNS catastrophes, in critically ill patients, or after generalized tonic-clonic status epilepticus "burns out" and no longer is manifested by motor activity (Niedermeyer and Ribeiro, 2000). The "twilight" form of status epilepticus is either absence or complex-partial status, neither of which is life threatening, although the latter may pose the risk of neurological morbidity. A good guideline is not to worsen the patient's level of consciousness by pharmacologic means. Low doses of a benzodiazepine and cautious loading with fosphenytoin or valproate usually suffice to control this kind of status. Phenytoin does not stop absence status epilepticus; therefore, valproate is a better choice for patients with known primary generalized epilepsy, or those in whom the EEG shows generalized discharges and no evidence of partial seizures is observed. Some controversy exists over the management of burned-out generalized status epilepticus (Krumholz, 1999; Drislane, 1999; Kaplan, 1999). Some argue that this type of nonconvulsive status epilepticus is as dangerous as convulsive status and must be treated as aggressively. However, this type of status often occurs in a critically ill patient who may not be able to tolerate the additional burden of high doses of antiseizure medications, particularly the barbiturates (Litt et al, 1998). Some studies have demonstrated that the prognosis in these patients depends more on the underlying illness than on the duration of status epilepticus. Certainly, treating these patients cautiously with a benzodiazepine, fosphenytoin, and valproate is reasonable. Patients who have more than one seizure but recover after each one may have incipient status epilepticus, especially if the interseizure interval is decreasing. These patients also can benefit from benzodiazepines. Sublingual lorazepam and rectal diazepam gel (Diastat) are options that may be less sedating than IV benzodiazepines. For further information, also see First Seizure in Adulthood: Diagnosis and Treatment, First Seizure: Pediatric Perspective, and Status Epilepticus. ANTISEIZURE MEDICATIONSSection 6 of 10
The treatment of epilepsy has become much more complicated over the past 15 years with the advent of 8 new drugs, not including fosphenytoin or IV valproate. The consulting neurologist must be familiar with the pharmacology and adverse effects of these medications. The half-life of each drug determines the length of time required to reach steady state, at which the drug level plateaus. Usually steady state is reached after 5 half-lives; the longer the half-life, the longer to reach the plateau. Gabapentin has a short half-life, approximately 6 hours, and no known serious adverse effects. Lamotrigine's half-life is very dependent on interactions with other drugs; it is approximately 15 hours in patients on enzyme inducers such as phenytoin or carbamazepine, approximately 70 hours in patients taking valproate, and 30 hours when administered alone or with both inducing drugs and valproate. Lamotrigine's most worrisome adverse effect is a serious skin rash (ie, Stevens-Johnson syndrome, toxic epidermal necrolysis). If a patient has stopped lamotrigine and then has a seizure, restarting the medication at the prior dose may be dangerous, since this may precipitate a rash even if the patient did not have one before. Starting at the appropriate initial dose is necessary, depending on what other medications the patient is taking and how long the patient was off the drug; then titrate up slowly. In this situation, starting the patient on another antiseizure medication during the time that the lamotrigine dose is being raised may be necessary. Topiramate has a half-life of approximately 12 hours in patients on an enzyme inducer and 21 hours in those who are not. Rapidly raising the dose of topiramate is likely to cause intolerable cognitive adverse effects. Tiagabine has a half-life 10 hours, but it may have a longer pharmacodynamic effect. If the dose is raised too quickly, unacceptable sedation occurs. Levetiracetam also has a short half-life of 6-8 hours, but a longer pharmacodynamic effect, and can be started at a low therapeutic dose of 500 mg bid. Zonisamide has a long half-life of approximately 60 hours, but often is sedating if started at a dose higher than 100 mg/d, while the therapeutic dose range is considered to be 200-400 mg/d. Oxcarbazepine is related closely to carbamazepine, but it can be titrated somewhat more rapidly; it may be started at 300 mg bid, a low therapeutic dose; bid dosing is adequate even though the half-life of its active metabolite, the monohydroxy derivative, is only about 10 hours. A drug more recently approved for the treatment of partial-onset seizures is pregabalin, which has a half-life of about 6 hours. A usual starting dose is 75 mg twice a day (Hitiris, 2006). When necessary to reach a high therapeutic level of a medication rapidly, IV fosphenytoin, valproic acid or levetiracetam is the drug of choice. Also see Antiepileptic Drugs: An Overview. NONEPILEPTIC SEIZURELIKE EVENTS IN THE EMERGENCY DEPARTMENTSection 7 of 10
Nonepileptic seizurelike events may be either physiologic or psychogenic. Physiologic events include syncope (especially convulsive syncope), cataplexy, migraine, transient ischemic attack, vertigo, and transient global amnesia. Convulsive syncope, in which the patient has myoclonic jerks or even a tonic-clonic sequence of events due to prolonged cerebral hypoperfusion, may be very difficult to differentiate from epileptic seizures. Usually episodes of convulsive syncope are preceded by a prodrome of lightheadedness, dimming of vision, roaring in the ears, nausea, diaphoresis, and palpitations. Most commonly the patient's head has been kept above the body during the syncopal episode, purposefully or accidentally, further worsening the hypoperfusion. Psychogenic nonepileptic seizures are common in the ED. In fact, in one study, 50% of patients presenting in status epilepticus were experiencing psychogenic seizures (Howell et al, 1989). Differentiating epileptic from psychogenic seizures in the ED is usually difficult and often impossible. Tongue biting, incontinence, self-injury, and postictal confusion suggest an epileptic seizure. Intact consciousness during a generalized convulsion, and prolonged duration with waxing and waning for hours suggest a psychogenic event. Keep in mind that these features may be observed in both epileptic and psychogenic attacks. The most definitive way to make the diagnosis of psychogenic attacks is to obtain an EEG during a seizure or immediately thereafter when some degree of postictal slowing of the background activity is expected. Even during a seizure, however, the EEG may show no abnormality in some simple partial seizures or seizures arising deep in the brain, or the tracing may be obscured by artifact. Erring on the side of calling the event an epileptic seizure until further workup is completed is probably best. Also, patients with psychogenic spells should be under the usual seizure precautions and activity restrictions, at least until the diagnosis is clear. Also see Psychogenic Nonepileptic Seizures. FOLLOW-UP CARE FOR PATIENTS PRESENTING WITH SEIZURES IN THE EMERGENCY DEPARTMENTSection 8 of 10
As noted in Evaluation and Treatment, follow-up care for patients presenting to the ED with seizures is critical. These patients need close follow-up care with a neurologist for both treatment and further evaluation. If the patient was started on a medication in the ED, the neurologist must decide whether to continue that medication, to discontinue medication, or to change to another, preferred drug for that patient. Most patients who are started on a drug in the ED are given phenytoin, which may not be the best drug for some types of epilepsy and some patients. The EEG and MRI are needed to determine the epilepsy syndrome, if possible, and to exclude serious intracranial pathology requiring medical or surgical intervention. For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education articles Seizures Emergencies and Epilepsy. SUMMARYSection 9 of 10
The neurologist plays an important role in the evaluation and treatment of patients seen in the ED for seizures. The neurologist most frequently serves as a consultant to the emergency physician. The involvement of the neurologist is important in helping the emergency physician to determine the appropriate workup and treatment. Perhaps most important is that early involvement of the neurologist ensures continuity of care. The neurologist also can serve an important role in educating ED staff about the optimal approaches to this common emergency. REFERENCESSection 10 of 10
Seizures in the Emergency Department excerpt Article Last Updated: Nov 14, 2006 |
