Seizures and Status Epilepticus
David Roh
Jan Claassen
INTRODUCTION
Seizures are frequently encountered in both the community and hospital setting. Epidemiologic studies in the United States have shown that 11% of the general population will have a seizure at some point in their life. Of these seizure patients, there is an estimated 1 million hospital visits due to seizures per year. The International League Against Epilepsy (ILAE) defines seizures as transient clinical events due to abnormally excessive or synchronous neuronal activity in the brain. These can manifest in a wide array of symptoms ranging from obvious convulsive activity to more subtle signs of twitching or altered mental status.
STATUS EPILEPTICUS
A failure to stop isolated seizures may lead to status epilepticus (SE). Its incidence has seen an increase in recent years with 5 to 30 cases per 100,000. SE is defined as convulsions lasting more than 5 minutes or two or more convulsions in a 5-minute interval without a return to preconvulsive neurologic baseline. Historically, SE had been defined as continuous convulsive seizure activity lasting greater than 30 minutes without complete recovery. However, the minimum time elapsed to qualify for SE was drastically shortened to 5 minutes based on the observation that convulsive seizures rarely last for more than a few minutes. Furthermore, seizures that are of longer duration typically do not stop spontaneously. Animal studies and human data have demonstrated irreversible brain injury can occur as early as 5 minutes of ongoing seizure activity. Delaying effective recognition and treatment of SE dramatically increases the patient’s morbidity and mortality. Thus, SE constitutes a neurologic emergency requiring prompt and decisive intervention.
CAUSES OF SEIZURES
It is important to identify any underlying cause for seizures, as management will be tailored to reverse these factors if possible (Table 6.1). In adults without a history of prior seizures, stroke is the most frequent underlying etiology of seizures. The most common cause of SE is a history of epilepsy. Frequent precipitating factors in these patients include medication noncompliance, low antiepileptic drug (AED) levels, and recent changes in AEDs. Other seizures due to underlying metabolic derangements (hypoglycemia, hyponatremia) can be commonly seen but will be difficult to control with AED agents alone. Subsequently, timely investigation into the underlying cause of the seizure will need to be implemented in the management of acute seizures. Many of these provoking factors may be elicited from the patient’s history or exam as discussed previously; however, laboratory and imaging workup can further elucidate these factors. See “Initial Workup” section for recommended testing.
TABLE 6.1 Etiology of Seizures | ||||||||||||||
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DIAGNOSIS
The diagnosis of acute seizures can be made on clinical grounds depending on the patient’s history and symptoms. Symptoms can range from obvious positive signs of rhythmic jerking and posturing to more subtle positive symptoms of twitching, nystagmus, automatisms, and eye deviation. Negative symptoms of seizures include staring, coma, lethargy, confusion, and aphasia. These negative symptoms may raise the suspicion of seizures in the appropriate context; however, the definite diagnosis requires an electroencephalogram (EEG). The differential diagnosis of seizures includes a wide variety of seizure mimics that produce sudden unexplained movements or alteration in level of consciousness (Table 6.2). If the patient is not exhibiting symptoms at the time of assessment, a focused history must be obtained from whoever witnessed the event.
FOCUSED HISTORY
Initial questions should be focused on what symptoms were seen, laterality of symptoms (hemibody or generalized), time of onset, length of activity, if the patient returned to baseline, seizure history, recent illness/fever, trauma, and relevant medications (Table 6.3). Medication history should include antiepileptics or agents that would lower seizure threshold (Table 6.4). These questions may allow the examiner to rapidly differentiate seizure versus SE, direct an initial diagnosis for the underlying etiology, and guide the diagnostic workup.
TABLE 6.2 Common Seizure Mimics | ||||||||
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FOCUSED EXAM
A focused general physical exam should rapidly screen the patient’s stability and identify life-threatening etiologies of seizures. These may include meningitis, hemorrhage, ischemic stroke, or mass effect (Table 6.5). Vital signs should be monitored with particular attention to hemodynamic stability and respiratory status. Focus should be paid to the presence of fever, nuchal rigidity, and rash. These findings, if present, should raise suspicion for central nervous system (CNS) infection, prompting further laboratory investigation and empiric treatment.
Observation and neurologic examination may detect obvious positive symptoms of seizures supporting the diagnosis. However, absence of obvious symptoms should not preclude the possibility of seizures. Nearly half of patients with generalized tonic-clonic SE will continue to have electrographic seizures after clinical symptoms disappear. This can result in continued subtle signs such as eye deviation, nystagmus, and facial twitching. Some of these subtle positive findings may have localizing value (Table 6.6). Comatose patients who have subtle lateralized facial or extremity twitching, nystagmus, or eye deviation should be considered to be in nonconvulsive SE until proven otherwise by EEG.
TREATMENT STRATEGY
Emergency EEG is indicated for patients who present with SE who fail to awaken after cessation of convulsive seizures. Nonconvulsive seizures occur in up to 40% of patients who fail to awaken after convulsive seizures. This can cause further depression of level of consciousness and increase resistance to antiepileptic therapy if not controlled. Affected patients will not exhibit obvious physical signs of seizures, but electrographic seizure activity will be detected on EEG. As a result, the clinician must be wary of the possibility of nonconvulsive status epilepticus (NCSE) if the patient does not awaken after cessation of seizure activity or displays subtle symptoms of continuing seizures. Please see Chapter 58 for further details on seizure semiology, localizing signs, and seizure syndromes.
TABLE 6.3 Focused History: Questions to Ask in the Patient with Seizure | |||||||||
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TABLE 6.4 Drugs that Lower the Seizure Threshold | |||||||
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EMERGENT TREATMENT OF STATUS EPILEPTICUS
PREHOSPITAL TREATMENT
The most important factor in the treatment of acute seizures is the amount of time it takes to administer the initial treatment. This requires a timely recognition of seizures by bystanders and notification of emergency medical services (EMS). Prehospital EMS care with patient stabilization and medication administration is vital in early treatment of acute seizures and has been associated with improved patient outcomes. Stabilization includes initial assessment of secure airway, stable breathing, and circulation. Once stabilized, prehospital care also involves attempts at obtaining intravenous (IV) access and assessing for reversible causes of seizures such as hypoglycemia.
Following initial assessment, treatment for convulsive seizures can be given by EMS. Benzodiazepines have been the AED of choice in the field (Table 6.7). IV agents have traditionally been used with lorazepam (4 mg) or diazepam (10 mg). In appropriate, targeted dosing, seizure patients that receive IV benzodiazepines have lower instances of respiratory depression/intubation than patients that have prolonged seizures without treatment. Subsequently, the efficacy and safety of IV benzodiazepine use, particularly IV
lorazepam, has been an important finding in the early prehospital treatment of convulsive seizures [Level 1].1
lorazepam, has been an important finding in the early prehospital treatment of convulsive seizures [Level 1].1
TABLE 6.5 Red Flags for Life-Threatening Causes of Seizures | |||||||||||||||
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