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Status Epilepticus Workup

  • Author: Julie L Roth, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
 
Updated: Feb 19, 2016
 

Approach Considerations

The approach to potential status epilepticus (SE) should be conducted similarly to that for any self-limited seizure, but clearly in an expeditious fashion. Prompt diagnosis facilitates medical intervention to abort or limit SE.

The workup should include stat laboratory work. Fever should prompt a thorough search for sources of infection, with blood culture and urinalysis. Lumbar puncture (after neuroimaging to rule out potential cerebral herniation) is indicated if a CNS infection is suspected. Fever, stiff neck, headache, and photophobia are signs and symptoms that may suggest such infection.

The risk of lasting morbidity or mortality is usually lower with focal SE than with generalized convulsive SE. This affords extra opportunities to pursue tests that can confirm the diagnosis, reveal associated etiologic processes (some of which may be morbid), and provide insight into fruitful treatment strategies.

Simple partial status epilepticus/epilepsy partialis continua

In patients with preserved consciousness and sensory or motor symptoms compatible with focal SE, a history of epilepsy may help focus the workup tremendously. In particular, if seizures in SE are the same as previous focal seizures, the patient is not apt to have a newly acquired CNS lesion.

Instead, the SE episode may reflect subtherapeutic anticonvulsant levels, new toxic or metabolic derangements, intercurrent infection (usually outside of the CNS), recent stress, or sleep deprivation, as in any breakthrough seizure in a patient with known epilepsy. In some situations, no new precipitant can be found, though one should be sought aggressively.

In patients without a previous diagnosis of epilepsy, an aggressive search for a new or preexistent focal CNS lesion is paramount. Because patients with established epilepsy are not immune to new CNS lesions, a search for a new CNS process should be considered if their established epileptic focus does not seem to account for the ongoing SE.

Search for a new focal lesion early because certain acute processes pose high rates of morbidity and may require treatment independent of the SE. For example, quickly finding a new cardioembolic stroke due to atrial fibrillation is pivotal because this condition must be dealt with swiftly, in parallel with focal SE, if both apply.

Complex partial status epilepticus

The approach to a patient with a confusional or stuporous picture that suggests complex partial SE (CPSE) is similar to the approach in simple partial SE and epilepsy partialis continua. The first pivotal step is including CPSE in the differential diagnosis. Numerous authors report that CPSE is often overlooked and that correct diagnosis is often considerably delayed. This problem stems from the close clinical overlap between CPSE and other, more common encephalopathies in hospitalized patients.

When CPSE occurs in the setting of previous epilepsy, search for new medical stressors (eg, toxins, metabolic derangements, alcohol, proconvulsant medications, subtherapeutic anticonvulsants, intercurrent illness, hypoxemia) that may trigger its expression.[54]

Another common clinical scenario leading to CPSE, especially in patients without previous epilepsy, involves overt yet self-limited generalized convulsion, often in the context of a new serious medical illness, after surgery, or after an acute CNS process. In this familiar scenario, the patient does not have the expected timely recovery to neurologic baseline after the brief convulsion.

Anticonvulsants are often started in response to the overt seizure, though frequently with inconsistent attention to blood levels. The patient's persistent stupor is initially misattributed to the concomitant medical illness or a diminished recuperative ability (in older patients) to the newly acquired CNS process. Potentially diagnostic EEGs may be wrongly deferred after that new-onset convulsion in this setting because the overt seizure is long over and the diagnosis of CPSE is overlooked.

Numerous authors have highlighted the frequent association of CPSE with previous or late generalized convulsive seizures. This constellation of features includes the following sequence:

  1. Serious medical, surgical, or neurological illness
  2. A brief convulsive seizure
  3. Protracted stupor with fluctuating neurologic findings, subtle nystagmus, or focal twitching

The presence of these elements should prompt consideration of CPSE and expedient EEG evaluation. After EEG results confirm CPSE, the workup proceeds as outlined for simple partial status epilepticus/epilepsy partialis continua.

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Laboratory Studies

The presence of SE should prompt a search for its etiology, and in particular for potentially reversible conditions. Clinical information should guide the ordering of laboratory tests.

Laboratory studies that should be obtained on an emergency basis include the following:

  • Electrolytes
  • Calcium
  • Magnesium
  • Glucose
  • Complete blood count
  • Renal function tests
  • Toxicologic screening
  • Anticonvulsant levels
  • Liver function tests

Emergent glucose assessment is particularly important because both hyperglycemia and hypoglycemia can be associated with SE. Rapid turnaround of anticonvulsant drug levels may be particularly helpful in guiding treatment choices in patients with well-established epilepsy who on long-term therapy.

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Arterial Blood Gases

Arterial blood gas (ABG) measurement may be useful to monitor oxygenation and ventilation efficacy and to discover any unexpected acid-base abnormalities. An episode of generalized seizures will typically result in a metabolic acidosis, but this should correct rapidly following seizure cessation as the lactate generated by vigorous muscle contractions is metabolized. Profound metabolic acidosis and continuing seizures might raise the possibility of isoniazid poisoning (see Isoniazid Toxicity in Emergency Medicine).

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Electroencephalography

EEG is the criterion standard for diagnosing EEG, and some authors believe that EEG should be a routine part of management of SE.[2, 3] Nevertheless, EEG is rarely available in the acute-care setting; normally, it is obtained through neurologic consultation. When EEG is unavailable for the acute workup, presumptive treatment strategies must occasionally be started before EEG confirmation becomes available.

Because of the possibility of subtle SE, an EEG should be strongly considered if the patient is not starting to awaken within 20-30 minutes after seizure cessation. High clinical suspicion for continued unresponsiveness from this subtle SE is necessary, along with timely consultations and occasional insistence on obtaining EEG.

Several groups have shown that electrical SE often persists when clinical seizure activity has ceased.[38, 55] DeLorenzo et al prospectively examined 64 patients who clinically appeared to have controlled SE. These patients were comatose and had no overt clinical signs of convulsive activity. However, EEG demonstrated persistent seizures in 48%, and 14% of these patients had nonconvulsive SE (predominantly of the complex partial type).[55]

EEG is often helpful in solidifying the diagnosis of focal SE, and it may be crucial in differentiating focal SE from some of the other mimics. Simple partial seizure activity occasionally lacks an EEG correlate. The absence of ongoing epileptiform activity does not completely exclude simple partial SE. However, absence of an EEG correlate should at least call the diagnosis of focal SE into question. Many patients with EPC have a repetitive discharge on EEG that is time-locked to the motor activity.

Because recurring complex partial seizures without interval neurologic recovery constitutes CPSE, a single EEG lacking ongoing partial seizure activity does not entirely preclude the diagnosis; the study may have been performed between seizures. Repeated or prolonged EEG recordings may be crucial in confirming CPSE

Although not always required for the diagnosis of status, EEG can be extremely useful to validate the diagnosis and often helps in categorizing the type of status. See the images below.

Focal status epilepticus. Electroencephalograph (E Focal status epilepticus. Electroencephalograph (EEG) in a patient with epilepsia partialis continua caused by Rasmussen encephalitis before hemispherectomy. The patient had long-standing, intractable partial epilepsy since the first decade of life. Seizures included complex partial with occasional secondary generalization and repetitive myoclonus involving the left side of the body. Note the frequent epileptiform discharges at 1-2 Hz involving the right frontocentral channels. These were evident on many of the patient's routine EEGs. Clinical myoclonus is often correlated with high-voltage bursts of such activity.
Focal status epilepticus. Electroencephalograph (E Focal status epilepticus. Electroencephalograph (EEG) in a 35-year-old patient with a history of intractable partial epilepsy, in complex partial status epilepticus. The patient underwent a rapid antiepileptic drug taper as an inpatient for long-term video/EEG monitoring as a presurgical candidate. On clinical observation, the patient abruptly stopped and stared, exhibiting automatisms. This first of 2 EEG fragments covers approximately 30 seconds and illustrates the start and evolution of a seizure in the right temporal lobe. The onset appears to be at Sp2 and T4. Note the time of the event, 18:35 on May 9.
Focal status epilepticus. This electroencephalogra Focal status epilepticus. This electroencephalographic (EEG) fragment was obtained at approximately 12:39 on May 10, 18 hours after the onset of complex partial status epilepticus originating in the right temporal lobe, in a 35-year-old patient with a history of intractable partial epilepsy. Other EEG acquisitions over the interval were identical. On clinical observation, the patient was lethargic, sluggish, and vague, with variable responsivity to examiners. Note the persistent epileptiform discharges at 1.5-2.5 Hz with phase reversal mainly at Sp2 though infrequently shifting to Sp1 and F7. The bulk of the discharges are maximal at Sp2, reflecting their mesial temporal origin, with rare, subtle, and low-amplitude reflection from lateral neocortical channels (F8). Background activities are slow with admixed beta frequencies. This finding corresponds to complex partial status epilepticus.
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Computed Tomography

CT scanning of the brain is often helpful in evaluating for a structural lesion (eg, brain tumor, infarction, abscess, hemorrhage) that may underlie SE. Noncontrast CT is the imaging procedure of choice for emergency department patients with SE. However, a neuroimaging study should never be allowed to impede rapid and aggressive treatment of the disorder. Imaging is often deferred if the patient is known to have epilepsy and the seizure pattern is not unusual for the individual.

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Magnetic Resonance Imaging

Brain MRI is rarely indicated in the acute phase of generalized convulsive SE. Although MRI provides more information than CT, it is more time consuming, and the additional information rarely affects immediate treatment and evaluation.

In contrast, in a patient with simple partial SE that does not match previous seizures, the search for an epileptic focus should include brain imaging, preferably with MRI (or CT if MRI is unavailable) to look for a new lesion (eg, new stroke, mass lesion). Currently, many centers offer advanced MRI, such as diffusion-weighted, perfusion, and susceptibility-weighted imaging.[56] These newer methods can be particularly helpful in identifying acute cerebral ischemia.

Nevertheless, MRIs may be problematic in focal SE because the SE itself can cause a wide range of MRI abnormalities, many of which are transient. Repeat imaging over weeks to months may be helpful to clarify their interpretation.

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Chest Radiography

Chest radiography may be used to assess for aspiration or endotracheal tube positioning.

If clinically indicated, other plain radiographs may be useful to assess fractures or dislocations.

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Lumbar Puncture

If CNS infection is in the differential diagnosis, consider a lumbar puncture (after appropriate head imaging to ensure safety).

Initiate antibiotic therapy if CNS or systemic infection is strongly suspected.

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Contributor Information and Disclosures
Author

Julie L Roth, MD Neurologist, Epilepsy and General Neurology, Comprehensive Epilepsy Program, Rhode Island Hospital; Assistant Professor, Department of Neurology, The Warren Alpert Medical School of Brown University

Julie L Roth, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society

Disclosure: Nothing to disclose.

Coauthor(s)

Andrew S Blum, MD, PhD Director, Adult Epilepsy and EEG Laboratory, Comprehensive Epilepsy Program, Rhode Island Hospital; Associate Professor of Neurology, The Warren Alpert Medical School of Brown University

Andrew S Blum, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Massachusetts Medical Society

Disclosure: Received royalty from Springer Publishing for editor of text, the clinical neurophysiology primer.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Norberto Alvarez, MD Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children's Hospital; Medical Director, Wrentham Developmental Center

Norberto Alvarez, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Jose E Cavazos, MD, PhD, FAAN Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director of the San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and American Neurological Association

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device. No conflict with any of the Medscape Reference articles that I wrote or edited.

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

Edward H Maa, MD Chief of Comprehensive Epilepsy Program, Department of Neurology, Denver Health and Hospitals; Assistant Professor, Department of Neurology, University of Colorado School of Medicine and Veterans Affairs Medical Center

Edward H Maa, MD is a member of the following medical societies: American Academy of Neurology and American Epilepsy Society

Disclosure: UCB Pharma Honoraria Speaking and teaching

Erasmo A Passaro, MD, FAAN Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab, Bayfront Medical Center, Florida Center for Neurology

Erasmo A Passaro, MD, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association, and American Society of Neuroimaging

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Forest Honoraria Speaking and teaching

Mark Spitz, MD Professor, Department of Neurology, University of Colorado Health Sciences Center

Mark Spitz, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society

Disclosure: pfizer Honoraria Speaking and teaching; ucb Honoraria Speaking and teaching; lumdbeck Honoraria Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Treatment algorithms for convulsive status epilepticus.
Focal status epilepticus. Electroencephalograph (EEG) in a patient with epilepsia partialis continua caused by Rasmussen encephalitis before hemispherectomy. The patient had long-standing, intractable partial epilepsy since the first decade of life. Seizures included complex partial with occasional secondary generalization and repetitive myoclonus involving the left side of the body. Note the frequent epileptiform discharges at 1-2 Hz involving the right frontocentral channels. These were evident on many of the patient's routine EEGs. Clinical myoclonus is often correlated with high-voltage bursts of such activity.
Focal status epilepticus. Electroencephalograph (EEG) in a 35-year-old patient with a history of intractable partial epilepsy, in complex partial status epilepticus. The patient underwent a rapid antiepileptic drug taper as an inpatient for long-term video/EEG monitoring as a presurgical candidate. On clinical observation, the patient abruptly stopped and stared, exhibiting automatisms. This first of 2 EEG fragments covers approximately 30 seconds and illustrates the start and evolution of a seizure in the right temporal lobe. The onset appears to be at Sp2 and T4. Note the time of the event, 18:35 on May 9.
Focal status epilepticus. This electroencephalographic (EEG) fragment was obtained at approximately 12:39 on May 10, 18 hours after the onset of complex partial status epilepticus originating in the right temporal lobe, in a 35-year-old patient with a history of intractable partial epilepsy. Other EEG acquisitions over the interval were identical. On clinical observation, the patient was lethargic, sluggish, and vague, with variable responsivity to examiners. Note the persistent epileptiform discharges at 1.5-2.5 Hz with phase reversal mainly at Sp2 though infrequently shifting to Sp1 and F7. The bulk of the discharges are maximal at Sp2, reflecting their mesial temporal origin, with rare, subtle, and low-amplitude reflection from lateral neocortical channels (F8). Background activities are slow with admixed beta frequencies. This finding corresponds to complex partial status epilepticus.
 
 
 
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