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|}'''For patient information, click [[Epilepsy (patient information)|here]]'''
|}'''For patient information, click [[Epilepsy (patient information)|here]]'''
{{SI}}
{{SI}}
{{CMG}}
{{CMG}}; {{AE}} {{ZMalik}}
 
{{SK}} [[Persistent Seizure]], [[Refractory Seizure]], [[Resistant Seizure]]


==Overview==
==Overview==
'''Status epilepticus''' (SE) refers to a life threatening condition in which the [[brain]] is in a state of persistent [[seizure]].  Definitions vary, but traditionally it is defined as one continuous seizure or recurrent seizures without regaining consciousness between seizures for greater than 30 minutes. Many doctors, however, believe that 5 minutes is sufficient to damage neurons and that seizures are unlikely to self-terminate by that time.
Status epilepticus is a life-threatening neurological medical emergency caused by the prolongation of a seizure that fails to terminate due to an imbalance between excitatory and inhibitory neurotransmitters/mechanisms in the brain. It is defined as a seizure lasting 5 minutes or more, or a recurrent seizure without a recovery phase. In 1983 Gastaut identified status epilepticus as, “when an epileptic [[seizure]] is so frequently repeated or so prolonged as to create a fixed and lasting condition”. There is no established system for the [[classification]] of status epilepticus. status epilepticus may be caused by [[epilepsy]], [[stroke]], [[infection]], metabolic imbalance, cerebral trauma or [[cerebrovascular accidents]], [[hypoxia]], [[eclampsia]], and [[drug toxicity]]. Status epilepticus must be differentiated from other disorders that may mimic the clinic presentation such as [[neuroleptic malignant syndrome]], [[psychogenic nonepileptic seizures]], [[delerium tremens]], low blood sugar, and movement disorders. The [[incidence]] of status epilepticus is approximately 7 to 40 cases per 100,000/year. Common risk factors in the development of status epilepticus include inadequate control of [[epilepsy]], [[hypoglycemia]], [[stroke]], alcohol use, metabolic abnormalities, [[anoxia]], [[hypoxia]], [[tumors]], and [[infections]]. Common complications of status epilepticus include [[cardiac dysrhythmia]], metabolic derangements, [[autonomic dysfunction]], neurogenic [[pulmonary edema]], [[hyperthermia]], [[rhabdomyolysis]], and [[aspiration pneumonia]]. Brain injury can be minimized by; airway patency, adequate oxygenation/circulation, prevention of [[hypoglycemia]], maintaining optimum body temperature, termination of a [[seizure]] by antiepileptic drugs. [[Lorazepam]] is a preferred [[benzodiazepine]] due to its low lipid solubility, rapid onset, long duration of action and high affinity to [[GABA]] receptor. [[Diazepam]] can be administered if [[lorazepam]] is not available or there is no IV access.
 
==Historical Perspective==
*In 1983 Gastaut identified status epilepticus as, “when an epileptic [[seizure]] is so frequently repeated or so prolonged as to create a fixed and lasting condition”.<ref>Gastaut H. Classification of status epilepticus. In: Delgado-Escueta AV, Wasterlain CG, Treiman DM, Porter RJ, eds. Status epilepticus. New York: Raven Press, 1983:15–35.</ref>
*In 2001, 2005 Shorvon defined it as “a term used to denote a range of conditions in which electrographic seizure activity is prolonged for 30 minutes or more and results in nonconvulsive clinical symptoms”.<ref>Shorvon S. The management of status epilepticus. J Neurol Neurosurg Psychiatry 2001;70 (Suppl 2):ii22–27</ref>
*Status epilepticus was included in the classification of seizures of the International League Against Epilepsy of 1970 and 1981.<ref>{{cite journal|title=A Proposed International Classification of Epileptic Seizures|journal=Epilepsia|volume=5|issue=4|year=1964|pages=297–306|issn=0013-9580|doi=10.1111/j.1528-1157.1964.tb03337.x}}</ref>


==Classification==
==Classification==
Status epilepticus can be divided into two categories&mdash;convulsive and nonconvulsive, the latter of which is underdiagnosed.
*There is no established system for the [[classification]] of status epilepticus.
===Convulsive===
*However, various types of status epilepticus may occur as any kind of [[seizure]] may evolve into a status epilepticus can.<ref>{{cite journal|doi=10.1001/archneur.1973.00490190028002.}}</ref>
[[Epilepsia partialis continua]] is a variant involving hour, day, or even week-long jerking. It is a consequence of [[vascular disease]], [[tumour]]s, or [[encephalitis]], and is drug-resistant.
**Generalized [[Convulsive]] Status Epilepticus(GCSE), [[seizures]] last more that five minutes with tonic-clonic movement. It is the most common neurological emergency.<ref name="ScottSurtees1998">{{cite journal|last1=Scott|first1=R. C|last2=Surtees|first2=R. A H|last3=Neville|first3=B. G R|title=Status epilepticus: pathophysiology, epidemiology, and outcomes|journal=Archives of Disease in Childhood|volume=79|issue=1|year=1998|pages=73–77|issn=0003-9888|doi=10.1136/adc.79.1.73}}</ref>
**Non-[[convulsive]] Status Epilepticus can be identified on [[electroencephalogram]]([[EEG]]) with no motor convulsive activity (e.g persistent [[absence seizure]])
**Focal [[seizure]] affecting a group of muscle with/without loss of [[consciousness]].
**Myoclonic status epilepticus with prolonged jerks and epileptiform discharges on [[EEG]].
**Refractory status epilepticus, continuous [[seizure]] not responding to treatment.<ref name="WonDubinski2019">{{cite journal|last1=Won|first1=Sae‐Yeon|last2=Dubinski|first2=Daniel|last3=Sautter|first3=Lisa|last4=Hattingen|first4=Elke|last5=Seifert|first5=Volker|last6=Rosenow|first6=Felix|last7=Freiman|first7=Thomas|last8=Strzelczyk|first8=Adam|last9=Konczalla|first9=Juergen|title=Seizure and status epilepticus in chronic subdural hematoma|journal=Acta Neurologica Scandinavica|volume=140|issue=3|year=2019|pages=194–203|issn=0001-6314|doi=10.1111/ane.13131}}</ref> <ref> Harrison's Manual of Medicine 19th Edition </ref>


Generalized [[myoclonus]] is commonly seen in [[coma]]tose patients following [[CPR]] and is seen by some as an indication of catastrophic damage to the [[neocortex]].<ref name="gen-myo-se">{{cite journal | first = Eelco F. M. | last = Wijdicks | coauthors = Parisi JE, Sharbrough FW | month = February | year = 1994 | title = Prognostic value of myoclonus status in comatose survivors of cardiac arrest | journal = Annals of Neurology | volume = 35 | issue = 2 | pages = 239–43 | pmid =8109907}}</ref>
==Pathophysiology==
 
*[[Seizures]] occur due to an imbalance between excitatory and inhibitory [[neurotransmitters]]/mechanisms in the brain.
===Nonconvulsive===
*Excitatory neurotransmitters are [[glutamate]], [[aspartate]], and [[acetylcholine]].
 
*Inhibitory neurotransmitters include [[GABA]].  
[[Complex partial status epilepticus]], or CPSE, and absence status epilepticus are rare forms of the condition which are marked by nonconvulsive seizures. In the case of CPSE, the seizure is confined to a small area of the brain, normally the temporal lobe. But the latter, absence status epilepticus, is marked by a generalised seizure affecting the whole brain, and an [[Electroencephalogram|EEG]] is needed to differentiate between the two conditions. This results in episodes characterized by a long-lasting stupor, staring and unresponsiveness.
*The disturbance in calcium ion-dependent potassium ion current and magnesium blockade of N-methyl-d-aspartate ([[NMDA]]) play a role in the prolongation of seizures.  
*Status epilepticus occurs due to failure in termination of [[seizure]].
*Prolonged status epilepticus is more likely to develop resistance to drugs and have poor [[prognosis]].


==Causes==
==Causes==
In known epileptics, this condition is associated with poor [[compliance (medicine)|compliance]] (adherence to medication regimen), [[alcohol]] withdrawal, and [[metabolism|metabolic]] disturbances. As a primary presentation it normally indicates a [[tumour]] or [[abscess]].
*Following are the conditions that could lead to a status epilepticus:
**[[Epilepsy]]: Approximately twenty-five percent of patients with status epilepticus have [[epilepsy]].<ref name="StasiukynienėPilvinis2009">{{cite journal|last1=Stasiukynienė|first1=Virginija|last2=Pilvinis|first2=Vidas|last3=Reingardienė|first3=Dagmara|last4=Janauskaitė|first4=Liuda|title=Epileptic seizures in critically ill patients|journal=Medicina|volume=45|issue=6|year=2009|pages=501|issn=1010-660X|doi=10.3390/medicina45060066}}</ref>
**Stroke<ref name="StasiukynienėPilvinis2009">{{cite journal|last1=Stasiukynienė|first1=Virginija|last2=Pilvinis|first2=Vidas|last3=Reingardienė|first3=Dagmara|last4=Janauskaitė|first4=Liuda|title=Epileptic seizures in critically ill patients|journal=Medicina|volume=45|issue=6|year=2009|pages=501|issn=1010-660X|doi=10.3390/medicina45060066}}</ref>
**Infections: CNS infections such as [[meningitis]], [[encephalitis]] or brain [[abscess]]. Other infections that cause fever, especially in children.
**Metabolic abnormalities: This could be a result of underlying [[renal]] or [[hepatic]] pathology causing [[hyponatremia]], [[hypoglycemia]] or [[hypocalcemia]].
**[[Cerebral]] trauma or [[cerebrovascular accidents]] due to [[hypertensive]] crisis.<ref name="LangenbruchKrämer2019">{{cite journal|last1=Langenbruch|first1=Lisa|last2=Krämer|first2=Julia|last3=Güler|first3=Sati|last4=Möddel|first4=Gabriel|last5=Geßner|first5=Sophia|last6=Melzer|first6=Nico|last7=Elger|first7=Christian E.|last8=Wiendl|first8=Heinz|last9=Budde|first9=Thomas|last10=Meuth|first10=Sven G.|last11=Kovac|first11=Stjepana|title=Seizures and epilepsy in multiple sclerosis: epidemiology and prognosis in a large tertiary referral center|journal=Journal of Neurology|volume=266|issue=7|year=2019|pages=1789–1795|issn=0340-5354|doi=10.1007/s00415-019-09332-x}}</ref>
**Alteration in [[anticonvulsive]] therapy including but not limited to sudden withdrawal or sub-optimal dosing, concomitant alcohol consumption, inadequate nutrition, starting a new medication that is non-compatible with anticonvulsive drugs and/or drug resistance.
**[[Hypoxia]]<ref name="LangenbruchKrämer2019">{{cite journal|last1=Langenbruch|first1=Lisa|last2=Krämer|first2=Julia|last3=Güler|first3=Sati|last4=Möddel|first4=Gabriel|last5=Geßner|first5=Sophia|last6=Melzer|first6=Nico|last7=Elger|first7=Christian E.|last8=Wiendl|first8=Heinz|last9=Budde|first9=Thomas|last10=Meuth|first10=Sven G.|last11=Kovac|first11=Stjepana|title=Seizures and epilepsy in multiple sclerosis: epidemiology and prognosis in a large tertiary referral center|journal=Journal of Neurology|volume=266|issue=7|year=2019|pages=1789–1795|issn=0340-5354|doi=10.1007/s00415-019-09332-x}}</ref>
**Drug toxicity<ref name="LangenbruchKrämer2019">{{cite journal|last1=Langenbruch|first1=Lisa|last2=Krämer|first2=Julia|last3=Güler|first3=Sati|last4=Möddel|first4=Gabriel|last5=Geßner|first5=Sophia|last6=Melzer|first6=Nico|last7=Elger|first7=Christian E.|last8=Wiendl|first8=Heinz|last9=Budde|first9=Thomas|last10=Meuth|first10=Sven G.|last11=Kovac|first11=Stjepana|title=Seizures and epilepsy in multiple sclerosis: epidemiology and prognosis in a large tertiary referral center|journal=Journal of Neurology|volume=266|issue=7|year=2019|pages=1789–1795|issn=0340-5354|doi=10.1007/s00415-019-09332-x}}</ref>
**[[Eclampsia]]


It can also be induced by [[nerve agent]]s such as [[soman]].<ref name="soman">{{cite journal | first = John H. | last = McDonough | coauthors = A. Benjamin, Joseph D. McMonagle, Thomas Rowland, Shih Tsung-Ming | month = February | year = 2004 | title = Effects of fosphenytoin on nerve agent-induced status epilepticus | journal = Drug and Chemical Toxicology | volume = 27 | issue = 1 | pages = 27–39 | pmid = 15038246 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=15038246&dopt=ExternalLink}}</ref>
==Differentiating Status epilepticus from other Diseases==
*Status epilepticus must be differentiated from other disorders that may mimic the clinic presentation such as [[neuroleptic malignant syndrome]], [[psychogenic nonepileptic seizures]], [[delerium tremens]], low blood sugar, and movement disorders. <ref name="Al-MuftiClaassen2014">{{cite journal|last1=Al-Mufti|first1=Fawaz|last2=Claassen|first2=Jan|title=Neurocritical Care|journal=Critical Care Clinics|volume=30|issue=4|year=2014|pages=751–764|issn=07490704|doi=10.1016/j.ccc.2014.06.006}}</ref>


===Drug Causes===
==Epidemiology and Demographics==
*The [[incidence]] of status epilepticus is approximately 7 to 40 cases per 100,000/year.
*Status epilepticus seems to be more common in males.


* [[Nelarabine]]
==Risk Factors==
* [[Rufinamide]]
*Common risk factors in the development of status epilepticus include inadequate control of [[epilepsy]], [[hypoglycemia]], [[stroke]], alcohol use, metabolic abnormalities, [[anoxia]], [[hypoxia]], [[tumors]], and [[infections]].<ref name="Fountain2000">{{cite journal|last1=Fountain|first1=Nathan B.|title=Status Epilepticus: Risk Factors and Complications|journal=Epilepsia|volume=41|issue=s2|year=2000|pages=S23–S30|issn=0013-9580|doi=10.1111/j.1528-1157.2000.tb01521.x}}</ref>


==Treatments==
==Screening==
*There is insufficient evidence to recommend routine [[screening]] for status epilepticus.


===Benzodiazepines===
==Natural History, Complications, and Prognosis==
*Common complications of status epilepticus include [[cardiac dysrhythmia]], metabolic derangements, [[autonomic dysfunction]], neurogenic [[pulmonary edema]], [[hyperthermia]], [[rhabdomyolysis]], and [[aspiration pneumonia]]. <ref name="SutterDittrich2018">{{cite journal|last1=Sutter|first1=Raoul|last2=Dittrich|first2=Tolga|last3=Semmlack|first3=Saskia|last4=Rüegg|first4=Stephan|last5=Marsch|first5=Stephan|last6=Kaplan|first6=Peter W.|title=Acute Systemic Complications of Convulsive Status Epilepticus—A Systematic Review|journal=Critical Care Medicine|volume=46|issue=1|year=2018|pages=138–145|issn=0090-3493|doi=10.1097/CCM.0000000000002843}}</ref>
*Permanent [[neurologic]] damage can occur with prolonged status epilepticus.
*Prognosis of status epilepticus depends upon the underlying cause, age, and medical condition of the patient. Overall mortality rate of status epilepticus is 7%–39%.<ref name="TownePellock1994">{{cite journal|last1=Towne|first1=Alan R.|last2=Pellock|first2=John M.|last3=Ko|first3=Daijin|last4=DeLorenzo|first4=Robert J.|title=Determinants of Mortality in Status Epilepticus|journal=Epilepsia|volume=35|issue=1|year=1994|pages=27–34|issn=0013-9580|doi=10.1111/j.1528-1157.1994.tb02908.x}}</ref>
*Approximately 10 to 30% of patients with underlying [[brain]] condition who have status epilepticus die within 30 days.<ref name="Al-MuftiClaassen2014">{{cite journal|last1=Al-Mufti|first1=Fawaz|last2=Claassen|first2=Jan|title=Neurocritical Care|journal=Critical Care Clinics|volume=30|issue=4|year=2014|pages=751–764|issn=07490704|doi=10.1016/j.ccc.2014.06.006}}</ref>
*Patients with [[epilepsy]] and who develop status epilepticus have increased [[mortality]] risk. However, stabilizing condition and optimal maintenance of medication, sleep, stress factors and stimulants plays an important role in improving [[prognosis]]. <ref name="StasiukynienėPilvinis2009">{{cite journal|last1=Stasiukynienė|first1=Virginija|last2=Pilvinis|first2=Vidas|last3=Reingardienė|first3=Dagmara|last4=Janauskaitė|first4=Liuda|title=Epileptic seizures in critically ill patients|journal=Medicina|volume=45|issue=6|year=2009|pages=501|issn=1010-660X|doi=10.3390/medicina45060066}}</ref>


Shortly after it was introduced in 1963, [[diazepam]] became the first choice for SE. Even though other [[benzodiazepine]]s such as [[clonazepam]] were useful, diazepam was relied upon almost exclusively. This began to change in 1975 with a preliminary study on [[lorazepam]] conducted by
==Diagnosis==
Waltregny and Dargent, who found that its pharmacological effects were longer lasting than those of an equal dose of diazepam.<ref name="waltdar">{{cite journal | first = Alain | last = Waltregny | coauthors = Jérôme Dargent | month = September/October | year = 1975 | title = Preliminary study of parenteral lorazepam in status epilepticus | journal = Acta Neurologica Belgica | volume = 75 | issue = 5 | pages = 219–29 | pmid = 3939}}</ref> This meant it did not have to be repeatedly injected like diazepam,<ref name="lorazepam1979">{{cite journal | first = JE | last = Walker | coauthors = RW Homan, MR Vasko, IL Crawford, RD Bell, WG Tasker | month = September | year = 1979 | title = Lorazepam in status epilepticus | journal = Annals of Neurology | volume = 6 | issue = 3 | pages = 207–13 | pmid = 43112}}</ref> the effects of which would wear off 5–15 minutes later in spite of its 30-hour [[half-life]] (due to extensive redistribution of diazepam outside the vascular compartment as diazepam is highly lipid soluble). It has also been found that patients who were first tried on diazepam were much more likely to require [[tracheotomy|endotracheal tubing]] than patients who were first tried on [[phenobarbital]], [[phenytoin]],<ref name="vspbandpht">{{cite journal | first = Richard A. | last = Orr | coauthors = Robert J. Dimand, Shekhar T. Venkataraman, Valerie A. Karr, Kathleen J. Kennedy | month = September | year = 1991 | title = Diazepam and intubation in emergency treatment of seizures in children | journal = Annals of Emergency Medicine | volume = 20 | issue = 9 | pages = 1009–13 | pmid = 1877765 |  doi = 10.1016/S0196-0644(05)82981-6 | url = http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WB0-4G82KTB-G&_coverDate=09%2F30%2F1991&_alid=434858892&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=6696&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=fab697f11c8e05b7fe0405b1d34a6f7d}}</ref> or lorazepam.<ref name="vslorazepam">{{cite journal | first = Richard | last = Appleton | coauthors = A. Sweeney, Imti Choonara, Joan Robson, Elizabeth Molyneux. | month = August | year = 1995 | title = Lorazepam versus diazepam in the acute treatment of epileptic seizures and status epilepticus | journal = Developmental Medicine and Child Neurology | volume = 37 | issue = 8 | pages = 682–8 | pmid = 7672465}}</ref>
'''Diagnostic Study of Choice'''
*There are no established criteria for the diagnosis of status epilepticus. However clinical manifestation, duration, [[EEG]] findings can aid in the diagnosis and identification of the underlying cause.


Today, the benzodiazepine of choice is [[lorazepam]] 0.02-0.03mg/kg IV, for initial treatment due to its long (2–8 hour) duration of action and rapid onset of action, thought to be due to its high affinity for GABA receptors and to its low lipid solubility which causes it to remain in the vascular compartment.  If lorazepam is not available, then diazepam 0.1mg/kg IV or [[midazolam]] 0.05mg/kg IV should be given.<ref name="benzo-of-choice">{{cite journal | first = Trudy | last = Pang | coauthors = Lawrence J. Hirsch | month = July | year = 2005 | title = Treatment of Convulsive and Nonconvulsive Status Epilepticus | journal = Current Treatment Options in Neurology | volume = 7 | issue = 4 | pages = 247–259 | pmid = 15967088 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=15967088&dopt=ExternalLink}}</ref> If IV access cannot be obtained, [[midazolam]] 10mg (if wt>40kg) or 5mg (if wt<40kg) can be administered via IM route<ref name="pmid22335736">{{cite journal| author=Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y et al.| title=Intramuscular versus intravenous therapy for prehospital status epilepticus. | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 7 | pages= 591-600 | pmid=22335736 | doi=10.1056/NEJMoa1107494 | pmc=PMC3307101 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22335736  }} </ref>. Sometimes, the failure of lorazepam alone is considered to be enough to classify a case of SE as [[Wiktionary:refractory|refractory]].
'''History and Symptoms'''
*Status epilepticus is identified as a [[seizure]] lasting more than 5 mins or recurrent [[seizures]] without a recovery period.
*Patient may have a recent history of [[infection]] with [[fever]], head trauma, alteration in medication, sleep deprivation, alcohol use/withdrawal.  
*Past medical history of the patient could include stroke, prior [[seizures]], [[meningitis]], [[encephalitis]].  


===Phenytoin and fosphenytoin===
'''Physical Examination'''
*Consciousness may be impaired.
*Rhythmic tonic-clonic movement may be present in patients with generalized convulsive status epilepticus. Non-convulsive status epilepticus may appear on an [[EEG]].
*In the post-ictal period focal neurological deficit may be present.
*In suspected drug use, look for needle marks.
*Presence of [[papilledema[[ could suggest a brain mass/[[abscess]]. 


Phenytoin was once another first-line therapy, although the [[prodrug]] [[fosphenytoin]] can be administered three times as fast and with far fewer injection site reactions. If these or any other [[hydantoin|hydantoin derivative]]s are used, then cardiac monitoring is a must if they are administered intravenously. Because the hydantoins take 15–30 minutes to work, a benzodiazepine or barbiturate is often co-administered. Because of diazepam's short duration of action, they were often administered together anyway.
'''Laboratory Findings'''
*There are no diagnostic laboratory findings associated with status epilepticus.
*However, electrolyte, [[BUN]], [[creatinine]], [[glucose]], [[LFT]], toxicology, pregnancy test(in women of child-bearing age) and medication level should be checked to identify the underlying cause.


===Barbiturates===
'''Electrocardiogram'''
*There are no [[ECG]] findings associated with status epilepticus.


Before the benzodiazepines were invented, there were the barbiturates, which are still used today if benzodiazepines or the hydantoins are not an option. These are used to induce a  [[barbiturate|barbituric]] coma. The barbiturate most commonly used for this is phenobarbital. [[Thiopental]] or [[pentobarbital]] may also be used for that purpose if the seizures have to be stopped immediately or if the patient has already been compromised by the underlying illness or toxic/metabolic-induced seizures; however, in those situations, thiopental is the agent of choice.
'''X-ray'''
*There are no x-ray findings associated with status epilepticus.


The failure of phenobarbital therapy does not preclude the success of a lengthy comatose state induced by a stronger barbiturate such as [[secobarbital]]. Such was the case for Ohori, Fujioka, and Ohta ca. 1998, when they induced a 10-month long coma (or "anesthesia" as they called it) in a 26-year-old woman suffering from refractory status epilepticus secondary to [[encephalitis|viral encephalitis]] and then tapered her off the secobarbital very slowly while using [[zonisamide]] at the same time.<ref name="secobarbitalofo">{{cite journal | first = Nobuhira | last = Ohori | coauthors = Fujioka Y, Ohta M. | month = May | year = 1998 | title = [Experience in managing refractory status epilepticus caused by viral encephalitis under long-term anesthesia with barbiturate: a case report] | journal = Rinsho Shinkeigaku | volume = 38 | issue = 5 | pages = 474–7 | pmid = 9806000}} (Japanese)</ref>
'''Echocardiography or Ultrasound'''
*There are no [[echocardiography]]/[[ultrasound]] findings associated with status epilepticus.


===General anesthetics===
'''CT scan'''
*There are no [[CT]] scan findings associated with status epilepticus.
*In patients with a previous history of [[stroke]] may appear on CT scan.


If this proves ineffective or if barbiturates cannot be used for some reason, then a [[general anesthetic]] such as [[propofol]]<ref name="propofol">{{cite journal | first = X | last = Pourrat | coauthors = JM Serekian, D Antier, J. Grassin | title = [Generalized tonic-clonic status epilepticus: therapeutic strategy] | journal = Presse Médicale | volume = 30 | issue = | date = June 9, 2001 | pages = 1031–6 | pmid = 11433696}} (French).</ref> is tried; sometimes it is used second after the failure of [[lorazepam]].<ref name="propofol2">{{cite journal | first = Paul E. | last = Marik | coauthors = Joseph Varon | title = The management of status epilepticus | journal = Chest | year = 2004 | volume = 126 | issue = 2 | pages = 582–91 | pmid = 15302747 | url = http://www.chestjournal.org/cgi/content/full/126/2/582}}</ref> This also means putting the patient on artificial respiration. Propofol has been shown to be effective in suppressing the jerks seen in myoclonus status epilepticus, but as of 2002, there have been no cases of anyone going into myoclonus status epilepticus, undergoing propofol treatment, and then not dying anyway.<ref name="propofolmse">{{cite journal | first = Eelco F.M. | last = Wijdicks | year = 2002 | month = July | title = Propofol in myoclonus status epilepticus in comatose patients following cardiac resuscitation | journal = Journal of Neurology Neurosurgery and Psychiatry | volume = 73 | issue = 1 | pages = 94–5 | pmid = 12082068 | url = http://jnnp.bmjjournals.com/cgi/content/full/73/1/94}}</ref>
'''MRI'''
*Variable [[MRI]] changes have been noticed in patients with status epilepticus but it is not present in every patient.
*The findings suggest cytotoxic and vasogenic [[edema]] due to prolonged seizure activity.


===Lidocaine===
'''Other Imaging Findings'''
*There are no other imaging findings associated with status epilepticus.


The use of [[lidocaine]] in status epilepticus was first reported in 1955 by Bernhard, Boem and Hojeberg.<ref name="lidocaine1955">{{cite journal | first = CG | last = Bernhard | coauthors = Bohm E, Hojeberg S | month = August | year = 1955 | title = A new treatment of status epilepticus; intravenous injections of a local anesthetic (lidocaine) | journal = AMA Archives of Neurology and  Psychiatry | volume = 74 | issue = 2 | page = 208–14 | pmid = 14397899}}</ref> Since then, it has been used in cases refractory to phenobarbital, diazepam, and phenytoin, and has been studied as an alternative to barbiturates and general anesthetics.<ref name="lidocainepro">{{cite journal | first = Praveen | last = Aggarwal | coauthors = Jyoti Prakash Wali | month = May | year = 1993 | title = Lidocaine in refractory status epilepticus: a forgotten drug in the emergency department | journal = American Journal of Emergency Medicine | volume = 11 | issue = 3 | pages = 243–4 | pmid = 93257009 | doi = 10.1016/0735-6757(93)90135-X | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=8489668&dopt=ExternalLink}}</ref><ref name="lidocainepro2">{{cite journal | first = N | last = Sugiyama | coauthors = Hamano S, Mochizuki M, Tanaka M, Eto Y | month = November | year = 2004 | title = [Efficacy of lidocaine on seizures by intravenous and intravenous-drip infusion] | journal = No To Hattatsu | volume = 36 | issue = 6 | pages = 451–4 | pmid = 15560386}} (Japanese)</ref> Lidocaine is a [[sodium channel]] blocker and has been used where sodium channel dysfunction was suspected.<ref name="sodium-channel-dysfunction">{{cite journal | author = Sawaishi Yukio | coauthors = Yano Tamami, Enoki Masamichi, and Takada Goro | month = February | year = 2002 | title = Lidocaine-dependent early infantile status epilepticus with highly suppressed EEG | journal = Epilepsia | volume = 43 | issue = 2 | pages = 201–4 | pmid = 11903470 | doi = 10.1046/j.1528-1157.2002.25301.x}}</ref> However, in some studies, it was either ineffective or even harmful for most patients.<ref name="lidocainecon">{{cite journal | author = Tanabe Takuya | coauthors = Suzuki Shuuhei, Shimakawa Shuichi, Yamashiro Kuniteru<!--The original kanji for "Kuniteru(?)" were 國暉. Please find the actual pronunciation if that is incorrect!-->, Tamai Hiroshi | month = January | year = 1999 | title = Problems of intravenous lidocaine treatment in status epilepticus or clustering seizures in childhood | journal = [http://www.meteo-intergate.com/journal/journal-archive_cl1nohat.html No To Hattatsu] | volume = 31 | issue = 1 | pages = 14–20 | pmid = 10025129}} (Japanese)</ref> The last is not so surprising in light of the fact that lidocaine has been known to cause seizures in humans and laboratory animals at doses greater than 15&nbsp;µg/mL<ref name="pro-and-anticonvulsant">{{cite journal | first = John C. | last = DeToledo | month = June | year = 2000 | title = Lidocaine and Seizures | journal = Therapeutic Drug Monitoring | volume = 22 | issue = 3 | pages = 320–322 | pmid = 10850400}}</ref> or 2–3&nbsp;mg/kg.<ref name="pro-and-anticonvulsant2">{{cite web | author=Steven C. Schachter | title=Lidocaine | url=http://professionals.epilepsy.com/page/local_lidocaine.html | publisher=epilepsy.com/professionals}} Adapted from: {{cite book | author=Najjar S, Devinsky O, Rosenberg AD, et al | editor=ed. Ettinger AB and Devinsky O | title=Managing epilepsy and co-existing disorders | chapter=Procedures in epilepsy  patients | year=2002 | pages=499–513 | publisher=Butterworth-Heinemann | location=Boston | isbn=0-7506-7241-2}}</ref>
'''Other Diagnostic Studies'''
*[[Electroencephalogram]] (EEG) is very important in recognizing and classifying the type of status epilepticus supported by clinical semiology.


==References==
==Treatments==
{{Reflist|2}}
'''Medical Therapy'''
{{-}}
*Brain injury can be minimized by; airway patency, adequate oxygenation/circulation, prevention of [[hypoglycemia]], maintaining optimum body temperature, termination of a [[seizure]] by antiepileptic drugs.
{{Diseases of the nervous system}}
*For tonic-clonic status epilepticus treatment should be initiated in 5 minutes. For focal status epilepticus treatment should be initiated in 10 minutes.<ref name="TrinkaCock2015">{{cite journal|last1=Trinka|first1=Eugen|last2=Cock|first2=Hannah|last3=Hesdorffer|first3=Dale|last4=Rossetti|first4=Andrea O.|last5=Scheffer|first5=Ingrid E.|last6=Shinnar|first6=Shlomo|last7=Shorvon|first7=Simon|last8=Lowenstein|first8=Daniel H.|title=A definition and classification of status epilepticus - Report of the ILAE Task Force on Classification of Status Epilepticus|journal=Epilepsia|volume=56|issue=10|year=2015|pages=1515–1523|issn=00139580|doi=10.1111/epi.13121}}</ref>
*[[Benzodiazepines]] are the antiepileptic drug of choice for initial managment. <ref name="Al-MuftiClaassen2014">{{cite journal|last1=Al-Mufti|first1=Fawaz|last2=Claassen|first2=Jan|title=Neurocritical Care|journal=Critical Care Clinics|volume=30|issue=4|year=2014|pages=751–764|issn=07490704|doi=10.1016/j.ccc.2014.06.006}}</ref> [[Lorazepam]] is a preferred [[benzodiazepine]] due to its low lipid solubility,  rapid onset, long duration of action and high affinity to [[GABA]] receptor. [[Diazepam]] can be administered if [[lorazepam]] is not available or there is no IV access.
*Other [[antiepileptic]] drugs like [[fosphenytoin]], [[phenytoin]], [[levetiracetam]], and [[valproic acid]] can be co-administered.
*Status epilepticus is considered [[refractory]] to [[benzodiazepine]] if two rounds of the medication fail to terminate the seizure.
*In case of refractory status epilepticus continuous intravenous (IV) infusion of [[midazolam]], [[pentobarbital]], or [[propofol]] should be administered.<ref> Harrison's Manual of Medicine 19th Edition </ref>
*For status epilepticus induced by [[eclampsia]] in pregnant women, magnesium sulfate is the drug of choice.
 
'''Surgery'''
*Surgical intervention is not recommended for the management of status epilepticus.
*However, the underlying cause of status epilepticus including the brain [[abscess]] or brain [[tumor]] could benefit from a surgical procedure.


'''Primary Prevention'''
*There are no established measures for the primary prevention of status epilepticus.
*Prevention of epileptic [[seizure]] or [[seizures]] due to [[hypoglycemia]], [[alcohol]] abuse, [[hyperthermia]] can contribute to prevention of status epilepticus.


[[Category:Neurology]]
'''Secondary Prevention'''
[[Category:Medical emergencies]]
*There are no established measures for the secondary prevention of status epilepticus.
[[Category:Epilepsy]]
*Patients with a prior episode of status epilepticus can prevent future episodes by controlling the aforementioned risk factors.
[[Category:Emergency medicine]]
[[Category:Overview complete]]
[[de:status epilepticus]]
[[nl:Status epilepticus]]
[[ru:Эпилептический статус]]
[[fi:Status epilepticus]]


 
==References==
{{WH}}
{{WS}}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Synonyms and keywords: Persistent Seizure, Refractory Seizure, Resistant Seizure

Overview

Status epilepticus is a life-threatening neurological medical emergency caused by the prolongation of a seizure that fails to terminate due to an imbalance between excitatory and inhibitory neurotransmitters/mechanisms in the brain. It is defined as a seizure lasting 5 minutes or more, or a recurrent seizure without a recovery phase. In 1983 Gastaut identified status epilepticus as, “when an epileptic seizure is so frequently repeated or so prolonged as to create a fixed and lasting condition”. There is no established system for the classification of status epilepticus. status epilepticus may be caused by epilepsy, stroke, infection, metabolic imbalance, cerebral trauma or cerebrovascular accidents, hypoxia, eclampsia, and drug toxicity. Status epilepticus must be differentiated from other disorders that may mimic the clinic presentation such as neuroleptic malignant syndrome, psychogenic nonepileptic seizures, delerium tremens, low blood sugar, and movement disorders. The incidence of status epilepticus is approximately 7 to 40 cases per 100,000/year. Common risk factors in the development of status epilepticus include inadequate control of epilepsy, hypoglycemia, stroke, alcohol use, metabolic abnormalities, anoxia, hypoxia, tumors, and infections. Common complications of status epilepticus include cardiac dysrhythmia, metabolic derangements, autonomic dysfunction, neurogenic pulmonary edema, hyperthermia, rhabdomyolysis, and aspiration pneumonia. Brain injury can be minimized by; airway patency, adequate oxygenation/circulation, prevention of hypoglycemia, maintaining optimum body temperature, termination of a seizure by antiepileptic drugs. Lorazepam is a preferred benzodiazepine due to its low lipid solubility, rapid onset, long duration of action and high affinity to GABA receptor. Diazepam can be administered if lorazepam is not available or there is no IV access.

Historical Perspective

  • In 1983 Gastaut identified status epilepticus as, “when an epileptic seizure is so frequently repeated or so prolonged as to create a fixed and lasting condition”.[1]
  • In 2001, 2005 Shorvon defined it as “a term used to denote a range of conditions in which electrographic seizure activity is prolonged for 30 minutes or more and results in nonconvulsive clinical symptoms”.[2]
  • Status epilepticus was included in the classification of seizures of the International League Against Epilepsy of 1970 and 1981.[3]

Classification

  • There is no established system for the classification of status epilepticus.
  • However, various types of status epilepticus may occur as any kind of seizure may evolve into a status epilepticus can.[4]
    • Generalized Convulsive Status Epilepticus(GCSE), seizures last more that five minutes with tonic-clonic movement. It is the most common neurological emergency.[5]
    • Non-convulsive Status Epilepticus can be identified on electroencephalogram(EEG) with no motor convulsive activity (e.g persistent absence seizure)
    • Focal seizure affecting a group of muscle with/without loss of consciousness.
    • Myoclonic status epilepticus with prolonged jerks and epileptiform discharges on EEG.
    • Refractory status epilepticus, continuous seizure not responding to treatment.[6] [7]

Pathophysiology

  • Seizures occur due to an imbalance between excitatory and inhibitory neurotransmitters/mechanisms in the brain.
  • Excitatory neurotransmitters are glutamate, aspartate, and acetylcholine.
  • Inhibitory neurotransmitters include GABA.
  • The disturbance in calcium ion-dependent potassium ion current and magnesium blockade of N-methyl-d-aspartate (NMDA) play a role in the prolongation of seizures.
  • Status epilepticus occurs due to failure in termination of seizure.
  • Prolonged status epilepticus is more likely to develop resistance to drugs and have poor prognosis.

Causes

Differentiating Status epilepticus from other Diseases

Epidemiology and Demographics

  • The incidence of status epilepticus is approximately 7 to 40 cases per 100,000/year.
  • Status epilepticus seems to be more common in males.

Risk Factors

Screening

  • There is insufficient evidence to recommend routine screening for status epilepticus.

Natural History, Complications, and Prognosis

  • Common complications of status epilepticus include cardiac dysrhythmia, metabolic derangements, autonomic dysfunction, neurogenic pulmonary edema, hyperthermia, rhabdomyolysis, and aspiration pneumonia. [12]
  • Permanent neurologic damage can occur with prolonged status epilepticus.
  • Prognosis of status epilepticus depends upon the underlying cause, age, and medical condition of the patient. Overall mortality rate of status epilepticus is 7%–39%.[13]
  • Approximately 10 to 30% of patients with underlying brain condition who have status epilepticus die within 30 days.[10]
  • Patients with epilepsy and who develop status epilepticus have increased mortality risk. However, stabilizing condition and optimal maintenance of medication, sleep, stress factors and stimulants plays an important role in improving prognosis. [8]

Diagnosis

Diagnostic Study of Choice

  • There are no established criteria for the diagnosis of status epilepticus. However clinical manifestation, duration, EEG findings can aid in the diagnosis and identification of the underlying cause.

History and Symptoms

  • Status epilepticus is identified as a seizure lasting more than 5 mins or recurrent seizures without a recovery period.
  • Patient may have a recent history of infection with fever, head trauma, alteration in medication, sleep deprivation, alcohol use/withdrawal.
  • Past medical history of the patient could include stroke, prior seizures, meningitis, encephalitis.

Physical Examination

  • Consciousness may be impaired.
  • Rhythmic tonic-clonic movement may be present in patients with generalized convulsive status epilepticus. Non-convulsive status epilepticus may appear on an EEG.
  • In the post-ictal period focal neurological deficit may be present.
  • In suspected drug use, look for needle marks.
  • Presence of [[papilledema[[ could suggest a brain mass/abscess.

Laboratory Findings

  • There are no diagnostic laboratory findings associated with status epilepticus.
  • However, electrolyte, BUN, creatinine, glucose, LFT, toxicology, pregnancy test(in women of child-bearing age) and medication level should be checked to identify the underlying cause.

Electrocardiogram

  • There are no ECG findings associated with status epilepticus.

X-ray

  • There are no x-ray findings associated with status epilepticus.

Echocardiography or Ultrasound

CT scan

  • There are no CT scan findings associated with status epilepticus.
  • In patients with a previous history of stroke may appear on CT scan.

MRI

  • Variable MRI changes have been noticed in patients with status epilepticus but it is not present in every patient.
  • The findings suggest cytotoxic and vasogenic edema due to prolonged seizure activity.

Other Imaging Findings

  • There are no other imaging findings associated with status epilepticus.

Other Diagnostic Studies

  • Electroencephalogram (EEG) is very important in recognizing and classifying the type of status epilepticus supported by clinical semiology.

Treatments

Medical Therapy

  • Brain injury can be minimized by; airway patency, adequate oxygenation/circulation, prevention of hypoglycemia, maintaining optimum body temperature, termination of a seizure by antiepileptic drugs.
  • For tonic-clonic status epilepticus treatment should be initiated in 5 minutes. For focal status epilepticus treatment should be initiated in 10 minutes.[14]
  • Benzodiazepines are the antiepileptic drug of choice for initial managment. [10] Lorazepam is a preferred benzodiazepine due to its low lipid solubility, rapid onset, long duration of action and high affinity to GABA receptor. Diazepam can be administered if lorazepam is not available or there is no IV access.
  • Other antiepileptic drugs like fosphenytoin, phenytoin, levetiracetam, and valproic acid can be co-administered.
  • Status epilepticus is considered refractory to benzodiazepine if two rounds of the medication fail to terminate the seizure.
  • In case of refractory status epilepticus continuous intravenous (IV) infusion of midazolam, pentobarbital, or propofol should be administered.[15]
  • For status epilepticus induced by eclampsia in pregnant women, magnesium sulfate is the drug of choice.

Surgery

  • Surgical intervention is not recommended for the management of status epilepticus.
  • However, the underlying cause of status epilepticus including the brain abscess or brain tumor could benefit from a surgical procedure.

Primary Prevention

Secondary Prevention

  • There are no established measures for the secondary prevention of status epilepticus.
  • Patients with a prior episode of status epilepticus can prevent future episodes by controlling the aforementioned risk factors.

References

  1. ↑ Gastaut H. Classification of status epilepticus. In: Delgado-Escueta AV, Wasterlain CG, Treiman DM, Porter RJ, eds. Status epilepticus. New York: Raven Press, 1983:15–35.
  2. ↑ Shorvon S. The management of status epilepticus. J Neurol Neurosurg Psychiatry 2001;70 (Suppl 2):ii22–27
  3. ↑ "A Proposed International Classification of Epileptic Seizures". Epilepsia. 5 (4): 297–306. 1964. doi:10.1111/j.1528-1157.1964.tb03337.x. ISSN 0013-9580.
  4. ↑ . doi:10.1001/archneur.1973.00490190028002. Check |doi= value (help). Missing or empty |title= (help)
  5. ↑ Scott, R. C; Surtees, R. A H; Neville, B. G R (1998). "Status epilepticus: pathophysiology, epidemiology, and outcomes". Archives of Disease in Childhood. 79 (1): 73–77. doi:10.1136/adc.79.1.73. ISSN 0003-9888.
  6. ↑ Won, Sae‐Yeon; Dubinski, Daniel; Sautter, Lisa; Hattingen, Elke; Seifert, Volker; Rosenow, Felix; Freiman, Thomas; Strzelczyk, Adam; Konczalla, Juergen (2019). "Seizure and status epilepticus in chronic subdural hematoma". Acta Neurologica Scandinavica. 140 (3): 194–203. doi:10.1111/ane.13131. ISSN 0001-6314.
  7. ↑ Harrison's Manual of Medicine 19th Edition
  8. ↑ 8.0 8.1 8.2 Stasiukynienė, Virginija; Pilvinis, Vidas; Reingardienė, Dagmara; Janauskaitė, Liuda (2009). "Epileptic seizures in critically ill patients". Medicina. 45 (6): 501. doi:10.3390/medicina45060066. ISSN 1010-660X.
  9. ↑ 9.0 9.1 9.2 Langenbruch, Lisa; Krämer, Julia; Güler, Sati; Möddel, Gabriel; Geßner, Sophia; Melzer, Nico; Elger, Christian E.; Wiendl, Heinz; Budde, Thomas; Meuth, Sven G.; Kovac, Stjepana (2019). "Seizures and epilepsy in multiple sclerosis: epidemiology and prognosis in a large tertiary referral center". Journal of Neurology. 266 (7): 1789–1795. doi:10.1007/s00415-019-09332-x. ISSN 0340-5354.
  10. ↑ 10.0 10.1 10.2 Al-Mufti, Fawaz; Claassen, Jan (2014). "Neurocritical Care". Critical Care Clinics. 30 (4): 751–764. doi:10.1016/j.ccc.2014.06.006. ISSN 0749-0704.
  11. ↑ Fountain, Nathan B. (2000). "Status Epilepticus: Risk Factors and Complications". Epilepsia. 41 (s2): S23–S30. doi:10.1111/j.1528-1157.2000.tb01521.x. ISSN 0013-9580.
  12. ↑ Sutter, Raoul; Dittrich, Tolga; Semmlack, Saskia; Rüegg, Stephan; Marsch, Stephan; Kaplan, Peter W. (2018). "Acute Systemic Complications of Convulsive Status Epilepticus—A Systematic Review". Critical Care Medicine. 46 (1): 138–145. doi:10.1097/CCM.0000000000002843. ISSN 0090-3493.
  13. ↑ Towne, Alan R.; Pellock, John M.; Ko, Daijin; DeLorenzo, Robert J. (1994). "Determinants of Mortality in Status Epilepticus". Epilepsia. 35 (1): 27–34. doi:10.1111/j.1528-1157.1994.tb02908.x. ISSN 0013-9580.
  14. ↑ Trinka, Eugen; Cock, Hannah; Hesdorffer, Dale; Rossetti, Andrea O.; Scheffer, Ingrid E.; Shinnar, Shlomo; Shorvon, Simon; Lowenstein, Daniel H. (2015). "A definition and classification of status epilepticus - Report of the ILAE Task Force on Classification of Status Epilepticus". Epilepsia. 56 (10): 1515–1523. doi:10.1111/epi.13121. ISSN 0013-9580.
  15. ↑ Harrison's Manual of Medicine 19th Edition
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