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Table of Contents    
COMMENTARY
Year : 2021  |  Volume : 69  |  Issue : 2  |  Page : 360-361

Non-Convulsive Status Epilepticus in Critically Ill Patients


1 Department of Neurology, AIIMS, New Delhi, India
2 Lady Hardinge Medical College, Connaught Place, New Delhi, India

Date of Submission16-Mar-2021
Date of Decision23-Mar-2021
Date of Acceptance23-Mar-2021
Date of Web Publication24-Apr-2021

Correspondence Address:
Jasmine Parihar
Lady Hardinge Medical College, Connaught Place, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.314548

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How to cite this article:
Tripathi M, Parihar J. Non-Convulsive Status Epilepticus in Critically Ill Patients. Neurol India 2021;69:360-1

How to cite this URL:
Tripathi M, Parihar J. Non-Convulsive Status Epilepticus in Critically Ill Patients. Neurol India [serial online] 2021 [cited 2021 May 13];69:360-1. Available from: https://www.neurologyindia.com/text.asp?2021/69/2/360/314548




Non-convulsive status epilepticus (NCSE) is increasingly recognized in the critically ill with the availability of bedside continuous electroencephalogram (cEEG) monitoring. According to the international league against epilepsy, NCSE can occur in patients without coma and with coma.[1],[2] The underlying causes of NCSE vary according to the patient population being studied. In critically ill comatose patients, the causes include pre-existing epilepsy or post-convulsive status epilepticus, sepsis, dyselectrolytemia, renal or hepatic dysfunction, hypoxic brain injury, new-onset refractory status epilepticus (NORSE), autoimmune encephalitis, central nervous system infections, and drug-induced NCSE. Sepsis and anoxia the commonest among these. The exact incidence of NCSE in each of these causes has been rarely studied, and the study by Octaviana F, et al. highlighting the high incidence of NCSE in patients with metabolic encephalopathy is a welcome addition to the existing data.[1]

NCSE is common in ICU patients, and the diagnosis requires a high index of suspicion, especially in patients with fluctuating or unexplained alterations in mental status. However, in ICU settings, there is a constellation of causes responsible for altered sensorium in a given patient. The clinical presentations and electroencephalogram features of comatose patients with NCSE may vary. Some patients may have subtle clinical manifestations like sustained eye deviation, nystagmus, eye flickering, or facial twitching to suggest that patient has an ongoing seizure. However, most comatose patients have no discernible clinical correlate suggestive of seizures.[3] In such patients, the diagnosis of NCSE requires prolonged EEG monitoring.

cEEG is a more sensitive test than is routine EEG for detecting NCSE in the critically ill population with 2.5 to 3-fold greater detection with continuous EEG compared with routine EEG.[4] EEG abnormalities like diffuse slowing and generalized periodic discharges are common in metabolic encephalopathies. There are a wide variety of discharges seen in critically sick patients that may represent a continuum between interictal and ictal discharges. These include lateralized periodic discharges (LPDs), bilateral independent periodic discharges (BIPD), generalized periodic discharges (GPD), lateralized rhythmic delta activity, triphasic waves (TWs), and stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs). However, how much of these EEG changes contribute to the patients' clinical state or ongoing neuronal injury is unclear.

More classical findings like triphasic waves are common with hepatic encephalopathies though these can also be seen in other forms of encephalopathies. TWs are generalized as well as periodic in character and hence have been now termed as “GPDs with triphasic morphology.”[5] It is now well known that the TWs can disappear with AEDs even when these might not represent seizures. Hence, the differentiation of TWs other forms of GPDs that represent seizures may be crucial to avoid unnecessary AEDs. TWs are 100-300 μV, 1.5-2.5 Hz frontal-predominant waves with an initial sharp negative followed by a prominent positive deflection, and then a negative deflection. They have an anterior to posterior time lag and a slow background. In contrast, the epileptiform discharges associated with NCSE had a higher frequency, shorter duration of phase one, and less generalized background slowing.[6]

In addition to cEEG in patients with unexplained altered sensorium, other appropriate investigations like electrolytes, complete blood count, renal function tests, liver function tests, urinalysis, and urine toxicology screen should be carried out. The threshold for getting brain imaging and cerebrospinal fluid analysis should be low for such patients.

While the clearly ictal discharges should be treated, how aggressively the equivocal patterns be addressed is unclear. Chasing to treat the EEG changes with antiepileptic drugs without improvement in the patients' clinical status may prove harmful. These electrographic findings may represent acute symptomatic NCSE if occurring in close temporary relationship to metabolic, toxic, infectious, and inflammatory etiology. Hence, the treatment of the primary and other contributory pathologies should be the principal objective. For diagnosis of NCSE, an IV antiseizure drug trial using benzodiazepines have been traditionally used to see the electrographic and clinical response. Midazolam in small sequential doses (1 mg) is preferred due to shorter half-life, rapid action to avoid prolonged sedation. Whereas clinical improvement with EEG reversal back to normal establishes the diagnosis of NSCE, patients in whom EEG findings return to normal without clinical improvement could still be NSCE.[7] For example, patients with metabolic encephalopathy patient may not show clinical response as NSCE is not likely the sole reason for an obtunded state. The sedating effect of benzodiazepines given in order to stop EEG discharges may further contribute to sedation. Antiepileptic drugs should thus be chosen judiciously in such patients. The use of conventional AEDs like phenytoin and valproate that have stood the test of time and whose levels can be measured along with the newer, safer AEDs like levetiracetam are reasonable choices when AEDs have to be started in critically ill patients with established or suspected NCSE.

The underlying cause and the clinical examination may have a more remarkable prognostic ability than the EEG findings in critically ill patients. Octaviana F. ……….et al. reports no significant difference in the mortality rate of metabolic encephalopathy patients with or without NCSE, suggesting the importance of managing the underlying cause.[1]

Considering that not all EEG findings may represent an ictal activity or NCSE, continuous EEG monitoring may not be required in all critically ill patients. A patient may undergo a routine EEG, whose findings may guide the need for continuous EEG monitoring. 2HELPS2B seizure prediction risk score based on the one-hour EEG findings can estimate the need for continuous EEG in limited-resource settings.[8],[9]

To conclude, the electrographic findings fulfilling the criteria of NCSE can be seen commonly in critically ill patients. A myriad of causes may be responsible for encephalopathy patient's clinical status. Solely focusing on NCSE in such a setting may harm the patient given the side-effects of AEDs. In a non-improving patient with NCSE, a search for evidence of other causes should be continued. Use of titratable, non-sedating AEDs may be reasonable in such settings.



 
  References Top

1.
Octaviana F, Bestari AP, Loho AM, Indrawati LA, Wiratman W, Kurniawan M, et al. Nonconvulsive Status Epilepticus in Metabolic Encephalopathy in Indonesia Referral Hospital. Neurol India 2021;69:354-361.  Back to cited text no. 1
  [Full text]  
2.
Trinka E, Cock H, Hesdorffer D, Rossetti AO, Scheffer IE, Shinnar S, et al. A definition and classification of status epilepticus--Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia 2015;56:1515-23. doi: 10.1111/epi.13121.  Back to cited text no. 2
    
3.
Claassen J, Mayer SA, Kowalski RG, Emerson RG, Hirsch LJ. Detection of electrographic seizures with continuous EEG monitoring in critically ill patients. Neurology; 62:1743-8. doi: 10.1212/01.wnl. 0000125184.88797.62.  Back to cited text no. 3
    
4.
Limotai C, Ingsathit A, Thadanipon K, McEvoy M, Attia J, Thakkinstian A. How and Whom to Monitor for Seizures in an ICU: A Systematic Review and Meta-Analysis. Crit Care Med 2019;47:e366-e373. doi: 10.1097/CCM.0000000000003641.  Back to cited text no. 4
    
5.
Hirsch LJ, Fong MWK, Leitinger M, LaRoche SM, Beniczky S, Abend NS, et al. American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2021 Version. J Clin Neurophysiol 2021;38:1-29.  Back to cited text no. 5
    
6.
Hartshorn JA, Foreman B. Generalized periodic discharges with triphasic morphology. J Neurocrit Care 2019;12:1-8.  Back to cited text no. 6
    
7.
Struck AF, Ustun B, Ruiz AR, Lee JW, LaRoche SM, Hirsch LJ, et al. Association of an Electroencephalography-Based Risk Score With Seizure Probability in Hospitalized Patients. JAMA Neurol 2017;74:1419-24.  Back to cited text no. 7
    
8.
Beniczky S, Hirsch LJ, Kaplan PW, Pressler R, Bauer G, Aurlien H, et al. Unified EEG terminology and criteria for non-convulsive status epilepticus. Epilepsia 2013;54 Suppl 6:28-9. doi: 10.1111/epi. 12270.  Back to cited text no. 8
    
9.
Rai V, Jetli S, Rai N, Padma MV, Tripathi M. Continuous EEG predictors of outcome in patients with altered sensorium. Seizure 2013;22:656-61.  Back to cited text no. 9
    




 

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