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The most important indication for electroencephalography (EEG) in critically ill patients is to evaluate fluctuating or persistently abnormal mental status (or other focal neurological deficits) that cannot otherwise be explained. Commonly, these symptoms are a manifestation of physiological diffuse cerebral dysfunction (encephalopathy), or they may be due to seizure activity without apparent clinical manifestations. Such “nonconvulsive” seizures (NCS), that may only be detected by EEG, occur in at least 8–10% of critically ill patients. Continuous or frequent NCS is called nonconvulsive status epilepticus (NCSE), and may result in secondary neurological injury, including neuronal death or alteration of neuronal networks. Left untreated, NCSE can become increasingly refractory to treatment. EEGs may be indicated in acute brain injury to detect seizure activity. They are useful in monitoring the depth of anesthesia and in the management of refractory status epilepticus. EEGs may also be used in the intensive care unit to characterize paroxysmal clinical events and in prognostication after cardiac arrest or determining brain death.
This chapter describes the diagnosis, types, and management of nonconvulsive status epilepticus using a case-based approach. Generalized status epilepticus including nonconvulsive status epilepticus (NCSE) is a medical emergency that is best managed in an intensive care unit with continuous EEG monitoring. Refractory status epilepticus (RSE) is defined as the failure of seizure activity to terminate despite initial benzodiazepines and additional intravenous antiseizure medications. Refractory status epilepticus is an indication for intravenous anesthetics such as midazolam and propofol with the goal of titrating to burst suppression. Highly epileptiform bursts seen are associated with status epilepticus recurrence despite treatment with intravenous anesthetics, a condition known as super-refractory status epilepticus (SRSE). Additionally, this chapter also describes how to recognize status epilepticus cessation and an uncommon form of NCSE called absence status epilepticus.
This chapter focuses on several of the most common actionable EEG abnormalities. This includes defining and describing epileptiform discharges, which are abnormal EEG waves that serve as markers of increased seizure risk. This also includes seizures themselves, and their characteristics and electrographic criteria. Prolonged and repetitive seizures known as status epilepticus are described, including their specific electrographic characteristics and criteria. The treatment resistant form of status epilepticus known as refractory status epilepticus is also described. Finally, the chapter describes a high risk electrographic phenomenon known as brief potentially ictal rhythmic discharges (BIRDs).
Status epilepticus (SE) has traditionally been thought to cause cerebrospinal fluid (CSF) pleocytosis. However, attributing CSF pleocytosis solely to SE without addressing the underlying etiology may lead to poor outcomes. Leukocyte recruitment to CSF has been shown to peak around 24 hours after prolonged seizures in animal studies, suggesting that CSF pleocytosis within the first 24 hours of SE onset may be due to underlying causes. The goal of this study is to assess if SE is associated with CSF pleocytosis, independent of other causes within the first 24 hours of onset.
Methods:
We completed a historical cohort study of adult patients with SE admitted to the intensive care unit of Vancouver General Hospital between March 2010 and May 2019.
Results:
Of the 441 patients admitted with SE during the study period, 107 met our inclusion criteria leading to 111 lumbar punctures (LPs), with 4 patients receiving two LPs. CSF pleocytosis was seen in 12 of 72 patients who underwent an LP within the first 24 hours of SE onset. In all 12 patients, a secondary etiology for the pleocytosis was observed aside from SE. Of the six CSF samples collected after 24 hours of onset that demonstrated pleocytosis, four had no cause for pleocytosis other than SE.
Conclusions:
In all 12 patients with CSF pleocytosis in the first 24 hours of onset of SE, an underlying etiology was identified. Therefore, any pleocytosis noticed within the first 24 hours of onset of refractory SE should not be attributed solely to SE.
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