Page 1142 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 85: Seizures in the Intensive Care Unit 781

without obvious motor activity. NCSE in this setting demands emergent SE may cause neuronal injury in surviving patients. Some neuronal
treatment guided by electroencephalographic monitoring to prevent injury is caused by systemic factors; for example, hyperthermia causes
further cerebral damage since there are no clear clinical criteria to indi- cerebellar neuronal injury. However, neuronal injury continues during
cate whether therapy is effective. electrographic SE, even without motor manifestations or when physi-
NCSE can occur as a late stage of convulsive SE from any etiology, or ologic parameters are held in the normal range. This is illustrated most
as an initial form of SE from another cause. Failure to recognize NCSE clearly in experimental GCSE. Neuronal injury is prominent in the hip-
is common in patients presenting with nonspecific neurobehavioral pocampus and temporal lobe in primates with experimental GCSE. The
abnormalities, such as delirium, lethargy, bizarre behavior, cataplexy, injury persisted even when muscle activity was eliminated by paralysis,
or mutism. A high level of suspicion for this disorder should be main- and pulse, blood pressure, temperature, and oxygenation were kept
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tained in patients with unexplained alteration in level of consciousness normal.
or cognition who are admitted to the ICU. Neuronal injury during SE is due in part to the excitotoxic effects of
Two special circumstances with which the intensivist should be famil- glutamate-mediated neuronal seizure activity. Glutamate is the most
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iar are myoclonus and febrile seizures. Brief, shock-like, involuntary common excitatory neurotransmitter in the brain. It mediates transfer
muscle contractions constitute myoclonus. Myoclonic jerks are arrhyth- of information between neurons under normal conditions via several
mic, of variable amplitude, and involve both small and large muscles. In receptors. However, glutamate excessively activates the N-methyl-d-
patients with postanoxic coma, myoclonus may be continuous or evoked aspartate (NMDA) subtype of receptor in the robust conditions of SE.
by stimuli such a noise or touch. While this disorder has been associated NMDA receptors have a limited normal function, but during SE they
with epileptiform discharges in the EEG, not all episodes of myoclonus cause very prolonged depolarization of neurons. This results in intracel-
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are epileptic; an EEG can clarify whether it is epileptic in individual lular accumulation of calcium and other cellular changes that result in
cases. Postanoxic myoclonus also occurs in patients who have regained both immediate and delayed cell death. 37
consciousness (the Lance-Adams syndrome); in this setting the myoclo- There are two important clinical implications of the pathophysiology
nus is probably of cerebellar origin and is not a seizure. Febrile seizures of SE. First, neuronal injury continues during electrical SE even after
are specific to young children and are usually generalized motor convul- control of motor manifestations. Therefore it is imperative to exclude
sions that occur in association with fever, typically as the temperature is ongoing seizure activity if patients are pharmacologically paralyzed
rising. These seizures should not be confused with those that transpire after GCSE or do not awaken soon after motor activity stops. These cir-
in the setting of fever secondary to infection of the nervous system. cumstances require EEG monitoring to exclude ongoing seizure activity.
Febrile seizures are usually brief, but can be prolonged and recurrent, Second, pharmacologic treatment is aimed at augmenting inhibition, via
prompting admission to an ICU. drugs that act on γ-aminobutyric acid (GABA), such as barbiturates and
Clinical judgment is required to classify seizures in the ICU. Patients benzodiazepines. There will probably also be a role for NMDA antago-
in whom consciousness has already been altered by drugs, hypoten- nists. Ketamine is the only currently available NMDA antagonist, but
sion, sepsis, or intracranial pathology may be difficult to classify using others are likely to be helpful in the future.
only the ILAE classification because it depends heavily on whether the
seizure activity has altered consciousness. However, focal seizure activ- CLINICAL MANIFESTATIONS
ity on EEG or focal neurologic deficits often helps determine whether
the seizure is focal or generalized in onset. The ILAE continues to work Three problems complicate seizure recognition in the ICU: (1) occurrence
toward revising and updating the current classification system. The goal of complex partial or nonconvulsive seizures in the setting of depressed
is a multi-axis diagnostic scheme that incorporates anatomic, etiologic, consciousness, (2) masking of seizures by pharmacologically induced
therapeutic, and prognostic implications. For the most recent informa- paralysis or sedation, and (3) misinterpretation of other abnormal move-
tion regarding this ongoing project, refer to www.epilepsy.org. 36 ments as seizures. ICU patients often have decreased levels of conscious-
ness in the absence of seizures that are ascribable to the underlying disease
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PATHOGENESIS AND PATHOPHYSIOLOGY and its complications. An encephalopathic patient may be unable to
appreciate or report symptoms of seizure. Fluctuations in mental status
The systemic and cerebral pathophysiology of GCSE can be divided into are frequently subtle and may go unrecognized by staff. A decline in base-
early and late phases. The early phase of systemic manifestations results line alertness may reflect a seizure; an EEG may be required to confirm
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from an adrenergic surge and excessive muscle activity. The adrener- that one has occurred.
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gic surge causes tachycardia, hypertension, and hyperglycemia. These Patients receiving neuromuscular junction blocking agents do not
are augmented by extreme muscle activity that causes hyperthermia manifest the motor signs of seizures. Patients with refractory intracra-
and acidosis and can lead to muscle breakdown, rhabdomyolysis, and nial hypertension, severe pulmonary disease, or other critical illnesses
secondary acute renal failure. This stage is generally well compensated may be both paralyzed and sedated, making identification of seizures
by homeostatic mechanisms so that the excessive demands are met with particularly challenging. Tachycardia and hypertension are signs of
increased supply or other compensatory mechanisms. seizure that can be misinterpreted as evidence of inadequate sedation.
Most facets of GCSE begin to slow down late in GCSE, so only a Continuous EEG monitoring is warranted in this population if seizures
rare patient continues to have continuous convulsive motor activity for are suspected.
more than 1 hour. Cessation of continuous motor activity would seem Patients with metabolic disturbances, anoxia, and other types of ner-
to be a beneficial turn of events, but this is actually coincident with a vous system injury may demonstrate abnormal movements that can be
sharp increase in mortality and in complications. Although systemic confused with seizure. Asterixis, or flapping tremor, is a brief arrhythmic
factors such as heart rate and blood pressure normalize, they may be loss of tone that can appear in the setting of hepatic encephalopathy,
inadequate to meet increased demands of intermittent convulsions or hypercarbia, drug intoxication, or CNS pathology. Myoclonus in post-
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electrographic seizure activity, even in the absence of convulsions. Thus anoxic coma has been reported in the presence and absence of epilep-
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mortality increases dramatically for SE lasting longer than an hour. tiform discharges. Therefore, EEG is absolutely indicated in this setting to
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Death may result from a number of causes, but in a prospective study evaluate for ongoing seizures. Action myoclonus in a patient recovering
of cardiovascular changes during GCSE, 58% of patients had potentially from hypoxic encephalopathy is evoked during movements directed at a
fatal arrhythmias. Patients with atherosclerotic cardiovascular risk target, such as an examiner’s finger. It is frequently associated with cer-
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factors may have a gradual deterioration in hemodynamic parameters ebellar ataxia and postural lapses, which when combined with myoclonus
as their cardiovascular reserve is expended, while other patients decline can severely impair ambulation. Myoclonus associated with etomidate
acutely, presumably from arrhythmias. 40 is described, but whether it is cortically mediated remains unclear.
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