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Subpart IVD
Chapter
36
Clinical – Neurologic
Seizures
Sharon E. Mace, MD, FACEP, FAAP
Introduction
Approximately 5–10% of the population will
experience at least one non-febrile seizure during
their lifetime.
1,2
Seizures account for about 1–2%
of all emergency department (ED) visits.
3
Excluding those patients with a known seizure disorder,
another 300,000 individuals are diagnosed with a
seizure annually, with the diagnosis generally
made in the ED.
2,4
Of these, there are 200,000
new cases of seizures and epilepsy annually.
2
These numbers do not include febrile seizures.
Worldwide, febrile seizures are noted in 2–4% of
children
5
and are the most common seizure in
children < 5 years old, with an approximate incidence of febrile seizures at 75,000–100,000 in the
United States.
6
Excluding headaches/migraines, epilepsy is
the third most common neurological disorder in
the United States after stroke and Alzheimer’s
disease,
7
with “a prevalence greater than cerebral
palsy, multiple sclerosis and Parkinson’s disease
combined.”
2
Nearly 3 million individuals or 1% of
the general population in the United States are
diagnosed with epilepsy.
8
Worldwide, epilepsy
affects some 50 million individuals.
9
The number of individuals with epilepsy is
expected to increase for several reasons, including
the growing geriatric population and the number
of returning veterans. This is because there is an
increased incidence of epilepsy in the elderly and
an increased risk of developing epilepsy in individuals with a traumatic brain injury.
2
On a yearly basis in the United States, about
28% of all epilepsy patients need treatment in
EDs.
10
This is not surprising, considering that up
to 30% of patients treated for epilepsy continue to
experience seizures (“breakthrough” seizures).
6,11
Not only are patients with seizures common
in the ED, they are “labor-intensive” in that they
make considerable demands on EMS and ED
resources.
12
In one ED study of patients with
seizures, “advanced care, including intravenous
access, laboratory work, cardiac monitoring, or
oxygen administration” was required in 84% of
patients and over half of the patients (55%) were
administered antiepileptic drugs (AEDs).
12
Over
one-fourth of patients (27%) were admitted to the
hospital.
12
The annual costs (direct and indirect)
each year in the United States for epilepsy and
seizures is $17.6 billion.
12
One-third of individuals who have had a single
unprovoked seizure will go on to develop epilepsy.
One-fourth of children with mental retardation,
one in eight children with cerebral palsy, and
50% of children with both mental retardation and
cerebral palsy will develop epilepsy.
2
In adults, 10%
of Alzheimer patients and 22% of stroke patients
can be expected to develop epilepsy. Individuals
with a family member who has epilepsy are also
at an increased risk of developing epilepsy, which
suggests a genetic component to the disorder.
2
In
children, the estimated risk of developing epilepsy
is 8.7% if their mother has epilepsy and 2.4% if
their father has epilepsy.
2
Considering that the observation unit (OU), in
general, is a more cost-effective alternative to inpatient care, then placing some of these patients in the
OU should result in a shorter length of stay and at a
lower cost than inpatient admission,
13
although a
future study regarding the OU treatment of seizures
is warranted to verify this conclusion.
Definitions
A seizure is the clinical manifestation(s) of an
episode of an abnormal, excessive, hypersynchronous electrical discharge of a group of
cortical neurons that results in a temporary disruption of brain dysfunction.
14
A seizure is a
discrete, time-limited alteration in brain function
that may include changes in the level of consciousness, motor activity, sensation, and/or autonomic function. Convulsions refer to a specific
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21:05:10
type of seizure with involuntary muscular contractions as its fundamental manifestation.
Seizures are classified into primary or second-
ary.
15
Primary or idiopathic seizures are seizures
in which no identifiable cause is recognized. Secondary or symptomatic seizures are seizures that
are caused by a recognizable neurological condition, for example, central nervous system infection, brain tumor, stroke, head injury, or
intracranial bleed. A reactive seizure is a generally
self-limited seizure in an otherwise “normal” individual due to a specific etiology, such as a drug/
toxin or metabolic disorder (i.e., hypoglycemia),
and is not designated as epilepsy or a seizure
disorder.
14
Provoked seizures, also referred to as
acute symptomatic seizures,
16
are seizures that
have an obvious and immediate preceding cause
(e.g., hypoglycemia, an electrolyte abnormality,
exposure to a toxin/adverse event from a drug)
or are due to recent acute CNS injury (such as
head trauma, stroke, or CNS infection). The usage
of this terminology when due to an acute metabolic abnorm ality or drug/toxin exposure may be
acceptable since treatment of the underlying etiology should prevent recurrence of the seizure.
When used following acute CNS injury the term
can be misleading since the underlying cause is
irreversible and there is a strong predilection
toward seizure reoccurrence.
17
Epilepsy is a clinical condition characterized by
recurrent (two or more), unprovoked seizures,
generally attributed to genetic susceptibility or a
chronic acquired CNS pathology (such as head
trauma, hypoxic encepahalopathy or a stroke),
and has no immediate identifiable cause.
14
Epilepsy, by definition, does not include seizures
caused by reversible etiologies, such as hypoglycemia, electrolyte or metabolic abnormalities,
toxins/poisonings, drugs (illicit, prescribed or over
the counter), or alcohol withdrawal seizures. The
highest incidence of newly diagnosed seizures is in
the extremes of age: the elderly (> 65 years old)
and children (< 5 years old).
2
Seizure incidence is
highest during the first decade of life, particularly
during the first year of life.
12
There are many
physiological reasons responsible for an increased
susceptibility of the developing brain to seizure.
12
Seizure Classifications
Seizures are categorized into generalized or
partial seizures, although if there is insufficient
information to classify the seizure, it is designated
as “unclassified.”
15,16
A generalized seizure consists of an initial
involvement of both cerebral hemispheres
18
and
is characterized by a loss of consciousness (LOC).
Generalized seizures are further subdivided
according to the presence or absence of specific
motor acti vity. Generalized seizures include gen-
eralized or tonic-clonic (grand mal): muscle rigidity followed by clonic movements of the head and
extremities, absence (petit mal): star ing with
impaired awareness and responsiveness, atypical
absence: like absence but may have incomplete
and/or gradual loss of responsiveness with tonic,
clonic or atonic movements, atonic (drop attack):
sudden total loss of muscle tone ± LOC, myoclo-
nic: jerking of a muscle or group of muscles, and
tonic: bilateral stiffening seizures.
18
Partial (focal) seizures are seizures with an
initial onset arising from a localized area of the
brain (e.g., limited to part of one cerebral hemisphere).
18
Partial seizures are frequently due to a
structural lesion or localized injury to the brain.
Therefore, they require a diagnostic evaluation for
a focal lesion such as a tumor, arteriovenous
malformation (AVM), cerebrovascular accident
(CVA) or intracerebral bleed; although, most
individuals with partial seizures will have no etiology identified and have idiopathic (unknown)
partial seizures. Partial seizures are subgrouped
based on whether or not there is LOC. With
simple partial seizures, consciousness is maintained; the patient with complex partial seizures
may appear conscious, but is unaware and unable
to interact or respond to their environment and
has impaired consciousness.
In addition to these classifications of seizures,
there are various epileptic syndromes th at are
delineated by a constellation of features.
19
Some of the more c ommon are febrile seizures,
infantile spasms, Lennox-Gastaut syndrome,
benign Rolandic epilepsy,andjuvenilemyoclonic e pilepsy.
19
Pathophysiology of Seizures
Epileptogenesis is the series of events that changes
a normal neuronal network into a hyperexcitable
network.
20
A discussion of the pathophysiology
of seizures can facilitate an understanding of
the mechanisms underlying the occurrence of
seizures and how AEDs work.
Sharon E. Mace
040
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Neuronal circuits are composed of axonal conduction and synaptic transmission. Axonal conduction refers to the propagation of action
potentials along the neuronal axon. (Figures 36.1
and 36.2) A synapse is the membrane-to-membrane
contact of a nerve cell with another cell. The function
of a synapse is to transmit nerve impulses, usually via
a chemical transmitter substance. Key neurotransmittersinthebrainincludegamma(γ) aminobuty-
ric acid (GABA), glutamate, acetylcholine,
dopamine, serotonin, norepinephrine, and histamine. Synaptic transmission is the transmission or
spread of nerve impulses, generally from axon
terminal (presynaptic) to the postsynaptic membrane. Most commonly, synaptic transmission
occurs via release of the chemical transmitters into
the synaptic cleft, which then binds to a receptor
for that neurotransmitter. In some instances, synaptic transmission occurs by direct propag ation of
the bioelectrical potential from the presynaptic to
the postsynaptic membrane via a “gap junction” in
which the synaptic cleft is extremely small, usually
< 2 mm wide. (Figure 36.3) Both axonal conduction and synaptic transmission utilize ion channels. (Figures 36.4 and 36.5)
Cellular Physiology: Action Potential
The action potential is the fundamental mechanism of neuronal excitability. An action potential
occurs in an all-or-none manner due to ion fluxes
that result in a lowering of the resting membrane
potential to a threshold membrane potential,
which then causes depolarization to occur.
(Figures 36.4 and 36.5)
Cellular Physiology: Ion Channels
Ion channels are a macromolecular protein pathway or passageway for the movement of ions into
and out of the cell. Ion channels consist of proteins
located in a cell’s plasma membrane that have a
“pore” or opening for the movement (influx or
efflux) of inorganic ions (e.g., Na+, K+, Cl
_
,Ca
2
+
) in order to maintain or modulate the electrical
potential of the cell. Thus, ion channels play a key
role in the propagation of the action potential in
neurons. These ion channels span the cell’s membrane, thereby, transversing the lipid bilayer of a
cell’s plasma membrane. (Figures 36.4 and 36.5)
Movement of ions across the neuronal membrane determines the electrical membrane potential and generates the action potential. Sodium (Na
+) is maintained in relatively high concentration
outside the cell, while potassium (K+) is maintained in a relatively high concentration inside
the cell. This electrochemical gradient is maintained by the ATP-dependent sodium-potassium
pump that maintains the resting membrane potential in a polarized state at about 70 mV.
(Figure 36.5) When an ion channel is opened, the
ion moves passively into or out of the cell along its
electrochemical gradient. (Figures 36.4 and 36.5)
There are two types of ion channels that can
alter membrane potential and are accountable for
excitatory and inhibitory activity: ligand-gated and
voltage-gated. Conductance of ligand-gated channels is affected by a signal molecule or ligand (e.g.,
neurotransmitters), while the conductance of
voltage-gated channels is affected by altering the
transmembrane potential. Changes in intracellular
Figure 36.1 Neuron
The dendrites receive incoming signals from other neurons. The cell body directs the activities of the neuron (acts as a “control
center”) and synthesizes, breaks down, and reuses (recycles) neuronal proteins. The outgoing signal to other neurons flows along the
axon. The axon terminal contains neurotransmitters.
Figures courtesy of Dr. Sharon E. Mace of the Cleveland Clinic Emergency Services, Mr. Dave Schumick of the Medical Art and Photography Department,
and the Medical Art and Photography Department of the Cleveland Clinic, Cleveland, Ohio.
Seizures
040
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ion compartmentalization can also affect the membrane potential.
21
Sodium and calcium voltage
gated ion channels act to depolarize the cell membrane toward the action potential threshold and
are, therefore, excitatory.
21
Potassium voltagegated channels cause hyperpolarization of the cell
membrane away from the action potential and
thus, are inhibitory. Ion channels are composed
of an aggregation of polypeptide subunits. The
types of subunits in the ion channels that are
present in an individual neuron control the shape
of the action potential and can modify the kinetic
properties of the ion channel.
Ion Flows: Depolarization
Inward sodium conductance with an influx of
sodium leads to a decrease in the resting membrane
Figure 36.2 Transmission of Impulse
down Action Potential
Movement of the action potential from
the neuronal cell body to the neuronal
axon terminal along the axon, which
allows conduction to occur.
Conduction is the mechanism whereby
intracellular signaling or
communication within the neuron
occurs, which allows the neuronal cell
body to communicate with the
neuronal axon terminal. Conduction
involves movement of an action
potential, which is generated in the cell
body near the axon, down the axon to
the axon terminal. The action potential
occurs due to the movement of the
electrically charged ions across the
neuronal membrane.
Figures courtesy of Dr. Sharon E. Mace of the
Cleveland Clinic Emergency Services, Mr.
Dave Schumick of the Medical Art and
Photography Department, and the Medical
Art and Photography Department of the
Cleveland Clinic, Cleveland, Ohio.
Sharon E. Mace
040
21:05:10
potential until it reaches the threshold potential,
which triggers depolarization. (Figures 36.4 and
36.5) Sodium current fosters depolarization by
lowering the resting membrane potential to a subthresholdlevelandmayfosterburstfiringof
neurons. Increased inward calcium conductance
causing an influx of calcium ions via voltage-gated
channels also creates a drop in the resting membrane potential that leads to depolarization. Calcium influx also contributes to neurotransmitter
release, thereby, influencing ligand-gated channels
as well as affecting the firing pattern of neurons and
gene expression.
Ion Flows: Hyperpolarization
The conductance of hyperpolarizing currents is
predominately mediated by potassium channels,
and works to diminish or inhibit excitation.
Potassium conductance has many actions, including leak conductance and rectification. Leak conductance is a major influence on the resting
membrane potential. Rectification pertains to the
circumstance in which the directio n of ion flow
through a channel is altered depending upon the
voltage, which could be due to blocking of the ion
channel pore by other ions. Hyperpolarization will
turn on a rectifier of inward potassium conductance with potassium influx into the neuron causing
a change in potassium ion flow. Potassium conductances have a multitude of effects on neurons.
These include the M-current that hyperpolarizes
the resting membrane potential and reduces the
rate of cell firing; the A-current that sets the interspike interval and the rate of cell firing; and calcium activated potassium conductances that are
responsive to intracellular calcium levels, determine interburst interval and the rate of cell firing.
Synaptic Transmission: E xcitatory
Neuurotransmitters – Glutamate
The amino acid glutamate is the primary excitatory neurotransmitter, while GABA is the major
inhibitory neurotransmitter in the CNS. Glutamate receptors have been found postsynaptically on
excitatory principal cells, inhibitory interneurons
and some glial cells.
Figure 36.3 Neuro Transmission via Chemical Neurotransmission (Neurotransmitters) or Electrical Neurotransmission
With chemical neurotransmission, neurotransmitters are synthesized in the presynaptic neuron and then released into the synaptic
cleft and travel to the postsynaptic neuron. Chemical transmission occurs via signal molecules or ligands, for example,
neurotransmitters.
Electrical neurotransmission involves the use of voltage gated ion channels, including ions such as potassium, sodium or calcium.
Figures courtesy of Dr. Sharon E. Mace of the Cleveland Clinic Emergency Services, Mr. Dave Schumick of the Medical Art and Photography Department,
and the Medical Art and Photography Department of the Cleveland Clinic, Cleveland, Ohio.
Seizures
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There are multiple subtypes of inotropic (fast
synaptic transmission) glutamate receptors: ɑamino-3-hydroxyl-5-methyl-4-isoxazole-proprionic acid (AMPA), kainate, and N-methyl-D-asparate (NDMA). All of these receptors open ion
channels when coupled with glutamate.
Synaptic Transmission: Inhibitory
Neurotransmitters – GABA Gammaaminobutyric Acid
GABA is the main inhibitory neurotransmitter in
the central nervous system (CNS).
GABA receptors have been found on almost
all cortical neurons and on some glia. There are
at least two types of GABA receptors: GABA-A
and GABA-B. GABA-A receptors are loc ated
postsynaptically, are permeable to Cl- ions, and
when activated the Cl- influx hyperpolarizes the
neuronal cell membrane, thereby, inhibiting an
action potential. GABA-B receptors are located
presynaptically, act via second messenger
systems, usually open K+ channels and have a
hyperpolarizing current. This causes a decrease
in transmitter release because of their presynaptic location.
Pathophysiology and Types of Epilepsy
Genetic modifications in the structure of sodium
channels has been linked to various types of epilepsy from generalized epilepsy and febrile seizures
to infantile myoclonic epilepsy and temporal lobe
Figure 36.4 Action Potential
Action potential with resting
membrane potential at around 70
millivolts.
Figures courtesy of Dr. Sharon E. Mace of the
Cleveland Clinic Emergency Services, Mr.
Dave Schumick of the Medical Art and
Photography Department, and the Medical
Art and Photography Department of the
Cleveland Clinic, Cleveland, Ohio.
Sharon E. Mace
040
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epilepsy, while changes in the calcium channels
have been associated with childhood absence epilepsy.
22
Genetic mutations affecting the M-current
regulated by potassium ion channels are thought to
be responsible for several types of epilepsy: idiopathic generalized epilepsy, benign partial epilepsy,
and benign familial neonatal convulsions.
Pathophysiology and Antiepileptic Drugs
The pharmac ology of most AEDs can be related
to the pathophysiology. Numerous AEDs including phenytoin and carbamazepine interact with
the voltage-dependent sodium channels. The
AEDs levetiracetam and topiramate act partly
through effects on the voltage-gated potassium
channels.
In animal studies, ionotropic agonists of
the excitatory glutamate receptors (AMPA,
NDMA, and kainate) precipitate seizures, while
antagonists of these receptors prevent seizures.
Metabotropic agonists of the glutamate receptors
have varying effects, probably due to their diverse
mechanisms of signal transduction and their different locations.
19
GABA-A receptor agoni sts, which include the
benzodiazepines and barbiturates, decrease or
eliminate seizure activity. Some GABA-B agonists, for example, baclofen, cause hyperexcitability
and precipitate seizures.
Summary: Neuronal Excitability
Many variables can affect neuronal hyperexcitability leading to an increased susceptibility to seizures.
This has been referred to as “neuronal” or intrinsic
if inside the neuron/cell or “extraneuronal” or
extrinsicifintheextracellularspace.
21
Intrinsic or neuronal variables include intracellular ion concentrations, intracellular neurotransmitters (amount, available substrate, synthesis,
or breakdown), voltage-gated or ligand-gated
Figure 36.5 Action Potential Changes from Ion Flow Leading to Depolarization or Hyperpolarization
Figures courtesy of Dr. Sharon E. Mace of the Cleveland Clinic Emergency Services, Mr. Dave Schumick of the Medical Art and Photography Department,
and the Medical Art and Photography Department of the Cleveland Clinic, Cleveland, Ohio.
Seizures
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channels (number, type, location or distribution),
receptors (number, type, location or distribution), modification of receptors, activation of
second-messenger systems, and alteration of
gene expression.
Extra-neuronal (extrinsic) factors include
extracellular ion concentration, extracellular
neurotransmitters (amount, available substrate,
synthesis or breakdown), uptake of neurotransmitters, synapses, neuronal networks or anatomical regions of the brain.
18
The sprouting of new
axons or the destruction of neurons leading to an
imbalance of the excitatory/inhibitory neurons,
changes in connections between the neurons with
new or loss of connections are examples of how
neuronal networks could affect hyperexcitability
and the propensi ty for seizures. Current and
future AEDs will likely target these molecular,
cellular, and anatomic factors that lead to neuronal hyperexcitability and seizures.
Patient Evaluation
The first step is to determine whether the event
was actually a seizure. The differential diagnosis
is extensive and includes syncope, hyperventilation, transient ischemic attack, migraines, pseudoseizures, sleep phenomena (e.g., narcolepsy/
cataplexy), drug toxicity, movement disorders
(such as chorea, dystonia, myoclonic jerks,
tremors, tics), and additionally in children/
infants: breath holding spells and behavioral
events. In an adult study, 30–40% of those seen
in a first seizure clinic had experienced an earlier
unrecognized seizure.
23
Similarly, a pediatric
study noted “a high rate of diagnostic inaccuracy,
with one quarter of patients incorrectly diagnosed
as having a seizure rather than a nonepileptic
event” and the diagnosis of epilepsy “missed in
over one-third of children.”
24
In this clinic, the
diagnosis was epilepsy in 74%, nonepilepsy in
24%, and unclassifiable in 2%.
A detailed history of the event is crucial and
should include: prodrome/aura if any, onset
(abrupt or gradual), activity (if any): type/progression/localized or generalized/symmetric or
asymmetric, consciousness, bladder/bowel incontinence, duration, postictal confusion/lethargy/
headache, precipitating factors, associated symptoms (severe, persistent headache may indicate
intracranial pathology), and any injuries sustained during the event.
In a patient with known sei zures, determine
the patient’s baseline seizure pattern and whether
this episode is similar to previous seizures and
ascertain any precipitating factors: missed doses
of seizure medications, new or changes in medications including over the counter drugs or a
change from brand name to generic, alcohol/
substance abuse or withdrawal, emotional stress,
strenuous exercise, sleep deprivation, and any
intercurrent infections or illnesses.
A prior history of unexplained injuries,
tongue biting, enuresis or “passing out” may indicate unrecognized seizure activity. An important
question to ask is whether there are any previous
head injuries. The history should include medications including anticoagulants, allergies, social
history especially alcohol/substance abuse, and
family history (including seizures, other neurologic, congenital, and/or genetic disorders). Past
medical history should include systemic illnesses
(particularly HIV, cancer, CVA, other neurologic
disorders, coagulopathy, endocrine or metabolic
disorders, liver/kidney disease, previous trauma)
and any recent illnesses/injuries.
6
The physical examination should include
vital signs with a temperature and pulse oxygen
saturation, level of consciousness, brief mental
status examination, screening for injuries (especially the head and spine), neurologic/cardiac/
respiratory examination, as well as checking
the neck/spin e (e.g., supple or stiff, any injuries)
and skin for rashes, petechiae, stigmata of
inherited/congenital disorders, bruising, infections, malignancies, etc.
A dextrostix/accucheck or blood glucose is
generally indicated even in known seizure patients
to rule out hypoglycemia. If the patient is on an
anticonvulsant that can be measured, usually an
anticonvulsant level is obtained. In those with a
known seizure disorder and a single unprovoked
seizure similar to their previous seizure pattern,
the glucose and anticonvulsant level may be the
only tests that are warranted.
14
However, if this is a first-time seizure, or there
are complicating factors, or the diagnosis is uncertain, then further evaluation is usually indicated.
Laboratory studies to consider are glucose, electrolytes including calcium and magnesium, renal
function tests (BUN creatinine), toxicology studies,
and in women of childbearing age, a pregnancy
test. A seizure can cause a wide anion gap metabolic (lactic) acidosis and an elevated prolactin
Sharon E. Mace
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level immediately after the seizure, which generally
resolves within 15–30 minutes. This may be useful
in distinguishing a true seizure from a pseudoseizure, but must be obtained immediately after the
seizure before they normalize.
Depending on the clinical circumstances,
other tests may be useful. If an infection is being
considered, a CBC may be warranted. If meningitis or a subarachnoid hemorrhage is in the differential, then a lumbar puncture with cerebrospinal
fluid analysis is indicated. If this is a new onset
partial seizure, there are focal findings or any
concern for intracranial process, then a CT scan
is indicated. A chest radiograph may detect an
aspiration pneumonia, a tumor or other abnormality. If syncope is a possibility, an ECG is a
simple, easily obtained noninvasive test. An EEG
may reveal valuable information.
An EEG is infrequently obtained in the ED
except for usual circumstances, such as evaluation
for nonconvulsive status epilepticus in a comatose
or paralyzed patient,
15
but may be part of the OU
evaluation.
Patient Selection
Patients in whom any history or a valid history
could not be obtained in the ED may be placed in
observation until a confirmatory history and a reliable friend/family member are available to take
responsibility for the patient so the patient can be
safely discharged home. Repeat physical examination can be done, looking for any injuries that
may have occurred during the episode and for clues
to the etiology of the event, and to ascertain that the
patient has fully recovered from their postictal state.
Patients who need further evaluation to determine the etiology of their “seizure-like” episode,
whether to confirm a true seizure or an alternative
diagnosis, are appropriate candidates for an OU.
Additional testing – whether laboratory, neuroimaging, an EEG, monitoring or other specialized
diagnostic studies – can be completed in the OU.
If syncope is a possibility, then monitoring for
dysrhythmias and a diagnostic workup can be
done in the OU. (See Chapter 25 on syncope.)
Patients who need time to recover from a postictal or intoxicated state can be safely monitored in
the OU. Patients for whom there is a concern for
recurrent seizure activity can undergo repeat neurologic checks along with vital signs and be monitored in the OU. Patients with a known seizure
disorder, awaiting their laboratory tests including
an anticonvulsant level, may have their “loading
dose” of anticonvulsant medication administered
in the OU. Management of any conditions that
precipitated the seizure, such as an infection, should
be done in order to help prevent seizure recurrence.
Since 90% of patients with alcohol withdrawal
seizures will have additional seizures within a
6-hour time frame, it has been recommended that
these patients be “ admitted for observation and
further investigation.”
15
Exclusion
Patients with unstable vital signs, acute psychiatric problems, status epilepticus, any intracranial
lesion needing emergent surgical intervention,
bacterial meningitis or new significant intracranial pathology (such as acute stroke or intracranial bleed) should not be admitted to an OU.
Certain patient populations are not appropriate patients for an OU admission. Human
immunodeficiency virus (HIV) positive patients
are a high-risk population; tend to have more
serious, life-threatening etiologies for their
seizures than the general population w ith mass
lesions, meningitis, and HIV encephalop athy
occurring more frequently; and usually need a
more extensive diagnostic evaluation, which
is unlikely to be completed in < 24 hours.
12
Although most seizures in pregnancy are not
first-time seizures, the management of the pregnant patient with known or new-onset seizures is
more complicated than usual and requires a multidisciplinary approach with the involvement of
consultants. Initiation of treatment for first-time
seizure in a pregnant patient should incorporate
consultations from an obstetrician and a neurologist. Concern over risk to the fetus from AEDs
adds another layer of complexity. Seizures beyond
20 weeks of gestation raise the possibility of
eclampsia. It is best not to place complicated
patients with seizures, such as HIV patients or
pregnant patients, in the OU.
Observation Unit Management
The history is of fundamental importance after an
episode, yet it may be difficult or impossible to
obtain a valid history in the ED, especially in a
patient with an altered mental status or who is
postictal, particularly if the patient is unaccompanied and there are no family members or others
Seizures
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from whom to obtain a history. In the OU, there
is time for family or friends to come in and
provide information, time to make phone calls
and reach those who were present during the
event, and time for the postictal or the intoxicated
patient to recover and give information.
Repeat vital signs and neurologic checks can be
done in the OU, with observation for any recurrent
seizures or monitoring if syncope and dysrhythmias are a consideration. It has been suggested that
those with alcohol withdrawal seizures be admitted
for observation and additional evaluation.
15
A diagnostic workup can be done in the OU in
order to determine the etiology of the event. Was
this episode a seizure or syncope or another disorder? If this was a seizure, evaluation can be
done, which may involve additional laboratory
tests, a neurology consult, neuroimaging (CT or
MRI), lumbar puncture, EEG or other specialized
testing. In patients with a known seizure disorder,
once their anticonvulsant level is available, then a
loading dose of anticonvulsant may be administered, although the necessity of loading anticonvulsant medications has been questioned recen tly.
One caveat to remember is that patients with
epilepsy may have a non-epileptic seizure event or
syncope or other problems/pathology. Moreover,
distinguishing between a seizure and a seizurelike event can be difficult, especially in a busy
ED. Additional time in the OU may be needed
for determination of the etiology of the event.
Precipitating factors known to lower the
seizure threshold and that trigger breakthrough
seizures can be treated in the OU. Patients with a
mild blood glucose and/or electrolyte abnormality, or vitamin deficiency, can have intravenou s
fluids with supplemental electrolytes, vitamins,
glucose, and others administered to correct their
deficit. Conversely, fluids and insulin can be given
to lower an elevated blood sugar. Patients with a
non-life-threatening infection (e.g., uncomplicated cellulitis or pharyngitis) may have treatment
including antibiotics started in the OU. However,
patients with seizures and serious life-threatening
or other significant infections, such as meningitis
or encephalitis, are not candidates for the OU. If
the patient needs adjustment in their seizure
medications, then neurology consultation can be
obtained in the OU.
Inclusion criteria include stable patients, who
are not critically ill, who do not need emergent
surgical intervention, and who are anticipated to
be ready for discharge in < 24 hours. Seizure
patients appropriate for observation include
stable patients with new onset seizures, alcohol
withdrawal seizures, uncomplicated febrile
seizures, posttraumatic seizures following isolated
blunt head trauma with a negative CT scan, and
normal or baseline neurologic examination.
13
Patients with precipitating conditions for their
seizures that can be easily treated and are expected
to improve within a 1-day (24-hour) timeframe
can be placed in observation. Thus, patients with
less severe infections – such as a urinary tract
infection but not urosepsis, or pneumonia without hypoxia or respiratory distress, and/or electrolyte or glucose abnormalities but not diabetic
ketoacidosis – may have management of their
underlying illness that brought on their seizures
as well as evaluation or therapy for seizure disorder in the OU .
Summary
Patients with seizures are commonly encountered
in clinical practice. The OU allows a brief period
of time, < 24 hours, that allows for obtaining
further history and testing in order to determine
the etiology of a given episode, whether a seizure
or syncope or another cause. The OU affords time
to complete a diagnostic evaluation and to administer therapy for the seizure including administering antiepileptics, and allows for the postictal
and/or intoxicated patient to recover. The OU
also provides an opportunity to repeat evaluation
of the postictal patient to determine if he or she is
stable for discharge and to treat any precipitating
causes of the seizure.
References
1. Forsgren L, Bucht G, Eriksson
S, et al. Incidence and clinical
characterization of unprovoked
seizures in adults; a prospective
population-based study.
Epilepsia, 1996; 37(3):
224–229.
2. www.epilepsyfoundation.org/
aboutepilepsy/whatisepilepsy/
statistics.cfm (last accessed July
24, 2012).
3. ACEP Clinical Policy: Critical
issues in the evaluation and
management of adult patients
presenting to the emergency
department with seizures.
Ann Emerg Med, 2004; 43:
605–625.
Sharon E. Mace
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