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V Vol. 22, No.

7 July 2000

CE Refereed Peer Review

Status Epilepticus:
FOCAL POINT Clinical Features and
★Status epilepticus (SE) is a
medical emergency that requires
prompt treatment for both the
Pathophysiology
seizure activity and the resultant
University of Georgia
systemic abnormalities.
Simon R. Platt, BVM&S, MRCVS
John J. McDonnell, DVM, MS
KEY FACTS
■ SE is defined by a period of at ABSTRACT: Status epilepticus (SE) has been defined as continuous seizure activity lasting at
least 5 minutes or two or more discrete seizures between which there is incomplete recovery
least 5 minutes of continuous
of consciousness. SE is a medical emergency that requires prompt treatment to avoid neuro-
seizure activity.
logic morbidity. The etiologies of SE are similar to those for individual generalized convulsive
seizures. The pathophysiology of SE is also similar to that of an individual seizure event; how-
■ Several pathophysiologic ever, loss of the inhibitory mechanisms responsible for the cessation of an isolated event is
changes, including hypertension, suspected. Systemic effects of continuous seizure activity can be damaging if not identified
tachycardia, hypoglycemia, and treated promptly. This article discusses the clinical and physiologic features of SE as well
acidosis, and hyperthermia, as the pathophysiology of this disorder.
occur during SE.

S
■ Although the precise mechanism tatus epilepticus (SE) is a common medical emergency that requires prompt
underlying the pathophysiology treatment to avoid appreciable neurologic morbidity.1–5 Proper management
of seizures is unknown, it is involves prompt seizure control and treatment of the underlying etiology.3
thought to be related to abnormal Knowledge of the basic mechanisms of neuronal injury and systemic effects of SE
levels of excitation and inhibition provides the background required to determine the rapidity with which treatment
within a group of neurons in should be initiated. These considerations should be balanced carefully against the
which synchronous discharge side effects of aggressive pharmacologic agents to determine appropriate treat-
cannot be suppressed. ment. This article defines SE and addresses the clinical features, physiologic fea-
tures, and pathophysiology of the condition. Companion articles will discuss sys-
■ Precipitating factors must be temic and pharmacologic management as well as therapy for refractory patients
investigated to facilitate seizure and potential at-home treatment.
control and thereby prevent
irreversible cerebral damage. DEFINITION
Status epilepticus has been defined as a seizure that “persists for a sufficient length
of time or is repeated often enough that recovery between attacks does not occur.”6
This definition has been modified to state that SE represents seizures that persist for
20 to 30 minutes, based on the duration necessary to cause injury to the central
nervous system.3,4,6,7 This description is misleading, however, because SE is usually
treated clinically well before this arbitrary time has elapsed.7 A more practical defini-
tion of SE is that it is a continuous series of two or more discrete seizures lasting at
least 5 minutes between which there is incomplete recovery of consciousness.6–8
Compendium July 2000 Small Animal/Exotics

This definition of SE guides TABLE I tic seizures were reported in


clinicians in treatment specif- Classifications and Causes of Seizures 7% of the cases.12 Dogs with
ically intended to reduce Responsible for Status Epilepticus in Dogs reactive epileptic seizures are
neurologic injury and is dis- Classifications and Percentage of Percentage of considered to have normal
tinct from the definition of Causes of Seizures Cases 12,a
Cases 14,b brain structure; the seizures
cluster seizures. Cluster are caused by intoxication or
seizures are two or more Primary epilepsy 26.8 28.0 by systemic, metabolic, or
seizures occurring over a rela- Secondary epilepsy 35.1 32.0 endocrine abnormalities. 13
tively brief period (i.e., min- Meningoencephalitis 22.7 12.0 Chronic processes that result-
utes to 24 hours) between Neoplasia 3.6 12.0 ed in SE included preexisting
which the patient regains Other 8.8 8.0 epilepsy in which SE is
consciousness.9 (including trauma caused by breakthrough
The essential element of and vascular disease) seizures or the discontinua-
SE is a failure of the mecha- Reactive seizures 6.7 12.0 tion of antiepileptic drugs.7
nisms that terminate individ- Metabolic 5.2 4.0 In almost 6% of the cases,12
ual seizures and produce a re- Intoxication 1.5 8.0 low antiepileptic drug con-
fractory period during which Other 31.4 28.0 centration was determined to
another seizure cannot oc- Low antiepileptic 5.7 Not evaluated be the cause of seizures.
cur.7 Thus, in SE seizures re- drug concentration We have recently completed
cur before full recovery from Not determined 25.8 28.0 a case-controlled cohort study
the pathophysiologic alter- evaluating 50 dogs with gen-
ations in brain function in- aBased on 156 dogs admitted a total of 194 times for SE or eralized convulsive SE.14 Of
12
duced by the previous sei- bcluster seizures. the dogs studied, 28% were
Based on 50 dogs admitted for SE only.14
zure.7 If recurrent convulsions diagnosed with primary
are allowed to persist without epilepsy, 32% secondary
treatment or with inadequate treatment, a progressive epilepsy, and 12% reactive epilepsy.14 A specific cause
diminution of convulsive activity occurs such that the could not be determined in 28% of the cases (Table I).
motor manifestations of SE become increasingly subtle. In the Bateman and Parent study,12 cerebrospinal fluid
In this state, patients may exhibit profound stupor or (CSF) abnormalities were documented in 75 (73.5%) of
coma, with convulsive activity consisting of only subtle the 102 dogs with either SE or cluster seizures. In our
twitches of the extremities or trunk or nystagmoid move- study, 12 (36%) of the 33 dogs with SE had abnormal
ment of the eyes.7 CSF compared with 3 (12%) of the 25 dogs admitted
Of adult human patients recently diagnosed with ep- for non-SE seizures.14
6,10
ilepsy, 12% to 30% first presented in SE. Approxi- An unbiased mortality rate of dogs with SE is un-
mately 100 to 150,000 cases of SE are reported in chil- known because many animals are euthanized before ag-
dren and adults in the United States each year.7,11 The gressive diagnostics and treatment are undertaken. The
prevalence of SE in veterinary medicine has not been overall mortality rate among human adults with SE
determined; however, dogs with either SE or cluster ranges from 3% to 22%.2,10,15 These findings are diffi-
seizures have been estimated to be 0.44% of the total cult to interpret considering the variety of underlying
hospital admissions.12 In addition, Podell and cowork- problems that can cause SE. These underlying factors
ers reported fatal SE in 3 of 50 dogs (6%).13 may also explain why the mortality rate associated sole-
ly with SE has not been evaluated in animals. In the
OUTCOMES AND CAUSES Bateman and Parent study,12 approximately 25% of 156
Emergent presentation of SE has recently been evaluat- dogs with SE or cluster seizures died or were eutha-
ed in veterinary medicine. In a study by Bateman and nized. No significant associations were observed be-
Parent,12 156 dogs admitted to a veterinary hospital for tween the outcome of dogs with SE or cluster seizures
SE or cluster seizures were retrospectively evaluated (Table and the breed, age at onset of seizure activity, type of
I). A specific cause for the seizures could not be deter- seizure activity at admission, or findings on CSF analy-
mined in 25.8% of the cases. Approximately 27% were sis.12 However, a significant negative association was
12
diagnosed with primary (genetic or idiopathic) epilepsy. identified between the outcome and the diagnosis of
Secondary or acquired epilepsy (having an identifiable granulomatous meningoencephalitis and the outcome
structural cause within the brain)13 was identified as the and loss of control of the seizure activity at 6 hours af-
cause of seizures in 35% of the cases, and reactive epilep- ter admission.12

C L U S T E R S E I Z U R E S ■ R E A C T I V?E? ?E ?P I ■
L E P?T?I?C? S■E I Z? U
? ?R ?E S■ ■? ?C?E?R E B R O S P I N A L F L U I D A N A L Y S I S
Small Animal/Exotics Compendium July 2000

Magnetic resonance (MR) breeds found in the overall


imaging or computed tomog- hospital population; all of the
raphy (CT) yielded positive pugs and Boston terriers—
findings in 19 (76%) of 25 with one exception—had sec-
dogs with either SE or cluster ondary epilepsy, to which
seizures.12 Of the 50 dogs eval- these breeds are considered
uated for SE in our hospital, predisposed.12
CT was used in 28, 13 (46%) Patients with SE usually
cases of which showed abnor- have clinically obvious sei-
mal findings.14 zures, such as tonic, clonic, or
Although no evidence exists tonic–clonic movements of
to indicate that early initia- the extremities.7 This activity
tion of appropriate treatment is classified as generalized con-
improves outcome in dogs vulsive or grand mal seizures
with seizures, such evidence and is usually accompanied by
does exist in human medicine Figure 1—The effects of status epilepticus (SE) on the marked impairment of con-
and remains an important ba- body. It is not always possible to obtain electroencephalo- sciousness.7,8 Typically, there is
sic tenet of treatment.12 In ad- graphic evidence of seizure discharges. Electrocardio- gradual recovery of conscious-
dition to the above correla- graphic evidence of heart rhythm disturbances may be de- ness following each convul-
tions, hospital visits during tected after SE occurs. Hyperthermic damage to muscles sion, but if the patient has not
which partial motor SE was leading to rhabdomyolysis may cause renal failure. The recovered fully to baseline be-
documented had a significant detection of myoglobinuria and reduced urine production fore the next convulsion oc-
association with poor out- after SE is vital to outcome. curs, the patient is considered
come for dogs.12 to be in generalized convul-
The mean duration of hospitalization for dogs with sive or tonic–clonic SE. Nonconvulsive SE is well recog-
SE or cluster seizures is 51.6 ± 42.6 hours with a mean nized in humans (in whom patients are classified as hav-
cost per hospital visit of $320 ± $175 (range, $45 to ing complex partial SE and absent SE).7 In veterinary
12
$1131). These figures are biased by the year of the medicine, these types of SE have not been well docu-
study and the types of seizures treated; however, they mented clinically or electroencephalographically. Howev-
are a good indication of the financial commitment that er, veterinary patients have been documented to have fo-
may be required to successfully treat a patient with SE. cal motor seizure activity without loss of consciousness.
Focal motor activity is classified as a partial seizure indi-
CLINICAL FEATURES cating involvement of only a focal area of the brain.17
In Bateman and Parent’s study of 156 dogs admitted There is the possibility of this activity being prolonged
to a veterinary hospital (between 1990 to 1995) with enough to be classified as partial motor SE or that it will
SE or cluster seizures, the mean patient age was 4.2 ± be followed by generalized (tonic–clonic) SE.17
12
3.3 years (range, 1.9 to 13.9 years). In our study, the Human patients who have electroencephalographic
mean age of the 50 dogs evaluated for SE at our hospi- evidence of SE with little or no visible motor activity
tal over the course of 9 years (1990 to 1999) was 5.05 are still at risk for central nervous system injury and re-
years (range, 0.15 to 15 years), with no statistical gen- quire immediate attention.10 Ongoing SE can produce
14
der prevalence ; however, the results of the Raw and neuronal death in experimental models of SE even
Gaskell study indicate that there is a male sex predilec- when metabolic factors are corrected and in paralyzed
tion for primary epilepsy.16 In the Bateman and Parent animals that are ventilated.3,7 In our clinical experience,
study, the sex distribution for severe seizures (i.e., SE we have found that nonconvulsive SE does occur in pa-
and cluster seizures) was broken down as follows: tients with resultant poor outcomes if intervention is
23.7% were castrated, 35.3% were sexually intact not instituted.
males, 26.3% were spayed, and 14.7% were sexually in-
tact females.12 The English foxhound, pug, teacup poo- PHYSIOLOGIC FEATURES
dle, Boston terrier, and Lakeland terrier were signifi- Several physiologic changes occur during the course
cantly overrepresented in the Bateman and Parent of SE, including hypertension, tachycardia, hypo-
study, but the authors urge cautious interpretation of glycemia, acidosis, and hyperthermia (Figure 1). The
this finding.12 The English foxhound, Lakeland terrier, initial physiologic response is a massive release of
and teacup poodle had low numbers of their respective epinephrine and norepinephrine into the circulation.4,7

P R I M A R Y E P I L E P S Y ■ T O N I C – C L O N?I C ? O■V E?M?E?N? T■


? ?M S ■? ? F? O
? C■A L ?M
? ?O?T O R A C T I V I T Y ■ N E U R O N A L D E A T H
Compendium July 2000 Small Animal/Exotics

This increase in circulating ciated morbidity and mortali-


Trans-membrane voltage-gated sodium–potassium channel
catecholamines results in in- ty. It is clear that seizures are
creased systemic, pulmonary, linked, at the lowest level, to
and left atrial blood pressure; membrane potentials, ionic
heart rate; plasma glucose fluxes, and the generation of
concentration,7,18,19 and cardiac action potentials. 27 In neu-
20
arrhythmias. Based on exper- rons, action potentials result
imental animal studies, it has from changes in the mem-
been suggested that the hyper- brane permeability to sodi-
glycemia may exacerbate SE- um, chloride, calcium, and
induced neuronal damage.21 potassium. These ions enter
Therefore, glucose administra- the cell by voltage-gated
tion during SE should be Figure 2—A voltage-gated sodium–potassium channel as- channels (Figure 2).
cautious unless true hypo- sists in the creation of an action potential when the sud- In the resting state, the ex-
glycemia can be established. den influx of sodium ions (Na+) alters the relative concen- tracellular sodium concentra-
Respiratory function is fre- trations of sodium and potassium (K+) in the cytosol. tion is much higher than the
quently impaired in early intracellular concentration
SE.22 Pulmonary edema is a and the sodium channels are
common finding in experi- minimally permeable. A sodi-
mental SE and has also been um-potassium-ATPase pump
reported on postmortem ex- maintains the high extracellu-
aminations following clinical lar sodium and intracellular
episodes of SE.23 potassium concentrations.
Acidosis, which is caused Membrane depolarization is
by a combination of respira- caused by a sudden increase
tory failure and the release of in the membrane permeabili-
systemic lactate during gener- ty to sodium, consequently
alized convulsive activity,7 is generating an action poten-
frequently reported in SE. tial.27 Immediately after the
Some degree of acidosis can action potential generation,
be found even in paralyzed Figure 3—Release of a neurotransmitter from the axonal sodium channels close and
terminal following the propagation of an action potential.
and artificially ventilated ani- The synaptic vesicles contain neurotransmitter substance potassium channels open to
mals.7 In late SE (usually after that is released into the synaptic cleft and binds to the allow the rapid efflux of
30 minutes of seizure activi- postsynaptic receptors. potassium from the intracel-
ty), many physiologic param- lular space. 27 As the action
eters return to baseline values potential reaches the axon ter-
or even drop below baseline.7 After an initial period of minal, voltage-dependent calcium channels allow entry
hypertension, blood pressure begins to decrease after 15 of calcium ion into the terminal, causing the release of
to 30 minutes of experimental SE and may be marked- a neurotransmitter (Figure 3).27 The generation of the
ly low after 2 hours of continuous seizure activity. 18,24,25
action potentials may be critical in the initiation and
Plasma glucose levels may begin to decrease to hypo- propagation of the seizure discharge. The theory that
glycemic levels.18,24,25 Renal failure may develop as a re- many normal cerebral neurons exhibit intrinsic burst-
sult of rhabdomyolysis with resultant myoglobinuria.26 ing activity in which populations of cells fire in a rhyth-
mic and repetitive manner is already well accepted.27
PATHOPHYSIOLOGY Seizures are likely if the balance between excitation or
Seizures are the clinical manifestation of rapid, exces- inhibition surrounding these cell populations is abnor-
sive neuronal discharges in the brain.4 However, the mal.27 The synchronous firing of populations of neu-
precise electrophysiologic and molecular mechanisms rons is ultimately responsible for a seizure event.27
that underlie the pathophysiology of seizures and SE Several neurotransmitters have been implicated in the
are poorly understood. A firm understanding of the generation of seizures. γ-Aminobutyric acid (GABA) is
pathophysiologic causes and effects of SE will enable a critical neuromodulator in the brain.27 GABA medi-
veterinarians to make informed treatment decisions for ates synaptic inhibition in the hippocampus by generat-
animals that present in SE, perhaps decreasing the asso- ing inhibitory postsynaptic potentials, which counter-

G L U C O S E A D M I N I S T R A T I O N ■? ?A?C?I D■O S?I?S? ?■ ■A C?T?I?O?N ■P O?T?E?N?T I A L S ■ S O D I U M C H A N N E L S


Small Animal/Exotics Compendium July 2000

balance excitatory inputs from other neurons, it may propa-


other brain regions.27 There gate to other areas of the
are two primary GABA recep- brain. It is hypothesized that a
tor subtypes—GABA A and population of cortical neurons
GABAB. GABAA is believed to within an epileptic focus un-
be more intimately involved dergoes paroxysmal synchro-
in the neurochemistry of nous depolarization termed
seizures.27 After GABA binds paroxysmal depolarizing shift
to GABAA, there is an influx (Figure 5).29 This results in an
of chloride ions through the abnormal burst of action po-
chloride channel, which re- tentials that continue in syn-
sults in hyperpolarization and chronous volleys without ap-
hence inhibition (Figure 4). A propriate inhibition.27 Although
large body of evidence cur- elevated extracellular potassi-
rently suggests that disruption um levels may induce seizures,
of GABAergic function may the appearance of seizures is
be central to the molecular also dependent on intact
pathophysiology of seizures.27 Figure 4—The γ-aminobutyric acid (GABA) receptor –
is synaptic inputs from the hip-
During a seizure, an extra- responsible for an influx of chloride ions (Cl ) into the pocampus, which appears to
neuron after binding with a benzodiazepine (BZD),
cellular elevation of potassi- GABA, or a barbiturate (BBT) such as phenobarbital. facilitate the transition from
um and a decrease in calcium normal to ictal cell firing.27
are responsible for enhancing The basic pathophysiology
neuronal excitability and facilitating seizure spread.4,28 of SE involves a failure of mechanisms that usually stop
If there is synchronization of the seizure discharge with an isolated seizure.7 This failure can arise from abnor-
mal excessive excitation or ineffective recruitment of in-
hibition.7 It is likely that numerous mechanisms are in-
volved depending on the underlying cause. Recent
experimental work has suggested that the failure of in-
• Easy Reference Index
hibition may be caused by a shift in the functional
Emergency Medicine • 364 Pages
properties of the GABA receptor that occurs as seizures
in Small Animal Practice • Color and
Black-and-White
become prolonged.7,10 Repetitive neuronal firing impos-
Photographs es a massive metabolic demand, which is exacerbated
✶ Cardiac Emergencies by glutamate-mediated excitotoxicity and decreased
✶ Trauma GABA inhibitory neurotransmission.7,10 This has be-
✶ Shock Emergency come known as the excitotoxic theory of neuronal
✶ Seizure-related Medicine
Disorders
damage.7
✶ Toxicology Many molecular signals are triggered by SE, activat-
✶ Thermal Emergencies ing receptors in neuronal membranes.7 Activation of
and much more the N-methyl-D-aspartate (NMDA) receptor has been
known to play a key role in neuronal signaling and de-
o f f ! $
10% 61 in Small A
nimal Prac
tice
layed neuronal death.28 It has been shown that NMDA
receptors become activated during continuous neuronal
0 0
68
stimulation; in several animal models, NMDA receptor
$ The
COMPENDIUM antagonists have been shown to block or delay seizure
COLLECTION
activity. However, little is known about the receptor’s
precise role.7 Excess concentrations of the excitatory
CALL
NOW 800 426-9119 amino-acid glutamate causes NMDA receptors to open
cation channels to calcium (Figure 6). Large concentra-
tions of calcium enter the neuron and then induce a
Email: books.vls@medimedia.com cascade of intracellular neurochemical events that can
to order your copy or request a catalog of the
VLS BOOKS kill the cell.7 Other possible neurotoxic substances re-
complete line of VLS books, journals, and videos.
VE T E R I N A RY L E A R N I N G SYS T E M S

leased during SE include aspartate, free fatty acids,


arachidonic acid, and free radicals.28

GABA RECEPTOR SUBTYPES


Compendium July 2000 Small Animal/Exotics

Brain injury during pro- evaluated in veterinary medi-


longed seizure events may also cine. Other disease processes
be related to a mismatch be- commonly associated with
tween substrate supply and de- SE are tumors, central ner-
mand.3,28 Compensatory fac- vous system infections, trau-
tors may be unable to meet ma, metabolic disorders (e.g.,
the considerable metabolic de- electrolyte disturbances), and
mand placed on the brain dur- vascular events.
ing seizures.3 SE lasting longer On initial presentation of
than 30 minutes can cause the patient, it is prudent to
brain damage, especially in the examine the skull and spine
limbic structures.10,28 In several for evidence of recent trau-
animal models of SE, histo- ma. This should be done by
pathologic evidence of neu- gentle palpation, with partic-
ronal damage was identified ular attention in the assess-
following prolonged seizure ment of crepitance, pain,
activity within CA1 and CA3 and asymmetry. Standard
sectors of the hippocampus; laboratory blood tests, in-
layers 3, 5, and 6 of the neo- cluding evaluations for glu-
cortex; Purkinje cells within Figure 5—The spread of an ictal discharge through the cose, sodium, and calcium
the cerebellum; the thalamus; cerebrum depends on the synchronization of individual level abnormalities; renal and
and the amygdala. 27 Animal neuronal electrical disturbances known as paroxysmal de- hepatic dysfunction; and
models of SE have also polarizing shifts (PDS). A generalized convulsive seizure is serum acetylcholinesterase lev-
demonstrated the deleterious the physical manifestation of the recruitment and syn- els should be performed.3,31
chronization of neuronal PDS throughout both cerebral
role that hyperthermia, hypox- It should be noted that liver
hemispheres.
ia, and hypotension play in enzymes may be increased
creating further neuronal shortly after seizure activity
damage.10 However, observa- because of the effects of hy-
tion of neuronal changes in poxia and hypotension. 4 If
well-ventilated animals in hypoglycemia is the potential
which adequate glucose levels cause of SE or if blood glu-
have been maintained suggests cose determination is un-
that ongoing seizure activity available, 500 mg/kg body
itself substantially contributes weight of 50% dextrose
to neuronal damage.10 In hu- (preferably diluted to 25%)
man studies, it has been sug- should be administered intra-
gested that SE may diminish venously over 15 minutes.3,7
neurocognitive abilities.27 Hyperglycemia can be detri-
mental to the brain in the hy-
UNDERLYING CAUSAL poxic environment created
FACTORS by SE. To counteract this po-
When treating animals with tential, intramuscular ad-
SE, the precipitating factors ministration of thiamine (vi-
must be recognized and treat- tamin B1) at 25 to 50 mg per
ed in order to facilitate seizure animal should precede glu-
control and ensure that the cose administration.3,7 Thi-
underlying cause is ministered amine is essential as a coen-
to before irreversible cerebral Figure 6—The glutamate receptor and its role in the pas- zyme in glucose utilization
damage results. Many cases of sage of calcium into the cell body. Excessive passage of by the brain.8 If intravenous
SE occur in patients with calcium into the cell because of excessive concentrations therapy is difficult to per-
known chronic seizure disor- of glutamate can be responsible for cell destruction. form, oral administration of
ders,30 although the true inci- (AMPA = alpha-amino-3-hydroxy-5-methyl-4-isoxazole; Karo® syrup can be a useful
dence of this has not been NMDA = N-methyl-D-aspartate) substitute.

BRAIN DAMAGE ■ HIPPOCAMPUS ■ HYPOGLYCEMIA ■ SEIZURE STABILIZATION


Small Animal/Exotics Compendium July 2000

If the patient has been on phenobarbital or other anti- tocol, it should not prevent the rapid institution of pa-
convulsants prior to SE, serum levels should be ob- tient stabilization.
tained. If encephalitis is suspected, a CSF analysis
should be considered as soon as seizure stabilization oc- ACKNOWLEDGMENT
curs. The use of glucocorticoids can reduce cerebral ede- The authors thank Ms. Allison Wright, Department
ma formation and modulate the inflammatory response of Educational Resources, University of Georgia, Athens,
in the brain after a hypoxic event.32 However, corticos- for providing the artistic content.
teroids have been shown to potentiate neuronal damage
when ischemia is present and inhibit neuronal repair.32 REFERENCES
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LESIONS ■ PIRIFORM/TEMPORAL LOBE REGION ■ SIGNAL INTENSITY


Compendium July 2000 Small Animal/Exotics

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