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7 July 2000
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
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
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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