V Vol. 22, No.
8 August 2000
CE Refereed Peer Review
FOCAL POINT
★ Because status epilepticus (SE)
frequently occurs outside the
hospital, prompt prehospital
treatment, including rectal and
intranasal administration of
drugs, can improve patient
management.
KEY FACTS
■ SE that does not respond to a
benzodiazepine or phenobarbital
requires more aggressive
treatment; potential reasons for
refractory seizure activity include
inadequate anticonvulsant doses,
an uncorrected metabolic
abnormality, intoxication,
or tumor.
■ Adequate doses of thiopental and
pentobarbital will usually control
the physical manifestations of
seizures, but severe hypotension
limits their safety.
■ The resources needed
to manage the potential
complications of intravenous
therapy in seizuring patients are
often inadequate, and may result
in severe systemic and cerebral
damage or death.
■ Rectal administration of
anticonvulsants is relatively easy
to carry out in the home and,
therefore, is useful in
emergencies.
Status Epilepticus:
Managing Refractory
Cases and Treating
Out-of-Hospital
Patients*
University of Georgia
Simon R. Platt, BVM&S, MRCVS
John J. McDonnell, DVM, MS
ABSTRACT: Status epilepticus (SE) is an emergency medical situation that may not respond
to benzodiazepine or phenobarbital treatment. This situation is termed refractory SE and re-
quires more aggressive treatment such as anesthesia. SE may also occur in the home environ-
ment where facilities are limited. The time that passes before treatment is instituted is crucial
in the prevention of permanent cerebral damage and may be important in saving the patient’s
life. For such patients, the efficacy of rectally delivered diazepam has been established. In-
tranasal delivery of anticonvulsants is being evaluated in dogs and may represent a future
method of at-home seizure control.
S
tatus epilepticus (SE) is a medical emergency that requires prompt treatment
to avoid appreciable neurologic morbidity.1–5 The proper management strat-
egy involves prompt control of seizures.3 Benzodiazepines (i.e., diazepam, lor-
azepam, midazolam, and clonazepam) are potent, fast-acting anticonvulsants that
form the cornerstone of early SE therapy.1-4 In animal screening tests, benzodi-
azepines have shown a broad spectrum of anticonvulsant activity and may at low
doses effectively inhibit seizure activity.6 However, there are situations in which
these drugs do not arrest continuous seizure activity and other treatments should
be employed. The companion articles in this series discussed the manifestations,
pathophysiology, and treatment of patients with SE. This paper explores the
treatment of refractory SE by veterinarians and at-home seizures by owners.
*A companion article entitled “Status Epilepticus: Clinical Features and Pathophysiology”
appeared in the July 2000 (Vol. 22 No. 7) issue of Compendium. The second installment,
entitled “Status Epilepticus: Patient Management and Pharmacologic Therapy,” can be
found in this issue. This is the final article in the series.
Compendium August 2000 Small Animal/Exotics

REFRACTORY STATUS EPILEPTICUS
Status epilepticus that does not respond to a benzodi-
azepine or phenobarbital is considered refractory and
requires more aggressive treatment5,7,8 (Figure 1). Poten-
tial reasons for resistant seizure activity include inade-
quate anticonvulsant doses, an uncorrected metabolic
abnormality, or the presence of intracranial disease
(e.g., a tumor).3,9 These patients are often difficult to
treat. Short-acting anesthetic drugs are commonly used
to treat resistant SE because these agents have a rapid
onset of action and short half-lives and reduce cerebral
metabolic rates.3 These drugs should be used only in an
intensive care setting because blood pressure and cen-
tral venous pressure should be monitored continuously.
General anesthesia prevents tonic–clonic movements
and allows control of respirations.
Continuous Benzodiazepine Infusion
Continuous benzodiazepine infusion has been shown
to be effective for treating refractory SE in humans and
animals.5,10 Continuous intravenous (IV) infu-
sions of diazepam were administered to 124 of
186 (66.8%) dogs with severe seizures,10 but
the efficacy of this treatment could not be de-
termined. The authors reported that continu-
ous diazepam infusions may be underused in
10
the management of dogs with seizures. The
its rapid clearance, chiefly eliminated by hepatic conju-
gation to inactive metabolites, and less profound hy-
potensive effects.2,3,13 However, propofol should be used
with caution and preferably in settings in which defini-
tive airway control and hemodynamic support are possi-
ble because hypoxemia secondary to apnea as well as
myocardial depression are primary side effects.2
When using propofol, seizures have been observed
during the induction of and emergence from anesthe-
sia, but the importance of these proconvulsant effects
in SE management is unknown.3,7 Whether the convul-
sive phenomena occasionally seen with the use of this
drug represent seizures, excitatory events, and/or a dis-
order of muscle tone is controversial.2 Experimental an-
imal models have documented the anticonvulsant ef-
fects of propofol.2 This drug has been shown to raise
the lidocaine seizure threshold in rats, arrest bupiva-
caine-induced seizures as effectively as thiopental at 10-
mg/kg doses, and be as potent as is diazepam at pre-
venting pentylenetetrazol-induced seizures in rabbits.2
Seizures persist despite treatment
with diazepam and phenobarbital
Medical team and
No
owner decide to use
Yes
aggressive treatment

dose should be calculated hourly (0.1 to 0.5 Options are: Consider:

1) Additional low-dose  1) Intubation/ventilation
mg/kg [0.23 mg/lb]) and is usually diluted in  boluses of diazepam 2) Arterial line for blood 
2) Continuous IV diazepam   gas evaluation
5% dextrose in water, with the volume used be-  infusion 0.1 mg/kg/hour 3) Urethral catheter
ing equal to the maintenance fluid requirement  in 2.5% dextrose/0.9%  4)  Continuous
 sodium chloride drip at   electrocardiogram
over the hour (Figure 1).5,10,11 The dose can be  maintenance rate 
delivered with an infusion pump. The infusion 3) No further treatment 
 except to optimize  Consider cause and institute
of diazepam should be used with caution be-  phenobarbital serum  maintenance therapy
 level
cause of its poor aqueous solubility, tendency
IV pentobarbital Yes
to crystallize in solution, and adsorption onto 1) 3–15 mg/kg to effect Phenobarbital
5
polyvinyl chloride tubings. Midazolam, which Seizures
2) Dopamine to maintain  infusion maximum
stop?
 blood pressure 24 mg/kg/day
is completely water soluble, has been used as a
safe, effective therapy for pediatric patients No No

with SE but is more expensive to administer.8 No

IV dopamine infusion
Severe Significant Yes
Seizures 2–10 µg/kg/min and/or
decreased hypotension/
Propofol No
blood pressure
stop
bradycardia?
IV dobutamine 2–10
µg/kg/min
In humans with refractory SE, IV infusions
Yes Yes
of anesthetic doses of propofol (2,6-diisopropyl-
3,7,12–14
phenol) have become standard. This ap- Poor prognosis consider: IV pentobarbital
proach has recently been evaluated in animals.15 1) Isoflurane anesthesia infusion 1 mg/kg/hour
2) Propofol infusion up to 6 hours
Propofol has shown barbiturate- and benzodi-  0.1–0.6 mg/kg/minute
azepine-like effects on the γ-aminobutyric acidA 3) IV mannitol 1 g/kg bolus
4)  IV furosemide 0.7 mg/kg
(GABAA) receptor and can suppress central ner-
vous system metabolic activity.12,13 Propofol can
be administered by IV bolus or by constant-rate Figure 1—Patients in status epilepticus that fail to respond to diazepam
and phenobarbital are considered to be refractory. This algorithm depicts
infusion (0.1 to 0.6 mg/kg/minute).3,14,15 The treatment options for these patients. IV = intravenous.
advantages of propofol over the barbiturates are

ANESTHETIC DRUGS ■ INFUSION PUMP ■ HYPOTENSIVE EFFECTS ■ AIRWAY CONTROL

Small Animal/Exotics
Several reports have documented the anticonvulsant ac-
tivity of propofol in humans.12 Stecker and colleagues
recently reported that propofol can control refractory
SE more quickly in humans than can high-dose barbi-
turates.12 Because of the pharmacokinetics of propofol,
it is believed that even if this drug failed to control
seizures and high-dose barbiturates were required, little
time would be lost and there would be no long-term
interference with other treatments.12 Heldmann and
colleagues recently studied the use of propofol in in
four cats and one dog with naturally occurring seizures
following the surgical attenuation of single extrahepatic
portosystemic shunts. 15 All of the patients, two of
which had seizures that were unresponsive to other an-
ticonvulsants, responded to propofol.15 All five animals
had regular indirect blood pressure measurements and
remained hemodynamically stable when the drug was
appropriately administered.15 All of the animals sur-
vived to discharge.
Barbiturates
Thiopental and pentobarbital have shown potential,
although unproven, cerebral protective effects in the
management of SE. Adequate doses of these drugs usu-
ally control the physical manifestations of seizures, but
severe hypotension limits their safety.4,7,8 Pentobarbital
sodium (Nembutal®; Abbott), used at standard safe
doses, is a general anesthetic with negligible anticonvul-
sant properties.4 Thiopental has been associated with a
higher degree of cardiac toxicity than has pentobarb-
ital.13 In one study, Roesch and colleagues reported more
ventricular arrhythmias in animals treated with thio-
pental than in those treated with pentobarbital at doses
lower than those required to cause a flat electroen-
cephalogram (EEG).13 At higher doses than those re-
quired to produce a flat EEG, only two of seven dogs
treated with thiopental survived whereas all 17 dogs
treated with pentobarbital survived.13 Pentobarbital
should be given to effect and not as a specific dose (3 to
15 mg/kg IV) because response varies widely among pa-
tients (Figure 1).
Patients treated with “barbiturate coma” commonly
require an extended period of mechanical ventilation in
an intensive care setting.5,8,12 In general, the side effects
of barbiturate coma include depression of myocardial
metabolism, vasodilation with a decrease in venous re-
turn, and decreased cardiac perfusion.16 These effects
can be minimized by using saline infusion and small
doses of dopamine. Patients can develop poikilothermia
and decreased urinary output during myocardial de-
pression and hypotension. Neurologic evaluation is dif-
ficult because spontaneous respiratory responses and
movements cease. We recommend reserving the use of
CARDIAC TOXICITY ■ SALINE INFUSION ■ POTASSIUM EFFLUX ■ ISOFLURANE
Compendium August 2000
these anesthetics for patients in which benzodiazepines
and phenobarbital fail.
Etomidate
Etomidate, which has shown GABA-ergic activity in
the brain, is a short-acting drug. The anticonvulsant ef-
fects of this agent in dogs and cats have not yet been
documented.4
Lidocaine
In 1955, IV lidocaine was first reported as a treat-
ment for SE in humans.17 Since that time, a number of
studies, mostly in Europe, have reported the efficacy of
lidocaine in refractory SE,9 although no large, double-
blind, placebo-controlled studies have proven the drug’s
efficacy in humans with SE.17 The exact mechanism by
which lidocaine terminates seizures is unknown at pres-
ent. Lidocaine decreases neuronal excitability by block-
ing voltage-dependent sodium channels in the cell
membrane.17 In addition, it reduces potassium efflux
into the extracellular space and decreases neuronal mi-
tochondrial metabolism and cerebral oxygen consump-
tion.17 Increased extracellular potassium increases the
concentration of the excitatory neurotransmitter gluta-
mate and may increase the recruitment of other neu-
rons into the seizure activity.17 Most reports on the use
of lidocaine in humans recommend a maintenance in-
fusion after initial termination of SE.17 Lidocaine has
been reported to cause seizures as well as myocardial
depression and cardiac conduction abnormalities. 17
However, the signs attributable to lidocaine toxicity are
rare clinically when the drug is used specifically for its
anticonvulsant properties. The optimal anticonvulsant
dose of lidocaine in humans and animals is unknown;
we do not recommend its use in SE until further inves-
tigations have been pursued.
Inhalational Anesthesia
Inhalational anesthetics have been recommended as a
treatment of last resort for patients with resistant SE.
The equipment and personnel necessary to administer
inhalational anesthesia may not be readily available and
the equipment can be cumbersome. Isoflurane, an in-
halational general anesthetic agent, may be efficacious
in the treatment of resistant SE.3 Not all of the volatile
anesthetic agents have antiepileptic potential; however;
enflurane may actually increase seizure activity.3 Isoflu-
rane, which has been studied extensively, does not un-
dergo hepatic metabolism and has a rapid onset of ac-
tion.3 Obviously, isoflurane therapy requires ventilation
and intensive care monitoring; hypotension may occur
during therapy.3
Compendium August 2000
Muscle Relaxants
Curarization, which allows control of respiration,
prevents tonic and clonic movements and physical in-
jury9; however, it does not prevent ongoing cerebral
seizure activity.9 Animal studies indicate that prolonged
seizure activity—even in paralyzed, ventilated ani-
mals—results in irreversible cerebral damage.9
OUT-OF-HOSPITAL STATUS EPILEPTICUS
Patients that present with SE demonstrate massive
uncontrolled muscle activity that often makes it diffi-
cult to administer essential anticonvulsant medications
into the vein. In out-of-hospital situations, the re-
sources to manage potential complications of IV thera-
py are inadequate; therefore, severe systemic and cere-
bral damage may result and can lead to death in some
dogs.18 However, if prompt prehospital seizure treat-
ment can be given, fewer antiepileptic drugs (AEDs)
are required and seizures tend to be shorter.1,19 Rectal
(PR), intranasal (IN), and buccal/sublingual routes of
administration may be useful in these settings, especial-
ly because the absorbed drug bypasses the liver (thereby
avoiding the problem of first-pass metabolism).19 IV
and intramuscular (IM) injections during SE can pose
risks to patients and caregivers and are often difficult to
administer 20; therefore, PR and IN administration,
which needs further study, will be used more routinely.
IN anticonvulsants have been used successfully in treat-
ing humans with SE.20
Because administering benzodiazepines by these
routes is not licensed, these methods must be used with
caution. Benzodiazepines are also Schedule IV drugs
and are not approved for animal use by the FDA.4 Di-
azepam, however, remains the drug of choice for treat-
ing SE in dogs and cats.4 Clients should be instructed
that at-home treatment of seizures must not replace im-
mediate veterinary attention for systemic stabilization.
Indications for immediate veterinary care may include
seizures that do not respond within 10 minutes to the
at-home therapy prescribed; seizures that respond but
recur within 24 hours; and systemic concerns such as
depressed respiratory effort, obtundation, and blind-
ness. The dangers of being in close contact with a
seizuring dog should also be emphasized to clients.
Rectal Drug Administration
Rectal AED administration, which is relatively easy
to perform in the home environment, can be useful in
emergencies. The absorption of lipid-soluble drugs by
the membranes of the colon and rectum is rapid and
complete.21 Diazepam can be administered into the rec-
tum using plastic administrators (e.g., teat infusion
cannulas, tomcat catheters) with a water-soluble lubri-
ANTIEPILEPTIC DRUGS ■ THERAPEUTIC CONCENTRATION ■ PHARMACOKINETIC STUDIES
Small Animal/Exotics
cant.11 The efficacy of diazepam delivered PR depends
on the time needed for the drug to reach the therapeu-
tic concentration and how much of the agent is needed
for the individual dog. In humans, the therapeutic con-
centration is estimated to be approximately 150 to 300
ng/ml.22 If this is also true in dogs, several canine stud-
ies have demonstrated that this level can be reached
well within 30 minutes—the time before serious neuro-
logic morbidity occurs.22 The actual therapeutic level in
dogs has not been well documented and may range
from 300 to 1500 ng/ml.23
Podell and colleagues evaluated the use of PR di-
azepam at home for cluster seizures in dogs.24 The au-
thors reported fewer seizures per cluster, reduced owner
cost for emergency room visits, and good owner com-
pliance.24 In pharmacokinetic studies, 0.5 mg/kg of di-
azepam delivered PR produced a mean peak total ben-
zodiazepine concentration of approximately 500 ng/ml
in four healthy beagles.25 A separate study using six
healthy mixed-breed dogs found that the mean peak to-
tal concentration of benzodiazepines was 474 ng/ml
with a dose of 1 mg/kg.23
The effect of concurrent long-term oral phenobarbi-
tal administration on diazepam delivered PR has re-
cently been evaluated.22 The mean peak concentrations
of diazepam after PR administration in six dogs fell
from 629 to 274 ng/ml after the dogs were given phe-
nobarbital (2.5 mg/kg every 12 hours for 30 days).22
These results demonstrated that dogs receiving chronic
phenobarbital therapy may require a higher dose of PR
diazepam than those dogs that have not been previously
treated with this drug. These phenomena resulted from
the increased activity of the hepatic microsomal enzyme
system caused by phenobarbital administration.
Pilot studies on the use of 0.2 mg/kg IV and 0.5 to
1.0 mg/kg PR lorazepam in normal dogs suggest that
lorazepam may not be acceptable for PR administration
because of an extensive first-pass effect.26 However, lor-
azepam can reach therapeutic blood concentrations
when administered IV.26
Rectal administration of a parenteral solution of di-
azepam (0.5 mg/kg) is approximately 80% effective in
controlling prolonged seizures in children, usually
within 15 minutes.27 European studies have emphasized
the safety and efficacy of at-home use of PR diazepam
in treating seizures.27 Previous canine studies have failed
to document any adverse cardiovascular or respiratory
effects when diazepam is administered PR.22,28
A gel formulation of diazepam in a prefilled (5
mg/ml) single-dose syringe for PR administration (Dia-
stat®; Athena Neurosciences) has become available
in the United States for the treatment of seizure clusters
in children and adults.29 In a randomized study, admin-
Small Animal/Exotics
istration of a single dose of Diastat® in
humans was significantly more effec-
tive than was placebo in reducing the
number of seizures.29 In addition, Dia-
stat® increased the probability that pa-
tients would remain seizure free for 12
hours after treatment compared with
patients who received the placebo. Re-
ported adverse effects of Diastat® (e.g.,
sedation) are consistent with the
known safety profile of diazepam. Dia-
stat® seems to have no observable de-
pressive effects on respiratory rate.29
PR administration of diazepam gel Figure 2—Intranasal administration of diazepam. Rapid uptake of the drug results in
may be useful for out-of-hospital man- part from the profuse vascular supply of the nasal turbinate mucous membranes.
agement of SE; however, its expense The close proximity of the cribriform plate and nasopharynx should also be noted.
may prohibit its use in animals.
In humans, the use of diazepam suppositories is of
limited value in the treatment of SE because therapeu-
tic plasma concentration is not reached until after 20
minutes.30 One author (S. P.) is now evaluating the mer-
its of diazepam suppositories compared with parenteral
diazepam administered PR.
Canine studies have previously demonstrated the im-
portance of the drug formulation and the vehicle used
in determining the bioavailability of PR diazepam.31
Parenteral diazepam is compounded with 40% propy-
lene glycol and 10% ethyl alcohol. This commercially
available formulation is not approved for use as a PR
27
drug. When this formulation of diazepam solution
was administered in high doses to rats, no significant
gross or microscopic changes in the rectal mucosa were
observed.21 Although this provides evidence of its local
safety, a potential complication of the use of PR di-
azepam in dogs may be the development of a perirectal
abscess, which was recorded in one dog.32 This compli-
cation may be a technique-associated problem rather
than a direct reaction to the drug; therefore, PR admin-
istration protocol should be reviewed thoroughly with
owners. Requiring the use of a glass ampule, needle,
and syringe for dispensing and tubing for administra-
tion, this method of delivery not only has the potential
for dosing error but is awkward and may cause poten-
tial injuries to patients or caregivers.27
Compounding pharmacies can help prepare diazepam
suppositories. Logistical problems created by the use of
syringes and the technical abilities required by the clients pass metabolism after IN dosing.34 This property may
in dosing their pets from a glass ampule can be avoided
by using suppositories. This practice may also reduce
concerns regarding scheduled drug misuse and abuse.
The dosages we use range from 0.5 mg/kg to 2.0 mg/kg.
With peak plasma concentrations occurring within
10 minutes after administration, PR administration of
SUPPOSITORIES ■ DRUG FORMULATION ■ SYSTEMIC EFFECTS ■ THRESHOLD
Compendium August 2000
midazolam in humans has been shown to be safe and
effective.33 After rectal instillation of a midazolam hy-
drochloride solution (0.3 mg/kg) in healthy human
volunteers, a mean bioavailability of 52% was found.31
Clinical effects, measured in terms of sedation and
EEG activity, were comparable to those obtained with
IV administration.31
Intranasal Drug Administration
In recent years, IN drug administration for systemic
effects has received increased attention because of its
convenience and reliability (Figure 2).34 IN AEDs have
been used successfully in humans with SE.35 Midazo-
lam, which has been shown to be quickly absorbed by
the nasal mucosa, can reach levels that equal or sub-
stantially exceed the threshold for sedation in hu-
mans.35,36 The duration of action following IN adminis-
tration is similar to that after oral dosing, although the
onset of action is earlier.32 Peak plasma concentrations
were reported 10 minutes after administration in hu-
mans and plasma concentrations of midazolam exceed-
ing therapeutic values were seen within 3 minutes after
IN administration in children.36,37 Maximum plasma
concentration for IN midazolam, triazolam, and flu-
razepam in dogs has been achieved within about 15
minutes.34 The bioavailability of these drugs following
IN delivery was more than two times greater than after
oral absorption.34 The difference in bioavailability has
been postulated to be caused by a reduction in first-
allow the use of lower doses of the IN drug. We have
shown that the time needed to reach the maximum
benzodiazepine plasma concentration for IN diazepam
(0.5 mg/kg) in dogs was within 6 minutes.38 Lorazepam
and midazolam are currently being evaluated in normal
dogs by one of the authors (S. P.) for their potential use
Compendium August 2000
in an IN dosing regimen. At present, no data exist on
the use of lorazepam in clinical studies.
The onset of the sedative effects of midazolam was
seen within 3 minutes after the drug was administered
IN to rabbits.37 The fast response time may be an indi-
cation of the previously described direct pathway from
the nasal cavity to the brain.30 It has also been suggested
that drugs instilled into the nasal cavity may directly
reach the brain by the cribriform plate and that the
concentration in the central nervous system may be
higher than that reflected by measurements of plasma
concentrations.37 Radiographic studies performed on
rabbits using contrast dye showed that administered
liquid IN reaches the vomeronasal gland, which has a
rich vascular supply, and that some liquid, albeit a
small amount, may be swallowed.37 Further studies to
better understand the uptake and absorption from the
nasal cavity are required.
A problem identified with the use of IN diazepam
has been the excessive volume that may be required in
large patients. Unfortunately, only a few formulation
studies of solubility have been performed on diazepam
in an attempt to administer larger doses of the drug in
smaller volumes.30 In a rabbit study, a comparison was
made of the pharmacokinetic parameters after a single
IN administration of diazepam in various formula-
tions compared with a single IV injection.30 The au-
thors reported that nasal application of diazepam in a
water-free, low-molecular-weight glycol might be of
clinical importance.30 When midazolam was adminis-
tered as drops of aqueous solution, mean bioavailabili-
ty was 55%.39 If the midazolam is given as an IN spray,
the bioavailability is approximately 85%.39 The dis-
parity is caused by that portion of the drug that is
expelled out of the nostrils or swallowed and then ab-
sorbed by the gastrointestinal tract. The mean bio-
availability of oral midazolam in children has been es-
timated to be 15% to 27%, depending on the dose.39
This low bioavailability is chiefly the result of exten-
sive first-pass metabolism producing 1-hydroxymida-
zolam as the main metabolite. 39 Thus, even if the
mean bioavailability of unchanged midazolam after
IN administration is only 55%, formulation of active
metabolite after intestinal absorption of the remaining
dose could theoretically result in a total pharmacolog-
ic effect approaching that achieved after parenteral ad-
ministration.39
The development of an accurate IN delivery system
may allow for greater drug absorption through the
nasal mucous membranes, less oral intake, and a more
profound effect. We cannot yet make any recommen-
dations regarding IN anticonvulsant treatment in dogs
and cats.
CRIBRIFORM PLATE ■ PARAMETERS ■ BIOAVAILABILITY ■ ARTERIAL LEVELS
Small Animal/Exotics
Buccal Administration
A recent study on the buccal absorption of midazolam
in humans demonstrated a rapid increase in venous mi-
dazolam concentrations for the first 20 to 30 minutes
after administration19; however, this study also revealed
direct evidence of a more rapid cerebral effect identified
by spectral analysis of EEG recordings.19 Rapid clear-
ance of the drug from the arterial circulation into the
brain and fat may be the mechanism that results in ini-
tial venous blood levels being lower than arterial levels.19
To the authors’ knowledge, the buccal route of anticon-
vulsant delivery has not been evaluated in animals.
SUMMARY
Generalized convulsive SE has been recognized for a
long time and characterized by recurrent or prolonged
generalized seizure events and profound impairment of
consciousness. Generalized SE must be treated early to
achieve the greatest probability of success. Morbidity
and mortality are largely determined by the underlying
etiology, but inadequate treatment further worsens a
poor prognosis. If treatment cannot be established ear-
ly, the probability of permanent neurologic damage be-
comes more likely. Because SE often starts in the home,
rapid treatment becomes a logistical problem. Dispens-
ing parenteral benzodiazepines for PR administration is
one option at present, although the use of these drugs
is not licensed in veterinary patients and thus should be
carefully managed. The success of this therapy relies on
complete client education, a thorough knowledge of
the properties of the drugs and methods of delivery, as
well as careful documentation of all client communica-
tions and the drugs dispensed.
ACKNOWLEDGMENTS
The authors thank Ms. Allison Wright and Ms. Emily
Pritchard, Department of Educational Resources, Univer-
sity of Georgia, Athens, for the artistic content.
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About the Authors
When this article was submitted for publication, Drs. Platt
and McDonnell were affiliated with the Department of
Small Animal Medicine, College of Veterinary Medicine,
University of Georgia, Athens. Dr. Platt is now affiliated
with The Animal Health Trust, Centre for Small Animal
Studies, Suffolk, England. Dr. McDonnell is affiliated with
the Veterinary Medical Center, Tufts University, North
Grafton, Massachusetts. Both authors are Diplomates of
the American College of Veterinary Internal Medicine
(Neurology).