FIGURE 72.1 Diagnostic approach to seizures. The most common causes are in bold type.
An LP with analysis of the cerebrospinal fluid (CSF) is the only way to make
the diagnosis of meningitis and should be performed when meningitis is being
considered. An elevated CSF protein, CSF pleocytosis, and a low CSF glucose
level are all suggestive of CNS infection. CSF cultures, Gram stain, latex studies,
and polymerase chain reaction may identify a specific agent. Ideally, CSF
cultures should be obtained before antibiotic therapy is initiated. However, in the
critically ill or unstable patient, antibiotics should not be withheld until an LP is
performed. Furthermore, in cases in which a potential metabolic disease is being
considered, CSF lactate, pyruvate, and/or amino acid level determinations can be
used to diagnose a specific metabolic disorder. In these cases, it is often helpful to
collect an extra tube of CSF for later analysis. In any patient with signs of
increased intracranial pressure, an LP should not be performed until head imaging
can be done.
Electrolyte abnormalities may also cause seizures, with hyponatremia,
hypocalcemia, and hypomagnesemia being the most common. Unfortunately,
seizures caused by electrolyte derangements are often refractory to anticonvulsant
therapy and patients will continue to seize until the underlying abnormality is
corrected. In general, the routine screening for electrolyte abnormalities in a
patient with brief seizure is of low value. Serum electrolytes should be measured
in all patients with seizure with significant vomiting or diarrhea; patients with
underlying renal, hepatic, neoplastic, or endocrinologic disease; patients who are
taking medications that may lead to electrolyte disturbances; or patients who have
seizures that are refractory to typical anticonvulsant management. Another
clinical scenario involves hyponatremic seizures in infants, typically younger than
6 months, after prolonged feedings of dilute formula (“infantile water
intoxication”). Other patients may be evaluated on a case-by-case basis. IV
calcium, magnesium, and hypertonic (3%) sodium chloride should be used to
treat the appropriate abnormal condition. In the case of hyponatremia, 3% sodium
chloride should be infused rapidly until the seizure activity has been stopped;
subsequent to seizure resolution, a slower rate of sodium correction should be
used to avoid possible central pontine myelinolysis.
Rarely, other chemistries can be helpful in identifying specific organ
dysfunction, either as a cause of the seizure activity or as an assessment of
systemic injury. An elevated blood urea nitrogen or creatinine level suggests renal
insufficiency (with associated findings such as hypertension and electrolyte
disturbances) as a potential cause.
Elevated liver function tests (transaminases or coagulation times) can be a
reflection of hepatic failure. Metabolic acidosis or hyperammonemia can suggest
an underlying metabolic disorder. In patients with prolonged seizures, an arterial
or venous blood gas level can help in assessing adequacy of ventilation and a
creatine kinase level can identify possible rhabdomyolysis.
Toxicologic screening can also be helpful in the seizing patient because certain
ingestions are managed with specific antidotes or treatments. In general, the
toxicologic screen should be directed at agents known to cause seizures (Table
72.1 ) or those suggested by a clinical toxidrome.
Radiologic imaging of the patient with seizure generally consists of a
computed tomography (CT) scan for emergent imaging or, preferably, a magnetic
resonance imaging (MRI) study if the patient’s condition allows. The following
situations should be considered emergent:
(i) a patient who has signs or symptoms of elevated ICP,
(ii) a patient who has a persistent focal neurologic deficit (Todd paresis vs. stroke),
and in selected patients with a focal seizure or,
(iii) a patient who has seizures in the setting of head trauma,
(iv) a patient who has persistent seizure activity or status epilepticus, or
(v) a patient who appears toxic.
Until C-spine injury is ruled out, it is important to maintain C-spine
immobilization when head trauma is a concern.
Patients with transient generalized seizures in whom a cause of the seizure
activity is identified probably do not require any further head imaging studies.
Patients with transient generalized seizures in whom no cause is identified and
who appear clinically well can have their head imaging performed on a
nonemergent basis in coordination with a pediatric neurologist.
In the past, because of easier availability and lack of a need for sedation for
most patients, CT scans were most often the study of choice in the ED for a
patient who presented with a seizure. However, given the heightened awareness
of the risks of ionizing radiation associated with CT scans, patients who do not
require emergent imaging may have an MRI study instead. An MRI study also
has several other advantages; MRI is better at identifying underlying white matter
abnormalities, disorders of brain architecture, lesions of the neurocutaneous
syndromes, lesions in the posterior fossa and the brainstem, and small lesions.
EEG is an important diagnostic tool in the evaluation of seizure types, response
to treatment, and prognosis. A limited EEG screen in the acute setting can rule
out subclinical or nonconvulsive SE and help with differentiating seizures from
some cases of psychogenic nonepileptic seizures or PNES (formerly known as
pseudoseizures). When there is uncertainty regarding ongoing seizure activity, an
urgent electroencephalogram (EEG) should be obtained. In the emergency
department, this can be a limited study, with application of only a few electrodes
to determine if the background is consistent with a normal awake individual (i.e.,
psychogenic nonepileptic seizure) or the diffusely slow and depressed
background of SE. Over recent years, various products and protocols have
emerged for quick lead placement (e.g., helmets, etc.) among actively seizing
patients.
EMERGENCY TREATMENT OF AN ACTIVE SEIZURE
Prolonged seizure activity is a true medical emergency. Although the duration of
seizures used to define status has varied over time, an accepted definition for the
purposes of clinical practice defines SE as a single unremitting seizure lasting
longer than 5 minutes or frequent clinical seizures without an interictal return to
the baseline clinical state. This corresponds with the time at which urgent
treatment should be initiated, which is the new focus of the definition.
With this proactive, management based definition, following stabilization of
the ABCs, further treatment is directed at stopping any seizure activity. This
section will focus on three elements of seizure management: prevention and
preparation, antiepileptic medication use, and post stabilization measures.
Prevention and Preparation
PEM providers often encounter patients who start seizing during the ED visit.
Many of these patients are patients with known epilepsy, some are being treated
with antiepileptic drugs (AEDs), and for some increased seizure frequency or a
breakthrough seizure is the reason for the ED encounter. The PEM clinician will
be best advised to assess these patients promptly and be able to answer the
following questions:
What AEDs is this patient taking, what is the dosage and when is the next dose
due? Were any doses missed? Were any doses possibly un(der)absorbed (e.g.,
vomiting or diarrhea)? Are the parents aware of any recent AED levels of any of
the medications involved? When in doubt, AED levels should be obtained
promptly. Subtherapeutic levels of AEDs are found in nearly a third of pediatric
epilepsy patients actively seizing in the ED. Furthermore, some AEDs, including
phenytoin, carbamazepine, gabapentin, tiagabine, and vigabatrin, can precipitate
generalized convulsive SE, particularly the myoclonic type, as well as
nonconvulsive (absence) SE.
What is the active seizure plan for this patient? Many children with refractory
epilepsy have their own status epilepticus (SE) plan, which may different that the
one proposed for first time seizures. These patients should be advised to seek
such a plan with their primary neurologist if they have not yet done so. History of
prior SE episodes, including whether certain AEDs were successful or failed, may
guide the PEM clinician in decisions about treatment.
If any drug needs to be loaded on an active alert patient, it should be loaded
promptly in the fastest way possible (which may very well be oral
administration). Also, oral administration is less likely to generate excessive
sedation and respiratory depression.