Acute Symptomatic Seizures in Children and Adults: Evaluation and Treatment



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Acute Symptomatic Seizures in Children and Adults: Evaluation and Treatment


J. Stephen Huff1 and Jessica L. Carpenter2


1 Departments of Emergency Medicine and Neurology, University of Virginia, Charlottesville, VA, USA
2 Department of Neurophysiology, Children’s National Medical Center, George Washington University, Washington, DC, USA






Introduction


The approach to any patient in the emergency department or hospital who has had an apparent seizure begins with assessment of airway integrity, ventilation, and circulatory support. If required, intervention may involve a variety of airway maneuvers such as repositioning the patient’s head, suctioning, insertion of a nasopharyngeal airway, bag–valve–mask-assisted ventilations, or consideration of endotracheal intubation or a laryngeal mask airway if consciousness is impaired or respirations are deemed inadequate. For any patient with altered consciousness, intravenous access should be obtained. Rapid bedside determination of blood glucose should be performed, and if hypoglycemia is found, intravenous dextrose or intramuscular glucagon should be administered. If rapid glucose determination is not available and the possibility of hypoglycemia exists, intravenous dextrose should be administered. Intravenous thiamine should be given before or concurrently with dextrose infusion if there is the possibility of poor nutrition or a malabsorptive state.


The differential diagnosis for convulsive events includes syncope, convulsive concussion, movement disorder, sleep-related event, nonepileptic seizure, rigors, and other etiologies that are discussed in Chapter 5. In this chapter, we discuss patients diagnosed with acute symptomatic or provoked seizure(s). By definition, an acute symptomatic seizure occurs at the time or within seven days of an acute neurological, systemic, metabolic, or toxic insult. After patient stabilization, the clinician’s task is to discriminate between provoked and unprovoked seizures.


Some basic groupings of patients readily become apparent. Has the patient had a single seizure and returned to a waking state and baseline neurological function, or has the patient had a series of seizures? Has the patient failed to regain consciousness now that the convulsion has stopped? Was the seizure associated with fever or intoxication? Is there a head injury present? Diagnostic evaluation and treatment decisions are guided by these groupings. Recognition of status epilepticus, including subclinical status epilepticus, is critical. Management of status epilepticus is considered in Chapter 31.


Common causes


About 25–30% of first seizures are provoked or acute symptomatic seizures. Causes of acute symptomatic seizures may be grouped into primary central nervous system (CNS) etiologies such as hypoxia, stroke, trauma, infection, and inflammation and systemic causes such as electrolyte abnormalities, toxins, infection/sepsis, and fever (Table 30.1). In emergency departments, ethanol-related seizures are likely the most commonly encountered provoked seizures in adults. Hypoglycemia and electrolyte disturbances, notably hyponatremia, are also relatively common. Other etiologies are less likely but may be vital to detect and treat.


Table 30.1. Causes of acute symptomatic seizures.































Neurological
Stroke (e.g., ischemic, hemorrhage)
Hypoxic brain injury
Traumatic brain injury
Neoplasm (primary or metastatic)
CNS infection (e.g., meningitis, encephalitis, abscess)
Inflammatory (e.g., ADEM, lupus cerebritis, NMDAR Ab encephalitis)
Systemic
Sepsis
Fever (i.e., febrile seizures)
Toxic/metabolic
Electrolyte disturbance (e.g., hypoglycemia, hyponatremia, hypocalcemia)
Acute intoxications (e.g., antidepressants, theophylline)
Withdrawal syndromes (e.g., ethanol, benzodiazepines, barbiturates)

ADEM, acute disseminated encephalomyelitis; CNS, central nervous system; NMDAR Ab, anti-N-methyl-D-aspartate receptor antibody.







image CAUTION!

“Don’t miss” diagnoses for etiologies of acute symptomatic seizures include infection, hypoxia, trauma, neoplasms, electrolyte disturbances, and ingestions/toxins.





Common causes of acute symptomatic seizures in children are similar to those of seizures in adults, with infection representing a larger percentage. Febrile seizures are common, occurring in 2–5% of all children. A febrile seizure, by definition, is any convulsion in a child between the ages of 6 months and 5 years associated with a fever (T > 38°C) at the time of illness, without a CNS infection. Febrile seizures can be classified as simple or complex (Table 30.2), with simple febrile seizures being associated with a good neurodevelopmental outcome (including only a slight increase risk of epilepsy later in life). Febrile seizures tend to run in families – recent studies have identified several genetic mutations (e.g., SCN1A in generalized epilepsy with febrile seizures plus [GEFs+]) associated with an increased risk for this type of provoked seizure. There has long been concern that children with febrile status epilepticus (FebSTAT) may be a specific subset of children with febrile seizures that are at increased risk of epilepsy later in life. This question is the focus of a large prospective study of children with prolonged FebSTAT. Thus far, the study has demonstrated an increased risk for hippocampal injury after prolonged febrile seizures, but the true risk for epilepsy is still to be determined.


Table 30.2. Febrile seizures.




















Simple febrile seizures
<15 min in duration
Nonfocal (i.e., generalized, including onset)
Does not recur in a 24-h period
Complex febrile seizures
>15 min in duration
Focal (or postictal focal weakness)
Recurrent within a 24-h period




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Mar 12, 2017 | Posted by in NEUROLOGY | Comments Off on Acute Symptomatic Seizures in Children and Adults: Evaluation and Treatment

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