Febrile seizures

Diagnostic workup
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By Renée Shellhaas MD MS, Carol S Camfield MD, and Peter Camfield MD

The initial workup of a febrile seizure should include a thorough history from a reliable witness and a careful pediatric and neurologic examination (Freeman 1980). If the cause of fever can be identified and if the child presents no disturbance of consciousness, it is usually not necessary to obtain further laboratory evaluation (American Academy of Pediatrics 1996; 2011). Implementation of evidence-based protocols for evaluation and management of children with febrile seizures can decrease the rate of hospital admission and of unnecessary testing (Callegaro 2009). Without standard protocols, however, many centers report lack of adherence to published guidelines (Sakai 2009; Shaked 2009).

Measurements of serum electrolytes (particularly sodium), glucose, blood urea nitrogen, calcium, and phosphorus levels should be reserved for children for whom there is a reasonable suspicion that 1 or more may be abnormal (Hirtz 1989). These tests are not recommended if their sole purpose is to identify the cause of a simple febrile seizure (American Academy of Pediatrics 2011). It should be noted that a serum sodium less than 135 umol/L is often noted in children who present with a febrile seizure. Recent studies have reported no difference in serum sodium levels between children with initial single simple and recurrent (within 24 hours) brief febrile seizures (Thoman et al 2004; Maksikharin and Prommalikit 2015). Rates of bacteremia are low, 2%, as are other serious bacterial illnesses (Shah et al 2002). Therefore, blood cultures and complete blood count are not routinely necessary.

A retrospective study of all cases of first simple febrile seizure presenting to an American tertiary care emergency department from 1995 to 2006 demonstrated a cerebrospinal fluid pleocytosis in 10 (3.8%; 95% confidence interval: 1.9% to 6.9%) of the 260 infants who underwent a lumbar puncture, with no pathogens isolated on bacterial culture. No patient in this study who was initially diagnosed with a first simple febrile seizure went on to develop bacterial meningitis (Kimia 2009). The same group analyzed the yield of lumbar puncture among 340 children with their first complex febrile seizure (Kimia 2010). Fourteen of the 340 patients had a CSF pleocytosis, and 3 had acute bacterial meningitis. These patients had additional signs and symptoms, which raised suspicion for meningitis. In another study, among 136 children with febrile status epilepticus who had a nontraumatic lumbar puncture (less than 1000 red blood cells/mm3), 96% had less than or equal to 3 white blood cells/mm3 (Frank et al 2012). In another study, among 136 children with febrile status epilepticus who had a nontraumatic lumbar puncture (less than 1000 red blood cells/mm3), 96% had less than or equal to 3 white blood cells/mm3 (Frank et al 2012). The authors caution that these studies apply only to populations with high rates of vaccination against Haemophilus influenzae type B and Streptoccocus pneumonia.

Neuroimaging should not be performed in the routine evaluation of a child with a first simple febrile seizure (American Academy of Pediatrics 2011). A CT or MRI should be performed only when an underlying structural lesion is suspected (American Academy of Pediatrics 1996; Hirtz et al 1997). Even in complex febrile seizures, in most cases, neither an emergent head CT nor MRI is necessary (Hampers et al 2006; Teng et al 2006; Hesdorffer et al 2008). Hesdorffer has suggested that associated brain abnormalities do not alter the clinical management of the febrile seizure and that the recommendation remains that brain MRI is unnecessary in children with a simple febrile seizure (Hesdorffer et al 2008). Of course, neuroimaging might be considered when the child has significant focal neurologic or developmental abnormalities, neurocutaneous lesions, or abnormal head size.

An EEG should not be routinely performed in the evaluation of a neurologically healthy child with a first simple febrile seizure, either at the time of presentation or within the following month (American Academy of Pediatrics 2011). A recent Cochrane Review concluded that there are no high-quality studies to support or refute the role of EEG, or the timing of EEG, after complex febrile seizures (Shah et al 2014). Abnormalities (most often focal slowing) are reported to occur in 45% of EEGs recorded for research purposes in the first 3 days after febrile status epilepticus (Nordli et al 2012). However, because abnormal EEGs do not reliably predict the development of epilepsy or recurrent febrile seizures, a routine EEG is not typically helpful in the clinical setting. Furthermore, in children with complex febrile seizures, EEG studies have not been predictive of the development of epilepsy (Joshi et al 2005).

In This Article

Introduction
Historical note and nomenclature
Clinical manifestations
Etiology
Pathogenesis and pathophysiology
Epidemiology
Prevention
Differential diagnosis
Diagnostic workup
Prognosis and complications
Management
References cited
Contributors