Opinion
Febrile convulsions in children WE READ with interest the article Understanding the pathophysiology behind febrile convulsions by Rebecca Innes (2015), published in the March issue of Nursing Children and Young People. The effort made by the author to explain the pathophysiology behind one of the most commonly encountered pathologies in childhood is commendable. Lots of myths exist among parents and health professionals about febrile convulsions in children because there remains an often-unfounded fear about serious brain damage and death. This, in turn, can lead to a ‘fever phobia’ among parents and, to a certain extent, healthcare professionals, leading to the overuse of antipyretics to control fever. The trend of using combination antipyretics is common in children (Paul et al 2015), however, is not in line with National Institute for Health and Care Excellence (NICE) (2013) guidelines. The author correctly highlights the physiological benefits of pyrexia: allowing more efficient immune responses and tissue repair, slowing down of viral replication and bacterial multiplication (Innes 2015). In trying to describe the pathophysiology of febrile convulsion, which remains largely unexplained, the author has outlined the pathophysiology of fever rather than febrile convulsion. This, in turn, runs the risk of creating uncertainty and confusion among readers who can misinterpret other serious conditions as febrile convulsion. Table 1
Siba Paul and colleagues comment on the pathophysiology and risk factors, in response to an article published this year Our response to the article by Innes should be considered as a source of additional information about febrile convulsion, which we think readers ought to be clear about. The first aspect that needs clarification is that the source of febrile illness in febrile convulsion is extracranial in origin (with no evidence of electrolyte imbalance). A febrile child with meningitis who has a convulsion during the illness cannot be classed as having a febrile convulsion. While the author mentions a simple febrile convulsion, she does not go on to classify types of febrile convulsion as simple and complex (Paul and Chinthapalli 2013). This is important, because the management of a child presenting with a simple febrile convulsion will be different from that of one having a complex febrile convulsion, as the latter may require admission and subsequent investigations (Paul et al 2015). Table 1 shows the features of the two types of febrile convulsions. Pathophysiology Little is known about the pathophysiology, but preliminary studies in children seem to support the hypothesis that the cytokine network is activated in fever and may have a role in the pathogenesis
Types of febrile convulsion
Simple febrile convulsion
Complex febrile convulsion
■ Evidence of generalised tonic-clonic seizure activity without focal features lasting less than ten minutes ■ Resolve spontaneously ■ Do not recur in the next 24 hours
■ Duration of febrile convulsion lasts more than ten minutes ■ Child may have two or more seizures in 24 hours ■ Child may not regain full consciousness within one hour after seizure terminated ■ Brief period of paralysis after the seizure (Todd’s paresis) ■ Presence of focal features, such as convulsion in one side of the body
14 June 2015 | Volume 27 | Number 5
of febrile convulsion in children (Tejani 2014, Innes 2015). Innes (2015) mentions that the most common background to febrile convulsion is immaturity of a child’s physiological reaction to infection. However, if that were true, febrile convulsions would be most common shortly after birth and the incidence would decline with increasing age. The peak age of onset of febrile convulsion is 18 months, with up to 50% of children having a first episode at between 12 and 30 months of age (Oluwabusi and Sood 2012). The truth is that the pathophysiology remains largely unexplained and trying to oversimplify the explanation could cause confusion among readers. Inheritance is largely considered to be polygenic; however, a small number of families have been identified with an autosomal dominant pattern of febrile convulsion inheritance, leading to the description of a ‘febrile seizure susceptibility trait’ (Tejani 2014, Paul et al 2015). Underlying mutations have been found in genes encoding the sodium channel and the gamma amino-butyric acid A receptor, which may partly explain the molecular mechanism of febrile convulsion in children. However, these tests are at an experimental stage and not available for routine clinical use (Paul and Chinthapalli 2013, Tejani 2014). Innes (2015) tries to explain different temperature levels above which neurological damage can occur, suggesting that an unregulated temperature will cause a greater risk for febrile convulsion. This can easily be misinterpreted by healthcare professionals, increase further fever phobia and may lead to the overuse of antipyretic medications. This is not in line with NICE guidelines (2013), which state that antipyretics do not prevent febrile convulsion and that a child’s response to antipyretic drugs NURSING CHILDREN AND YOUNG PEOPLE
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should not be used as an indication of the severity of illness. In the concluding section, Innes (2015) suggests that managing febrile convulsion involves prompt recognition, administration of antipyretic medication, other cooling strategies and careful monitoring. However, the rationale behind antipyretic administration – which is to alleviate the distress of the child which may, in turn, lead to better hydration (NICE 2013) – is not explained in the article. In a small number of complex febrile convulsion cases there may be a need for anticonvulsant medications, such as benzodiazepines. An algorithm for managing convulsive seizure is recommended by NICE CG137 (2012). Long-term outcome Two aspects of prognosis that Innes (2015) leaves uncovered and what most parents remain worried about are the risk of recurrence and developing epilepsy in later life. It is important to explain that about one third of children will go on to have further febrile convulsion during subsequent febrile episodes (Paul et al 2015). The risk factors for recurrence include: onset of first convulsion aged
Febrile convulsions in children WE READ with interest the article Understanding the pathophysiology behind febrile convulsions by Rebecca Innes (2015), published in the March issue of Nursing Children and Young People. The effort made by the author to explain the pathophysiology behind one of the most commonly encountered pathologies in childhood is commendable. Lots of myths exist among parents and health professionals about febrile convulsions in children because there remains an often-unfounded fear about serious brain damage and death. This, in turn, can lead to a ‘fever phobia’ among parents and, to a certain extent, healthcare professionals, leading to the overuse of antipyretics to control fever. The trend of using combination antipyretics is common in children (Paul et al 2015), however, is not in line with National Institute for Health and Care Excellence (NICE) (2013) guidelines. The author correctly highlights the physiological benefits of pyrexia: allowing more efficient immune responses and tissue repair, slowing down of viral replication and bacterial multiplication (Innes 2015). In trying to describe the pathophysiology of febrile convulsion, which remains largely unexplained, the author has outlined the pathophysiology of fever rather than febrile convulsion. This, in turn, runs the risk of creating uncertainty and confusion among readers who can misinterpret other serious conditions as febrile convulsion. Table 1
Siba Paul and colleagues comment on the pathophysiology and risk factors, in response to an article published this year Our response to the article by Innes should be considered as a source of additional information about febrile convulsion, which we think readers ought to be clear about. The first aspect that needs clarification is that the source of febrile illness in febrile convulsion is extracranial in origin (with no evidence of electrolyte imbalance). A febrile child with meningitis who has a convulsion during the illness cannot be classed as having a febrile convulsion. While the author mentions a simple febrile convulsion, she does not go on to classify types of febrile convulsion as simple and complex (Paul and Chinthapalli 2013). This is important, because the management of a child presenting with a simple febrile convulsion will be different from that of one having a complex febrile convulsion, as the latter may require admission and subsequent investigations (Paul et al 2015). Table 1 shows the features of the two types of febrile convulsions. Pathophysiology Little is known about the pathophysiology, but preliminary studies in children seem to support the hypothesis that the cytokine network is activated in fever and may have a role in the pathogenesis
Types of febrile convulsion
Simple febrile convulsion
Complex febrile convulsion
■ Evidence of generalised tonic-clonic seizure activity without focal features lasting less than ten minutes ■ Resolve spontaneously ■ Do not recur in the next 24 hours
■ Duration of febrile convulsion lasts more than ten minutes ■ Child may have two or more seizures in 24 hours ■ Child may not regain full consciousness within one hour after seizure terminated ■ Brief period of paralysis after the seizure (Todd’s paresis) ■ Presence of focal features, such as convulsion in one side of the body
14 June 2015 | Volume 27 | Number 5
of febrile convulsion in children (Tejani 2014, Innes 2015). Innes (2015) mentions that the most common background to febrile convulsion is immaturity of a child’s physiological reaction to infection. However, if that were true, febrile convulsions would be most common shortly after birth and the incidence would decline with increasing age. The peak age of onset of febrile convulsion is 18 months, with up to 50% of children having a first episode at between 12 and 30 months of age (Oluwabusi and Sood 2012). The truth is that the pathophysiology remains largely unexplained and trying to oversimplify the explanation could cause confusion among readers. Inheritance is largely considered to be polygenic; however, a small number of families have been identified with an autosomal dominant pattern of febrile convulsion inheritance, leading to the description of a ‘febrile seizure susceptibility trait’ (Tejani 2014, Paul et al 2015). Underlying mutations have been found in genes encoding the sodium channel and the gamma amino-butyric acid A receptor, which may partly explain the molecular mechanism of febrile convulsion in children. However, these tests are at an experimental stage and not available for routine clinical use (Paul and Chinthapalli 2013, Tejani 2014). Innes (2015) tries to explain different temperature levels above which neurological damage can occur, suggesting that an unregulated temperature will cause a greater risk for febrile convulsion. This can easily be misinterpreted by healthcare professionals, increase further fever phobia and may lead to the overuse of antipyretic medications. This is not in line with NICE guidelines (2013), which state that antipyretics do not prevent febrile convulsion and that a child’s response to antipyretic drugs NURSING CHILDREN AND YOUNG PEOPLE
Downloaded from RCNi.com by ${individualUser.displayName} on Jan 31, 2016. For personal use only. No other uses without permission. Copyright © 2016 RCNi Ltd. All rights reserved.
should not be used as an indication of the severity of illness. In the concluding section, Innes (2015) suggests that managing febrile convulsion involves prompt recognition, administration of antipyretic medication, other cooling strategies and careful monitoring. However, the rationale behind antipyretic administration – which is to alleviate the distress of the child which may, in turn, lead to better hydration (NICE 2013) – is not explained in the article. In a small number of complex febrile convulsion cases there may be a need for anticonvulsant medications, such as benzodiazepines. An algorithm for managing convulsive seizure is recommended by NICE CG137 (2012). Long-term outcome Two aspects of prognosis that Innes (2015) leaves uncovered and what most parents remain worried about are the risk of recurrence and developing epilepsy in later life. It is important to explain that about one third of children will go on to have further febrile convulsion during subsequent febrile episodes (Paul et al 2015). The risk factors for recurrence include: onset of first convulsion aged
