PEDIATRICS Vol. 122 No. 5 November 2008, pp. e1080-e1085 (doi:10.1542/peds.2008-1273)
ARTICLE |
Clinical Predictors of Lyme Disease Among Children With a Peripheral Facial Palsy at an Emergency Department in a Lyme Disease–Endemic Area
Division of Emergency Medicine, Children's Hospital Boston, Boston, Massachusetts
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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INTRODUCTION. Although Lyme disease can cause peripheral facial palsy in Lyme disease–endemic areas, diagnostic predictors in children have not been described.
OBJECTIVE. Our goal was to determine clinical predictors of Lyme disease as the etiology of peripheral facial palsy in children presenting to an emergency department in a Lyme disease–endemic area.
METHODS. We reviewed all available electronic medical charts of children 
20 years old with peripheral facial palsy who were evaluated in the emergency department of a tertiary care pediatric center from 1995 to 2007. We used the Centers for Disease Control Lyme disease definition: presence of erythema migrans lesion or serologic evidence of infection with Borrelia burgdorferi. We performed binary logistic regression with bootstrapping validation to determine independent clinical predictors of Lyme disease.
RESULTS. We identified 313 patients with peripheral facial palsy evaluated for Lyme disease. The mean age was 10.7 years, and 52% were male. Of these, 106 (34%) had Lyme disease facial palsy. After adjusting for year of study, the following were independently associated with Lyme disease facial palsy: onset of symptoms during peak Lyme disease season (June to October), absence of previous herpetic lesions, presence of fever, and history of headache. In the subset of patients without meningitis, both onset of symptoms during Lyme disease season and presence of headache remained significant independent predictors.
CONCLUSIONS. Lyme disease is a frequent cause of facial palsy in children living in an endemic region. Serologic testing and empiric antibiotics should be strongly considered, especially when children present during peak Lyme disease season or with a headache.
Key Words: Lyme disease • facial palsy
Abbreviations: ED—emergency department • CI—confidence interval • CSF—cerebrospinal fluid • aOR—adjusted odds ratio
Acquired unilateral facial weakness is most commonly because of paralysis of the peripheral facial nerve. Central causes, although rare in children, must be considered when a patient presents with sparing of the forehead musculature.1 Historically, the most commonly identified cause of an acquired peripheral facial palsy in children has been otitis media (often without mastoiditis).2 However, over the past several decades the prevalence of Borrelia burgdorferi infections has increased significantly.3 In endemic areas, such as the Northeastern United States, Lyme disease has become the most commonly identified cause of acquired facial palsy,2,4–7 especially among children.8
At the time of initial presentation, the etiology of a peripheral facial palsy will not be identifiable in most cases. Confirmatory serology to document B burgdorferi infection requires 3 to 5 days at most clinical laboratories. Lyme disease serology is a 2-tiered test: enzyme-linked immunosorbent assay screening with Western Blot confirmation. However, the appropriate therapy depends on the etiology. For Lyme disease facial palsy, initiation of antibiotic therapy is indicated,9 whereas for Bell's palsy, timely corticosteroid therapy improves time to resolution of symptoms.10 The clinician first treating a child with facial palsy must decide whether to initiate empiric therapy with antibiotics, steroids, or both without the availability of Lyme disease test results.
If children with Lyme disease facial palsy could be identified at the time of initial evaluation, diagnostic testing and therapeutic management could be optimized. We sought to identify independent predictors of Lyme disease facial palsy in children. We assembled a retrospective cohort of all children presenting to a single emergency department (ED) over a 12-year period with acquired peripheral facial palsy.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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Study Design
We performed a retrospective cohort study of all children
20 years of age who presented to the ED of a single large urban pediatric tertiary care center located in a Lyme disease–endemic area during a 12-year study period (October 1, 1995, to September 30, 2007). Case identification was conducted in 2 phases. First, for the initial screening, we created a computer-assisted key word screening tool called regular-expression matching.11 This technique provides a more comprehensive and inclusive search than key word searching by including misspelled and mistyped variations. The output of the search tool was further refined by manual medical chart review.
We included children who had peripheral facial nerve (cranial nerve VII) palsy. Patients with sparing of the forehead musculature had central facial nerve palsy and were not included in the study. If a patient had multiple ED visits to the study institution for the same episode of facial palsy, only the first visit was considered. We excluded patients for the following reasons: congenital facial palsy, known central nervous system malignancy, surgery in the area of the facial nerve within 1 week of ED presentation, Todd's paralysis, or more generalized paralysis including hemiparesis.
The complete hospital medical charts of all study patients were retrospectively reviewed (by Drs Nigrovic or Thompson) to determine patient demographics, date of presentation, onset and duration of symptoms, potential exposures (known tick bite or previous herpetic lesions), and clinical characteristics (fever, headache, muscle aches, joint pains, or rash). We defined the Lyme disease season as onset of symptoms between June and October. Laboratory databases were reviewed to determine serology results (for Lyme disease, Ebstein-Barr virus, and herpes simplex virus) and lumbar puncture results, if performed. Type and duration of medical treatment (including antibiotics and steroid treatment) initiated during the ED visit were also recorded.
Lyme Disease Definition
We defined a case of Lyme disease facial palsy if the study patient met the Centers for Disease Control and Prevention definition of Lyme disease: presence of an erythema migrans lesion or serologic evidence of infection with B burgdorferi.12 We considered patients to have positive results only if the Western blot were positive using the reference laboratory definitions. Serologic testing for B burgdorferi was performed by offsite commercial laboratories: ARUP (Salt Lake City, UT) and Immugen (Norwood, MA). Patients with a positive enzyme-linked immunosorbent assay and negative or absent Western blot were not considered to have Lyme disease.13
Statistical Analysis
We sought to identify predictors of Lyme disease as a cause of facial palsy within the subset of patients evaluated for Lyme disease. Patients evaluated for Lyme disease either had an erythema migrans lesion or Lyme disease serology sent. We performed univariate analysis using 
2 analysis (categorical predictors) and Mann-Whitney U test (continuous predictors). An independent physician (Dr Fine) reviewed a random selection of 8% of the medical charts of those patients evaluated for Lyme disease to assess interrater reliability. For each candidate predictor, we then calculated both the percentage agreement and 
statistic. We included predictor variables with at least moderate agreement (lower bound of the 95% confidence interval [CI] for the statistic > 0.4)]14 in the multivariable analysis.
We performed backward stepwise multivariate logistic regression to determine the relationship between a priori candidate predictors and Lyme disease as a cause of the child's facial palsy. Given the observed trends in both Lyme disease incidence and in frequency of serologic testing,3,15–17 we adjusted all of our analyses for year of presentation. Because of the association between cerebrospinal fluid (CSF) pleocytosis and Lyme disease facial palsy, we repeated the multivariate analysis in the subgroup of patients without meningitis (defined as either CSF pleocytosis [CSF white blood cell count < 10 cells per mm3]18 or no lumbar puncture performed because the treating physician had no clinical suspicion for meningitis). Only patients with complete data on all candidate predictors were included in the multivariable analysis.
To validate the selection of predictors for both the main and subgroup analyses, we performed boot-strapping resampling methods, with 1000 iterations of the multivariate analysis. Predictors that remained significant in >50% of analyses were retained.19,20
For all analyses, we used the Statistical Program for the Social Sciences.21 The study was approved by the institutional review board of the study institution.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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During the 12-year study period, there were 609 671 ED visits for children
20 years of age. We identified a cohort of 420 children with facial palsy who met the study criteria (0.07% of ED visits). Of these, 141 children (34% of patients with facial palsy) had an etiology for their facial palsy identified using laboratory tests obtained during their ED evaluation: 106 (75%) Lyme disease, 30 (21%) otitis or mastoiditis, and 5 (4%) facial nerve trauma. Children with no documented etiology were considered to have Bell's or idiopathic facial palsy (n = 279). The frequency of both Lyme disease testing and Lyme disease facial palsy varied significantly by month of symptom onset (Fig 1).
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Table 1 provides the clinical and laboratory characteristics of the 313 patients with facial palsy who were evaluated for Lyme disease. Of these, 106 children (34%) had Lyme disease facial palsy. Of these, the Lyme disease diagnosis was made by the presence of an erythema migrans rash (11 children [10%]), positive serologic test for Lyme disease (60 children [57%]), and an erythema migrans rash and a positive serologic test for Lyme disease (35 children [33%]). In the 46 children with erythema migrans rash, the rash preceded the onset of the facial palsy in all cases. Of the 95 patients with positive Lyme disease serologic tests, 73 (77%) patients had positive immunoglobulin M and 38 (40%) positive immunoglobulin G assays (16 patients had both positive immunoglobulin M and immunoglobulin G assays).
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A second physician repeated chart abstraction for 25 of the patients (8% of all children with facial palsy evaluated for Lyme disease). We included all candidate predictors with a
statistic of >0.414 in the multivariable analysis (Table 2). We did not include predictors in the multivariate analysis for which we were unable to calculate the statistic by standard methods.
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We identified the following independent predictors of Lyme disease facial palsy, after adjusting for year of presentation: onset of symptoms during peak Lyme disease season (June through October), headache, fever, bilateral facial palsy, and no previous history of herpetic lesions. The results of the multivariable analysis were then validated using bootstrap methodology. Four of the 5 significant predictors were selected in >50% of the bootstrap iterations (range: 79%–100%). Bilateral facial palsy was selected in only 43% of the iterations and was removed as a predictor. Table 3 provides the final multivariate analysis. In the subgroup of 267 patients without erythema migrans rash, the same 4 predictors were still associated with Lyme disease facial palsy (results not shown). Table 4 demonstrates the risk of Lyme disease facial palsy with 1, 2, or
3 high-risk Lyme disease predictors. Patients with 3 high-risk predictors had at least a 50% risk of having Lyme disease facial palsy.
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Ninety-four (30%) of the 313 children evaluated for Lyme disease underwent a lumbar puncture as part of the diagnostic evaluation. Of those, 55 children (59%) had a documented CSF pleocytosis with a CSF white blood cell count
10 cells per mm.3 Fifty-three of the patients with facial palsy and meningitis (98%) had proven Lyme disease (the other 2 patients had negative Lyme disease serology). In the subgroup analysis of 258 children with Lyme disease facial palsy without meningitis, the following remained independent predictors of Lyme disease facial palsy after adjusting for study year: onset of symptoms during the peak Lyme disease season [(adjusted odds ratio [aOR]: 3.9 [95% CI: 2.0–7.6]) and history of headache (aOR: 2.4 [95% CI: 1.1–5.2]). Both predictors were selected in >50% of the bootstrap iterations (Lyme disease season 98% and headache 74%). Overall 69 (22%) of 313 of the patients were admitted to the hospital (48% of those with Lyme disease facial palsy and 9% of other patients). Of the 104 patients with Lyme disease facial palsy and treatment information available, 98% were prescribed antibiotics (of which 64% were oral and 36% were parenteral), 14% corticosteroids, and 5% antivirals. Of the 201 study patients with Bell's palsy and treatment information available, 30% were prescribed antibiotics (of which 92% were oral and 8% parenteral), 56% corticosteroids, and 28% antivirals.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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We found that Lyme disease is a frequent cause of facial palsy in children (34% of those evaluated for the infection in our cohort). We identified an independent association between onset of symptoms during peak Lyme disease season, absence of previous herpetic lesions and presence of either headache or fever with Lyme disease facial palsy. Both onset of symptoms during Lyme disease season and presence of headache remained associated with Lyme disease in the subgroup of patients without meningitis. This model may allow prospective identification of children at high and low risk of Lyme disease facial palsy using clinical predictors available at the time of initial presentation.
The prevalence of Lyme disease among patients with facial palsy varies widely between published series. In several published adult studies, the prevalence of Lyme disease facial palsy has ranged from 2% to 25% depending on the geographic region and the population studied.6,8,22–26 However, the prevalence of Lyme disease facial palsy in children with facial palsy seems to be considerably higher. In 2 Scandinavian studies and 1 study from Delaware, the incidence ranged from 50% to 65%.2,5,7 The prevalence of Lyme disease among patients with facial palsy in our cohort was somewhat lower than these pediatric series, but may be more representative of the typical distribution of children evaluated in the emergency department for facial palsy. Importantly, the actual Lyme disease prevalence in our cohort may actually be lower than we reported because one third of our study patients did not have results of Lyme disease serology available. In the Scandinavian studies, only hospitalized children were included,5,7 whereas the Delaware study consisted of patients, living in a hyperendemic Lyme disease region referred to an otolaryngologist.2
One previous group of Finnish investigators identified independent risk factors of Lyme disease facial palsy using a prospective cohort of 503 patients with facial palsy.22 They identified the following independent predictors of Lyme disease: presentation during the summer season and presence of enlarged cervical lymph nodes and joint pains. Presentation during Lyme disease season is an independent clinical predictor in both studies. However, our study differs from the Finnish study in several important ways. First, our study included much younger patients (mean: 11 vs 46 years old). Second, we used the Center for Disease Control and Preventions case definition for Lyme disease, whereas the Finish investigators defined children with CSF pleocytosis alone as having Lyme disease facial palsy. However, pleocytosis has been found in facial palsy patients without Lyme disease.27 Third, we only included candidate predictors with high interrater reliability. Fourth, our study included a larger number of patients with Lyme disease facial palsy (106 vs 11 patients), allowing additional candidate predictors to be evaluated in the multivariate analysis, as well as bootstrap validation.
Only a small minority of facial palsy cases are bilateral. Although unilateral facial palsy is commonly idiopathic, the majority of bilateral facial palsy cases have an identifiable cause.28–31 The association of bilateral facial palsy and Lyme disease has been previously recognized.22,32 In our multivariate analysis, bilateral facial palsy was an independent predictor of Lyme disease. Because the predictor was not validated by bootstrap methods (selected in less than half of the 1000 iterations), we did not include bilateral facial palsy in our final multivariate analysis. However, bilateral facial palsy might be selected as a predictor of Lyme disease facial palsy in a larger size cohort or with an independent external validation. Clinicians treating patients with bilateral facial palsy should strongly consider obtaining diagnostic testing for Lyme disease.
The optimal treatment for a patient with facial palsy depends on the etiology which is often unknown at the time of initial patient presentation. For Lyme disease facial palsy, infectious disease experts recommend antibiotic therapy (although considerable controversy still exists as to the need for oral versus parenteral antibiotic therapy).9 For Bell's palsy, both corticosteroids and antivirals have been suggested as possible treatments although insufficient evidence had existed to conclusively demonstrate the efficacy of either therapy.33,34 A recent randomized placebo-controlled, multifactorial trial compared both prednisone and acyclovir to placebo for the treatment of adults with Bell's palsy who presented within 72 hours of symptom onset.10 Of note, the study was conducted in Scotland where B burgorferi is not endemic and, therefore, no patients with Lyme disease were included (F.M. Sullivan, PhD, written communication, 2007). The recovery of facial nerve function at 3 months was significantly better for patients treated with prednisone versus placebo but identical for acyclovir versus placebo. These results, however, may not be generalizable to regions with endemic Lyme disease.
The application of our multivariate prediction model has the potential to improve the quality of care for children with facial palsy living in Lyme disease–endemic areas. Patients with otitis media or local trauma causing their facial palsy will readily be identified by clinical history and physical examination. Otherwise, children with 1 high-risk predictor for Lyme disease facial palsy should have a Lyme disease titer sent with strong consideration for the initiation of an empiric antibiotic. Corticosteroids should be considered for children with no high-risk Lyme disease predictors. In our cohort, although most patients with Lyme disease facial palsy were started on antibiotics, so were a significant proportion of those patients with Bell's palsy. Corticosteroids were also given to a substantial minority of Lyme disease facial palsy cases and only half of those with Bell's palsy. This misallocation of treatment modalities suggests that prospective application of this predictive model has the potential to improve allocation of empiric therapies for children with facial palsy.
Our study has several important limitations. First, the study was retrospective and the predictors were assessed by medical chart review. We attempted to minimize this potential bias by selecting objective parameters that would be recorded accurately in the medical chart. We also had a second chart abstractor review a proportion of the records and we selected candidate predictors with good interrater reliability. Second, patients with positive Lyme disease serologic tests may have had a previous infection but Lyme disease may not have caused the acute facial palsy. We were unable to correct for this type of misclassification, and clinically felt that this occurred very rarely. Third, we may not have identified all the children with Lyme disease facial palsy. Not all patients with facial palsy had a Lyme disease test performed (or had a test results available from review of the hospital medical chart). However, the clinical characteristics of the untested patients are similar to those with Bell's palsy making it unlikely that a significant number of these patients had unrecognized Lyme disease facial palsy (data not shown).
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CONCLUSIONS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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We identified a large retrospective cohort of children with facial palsy evaluated in the ED of a single center in a Lyme disease–endemic region over a 12-year period. We identified 4 high-risk clinical predictors, which, if present, significantly increase the likelihood of Lyme disease facial palsy: presentation during peak Lyme disease season, no previous herpetic lesions, fever, and headache. Patients at risk for Lyme disease facial palsy should be strongly considered for Lyme disease serology and empiric antibiotic therapy. This multivariate predictive model has the potential to improve the clinical care of children from Lyme disease–endemic regions who develop peripheral facial palsy.
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ACKNOWLEDGMENTS |
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We thank Allen Steere, MD, for critical review of the manuscript. We also acknowledge David Hummel, MSc, for assistance with the computer code for the text search tool and Patrick Johnston, MMath, for assistance with calculation of the
statistic. |
FOOTNOTES |
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Accepted Jul 7, 2008.
Address correspondence to Lise E. Nigrovic, MD, MPH, Children's Hospital Boston, Division of Emergency Medicine, 300 Longwood Ave, Boston, MA 02115. E-mail: lise.nigrovic{at}childrens.harvard.edu
The authors have indicated they have no financial relationships relevant to this article to disclose.
| What's Known on This Subject In endemic areas, Lyme disease has become the most commonly identified cause of acquired peripheral facial palsy, especially among children. Although diagnostic test results for Lyme disease take many days, treating clinicians must make immediate therapeutic decisions for a child with facial palsy.
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| What This Study Adds
Using our large retrospective cohort of children with peripheral facial palsy, we identified high-risk clinical predictors that, if present, significantly increase the likelihood of Lyme disease facial palsy. Patients with
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PEDIATRICS (ISSN 1098-4275). ©2008 by the American Academy of Pediatrics
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