Objective: To characterize the causes and treatment of facial nerve paresis (FNP) in pediatric patients.
Method: Retrospective study in a tertiary care pediatric hospital. Thirty-four patients identified with partial or complete FNP evaluated between 1997 and 2003. A review of the medical records including sex, age, laterality, etiology, therapy, severity of paralysis according to House-Brackman (HB) six-point grading scale, duration, and degree of recovery.
Results: Thirty-five cases of FNP. Causes of FNP were infectious (13), traumatic (7), iatrogenic (5), congenital (4), Bell's/Idiopathic (3), relapsing (2) and neoplastic (1). Peak age distributions for both infectious and traumatic etiologies were bimodal: 1-3 and 8-12 years. Of the 13 infectious cases, 11 were associated with acute otitis media with effusion (AOME). Four (4/11) were bacterial-culture negative. Seven (7/11) were bacterial-culture positive, four (4/7) of which required prolonged, broth-medium culture. Bacteria cultured predominantly included Staphylococcus non-aureus species (5/7) and Propionobacterium acnes (3/7). One (1/13) was viral culture positive (Herpes Simplex Virus). All six patients who received intravenous steroids for OME-associated FNP received the doses within the first week of presentation and had complete recovery (HB I/VI); three of five patients who did not receive steroids had complete recovery. There were five iatrogenic cases; two (2/5) were planned surgical sacrifices and three (3/5) were complications of middle ear/mastoid surgery. Facial nerve function associated with infection returned in 0.5-2 months while, when associated with trauma, returned in 0.25-30 months.
Conclusions: In infectious or traumatic FNP, children aged 1-3 and 8-12 years are the primary groups involved. In AOME FNP, culture-identified organisms may not be representative of traditional pathogens. Infectious FNP averaged 1 month for recovery while traumatic FNP averaged 9 months. Intravenous steroid therapy may improve the outcome. Recovery was complete (HB I/VI) in 8/10 infectious and 4/6 traumatic cases.