LAUSR

We present a novel presentation of Horner syndrome (HS) in a child after button battery (BB) ingestion (BBI). The BB impacted in the cervical oesophagus disrupting the ipsilateral sympathetic chain. Acute presentation of HS may include ptosis, miosis and facial anhidrosis. A 1-year-old boy, with no medical or family history, attended with a 4-week history of sore throat, pyrexia, reduced intake, vomiting and a presumed swollen left upper eyelid, despite initial treatment with coamoxiclav for likely tonsillitis and chloramphenicol to the left eye. Clinical assessment revealed persistent pyrexia, a left eye 3 mm ptosis with miosis but tolerating solid food. Pharmacological testing for HS with apraclonidine 1% caused a resolution of the ptosis and miosis after 20 min, confirming an HS (Fig. 1a, b). A chest X-ray revealed a 23 mm BB lodged in the oesophagus at the level of the lower cervical spine (Fig. 2a, b). Rigid oesophagoscopy revealed the BB lodged in the oesophageal wall with circumferential white scarring noted after removal. Post-operative thoracic computer tomography (CT) scan demonstrated para-oesophageal air, consistent with a perforation (Fig. 2c). This was managed conservatively—nil by mouth, nasogastric feeding and intravenous co-amoxiclav. After 10 months, the HS has completely resolved (Fig. 1c). Aetiologies of HS in a paediatric population are summarised in Table 1. In children with acute dysphagia, unwitnessed foreign-body ingestion must be considered. Investigation of BBI with MRI could be catastrophic due to magnetism of BB. In five case series of 90 acquired Fig. 1 a Before application of apraclonidine 1%. Miosis left eye and partial ptosis. b Twenty minute post apraclonidine 1% instillation to both eyes. Reversal of ptosis, and mydriasis of left eye. c 10 months after initial presentation.