Impact of T3 thoracoscopic sympathectomy on pupillary function: a cause of partial Horner's syndrome?

Background: Thoracoscopic bilateral sympathicolysis of the T3 sympathetic ganglia is an effective treatment for palmar hyperhidrosis, though not without potential complications and consequences such as Horner's syndrome. The objective of our study is to evaluate the repercussion of T3 sympathetic denervation on pupillary tone in patients with primary hyperhidrosis.

Methods: A prospective descriptive study of 25 patients (50 pupils) ranging in age from 18 to 40 years with an indication of T3 sympathectomy for palmar hyperhidrosis or palmar-plantar hyperhidrosis from 1 December 2009 to 31 December 2010 was carried out. We excluded all patients with previous eye surgery or other ocular pathologies and those with pathologies that contraindicate denervation surgery and ocular study. All patients were evaluated before surgery and at 24 h and 1 month after sympathetic denervation. Pupil/iris (P/I) ratio was measured before and after instillation of sympathicomimetic eye drops containing 1% apraclonidine.

Results: No statistically significant differences were found when we compared the preoperative P/I ratio of the left eyes versus the right eyes (P = 0.917). We found statistically significant differences (P < 0.001) between the preoperative P/I ratio [0.40 mm (standard deviation, SD 0.07 mm)] and the postoperative basal ratio [0.33 (SD 0.05)] at 24 h. The P/I ratio at 24 h increased from 0.33 to 0.36 (SD 0.09), a nonsignificant increase (P = 0.45), after instillation of medicated eye drops. No differences were observed between the preoperative [0.40 (SD 0.07)] and 1-month basal values [0.38 (SD 0.07)], and instillation of apraclonidine no longer induced a hypersensitivity response.

Conclusions: T3 sympathectomy leads to subclinical pupillary dysfunction with a tendency for miosis, even though this impairment is not generally evident on standard physical examination or reported by patients. This subclinical dysfunction may be caused by injury to an undefined group of presympathetic nerve cell axons in caudocranial direction that communicate with the cervical sympathetic ganglia and whose function is mydriatic pupillary innervation.